Metabolic safety of growth hormone in type 1 diabetes and idiopathic growth hormone deficiency. - PubMed - NCBI J Pediatr. 2013 Oct;163(4):1095-8.e4. doi: 10.1016/j.jpeds.2013.04.045. Epub 2013 Jun 6. Metabolic safety of growth hormone in type 1 diabetes and idiopathic growth hormone deficiency. 1Division of Pediatric Endocrinology, Department of Pediatrics, Technical University München, Munich, Germany. Electronic address: Walter.Bonfig@lrz.tum.de. Abstract To evaluate metabolic consequences of growth hormone (GH) treatment in children with type 1 diabetes. STUDY DESIGN: This study is an analysis of metabolic changes in 37 patients with childhood-onset GH deficiency and type 1 diabetes, documented in the Diabetes Patienten Verlaufsdocumentationsystem database. Main outcome measures were changes in hemoglobin A1c and daily insulin requirements during GH therapy in children with GH deficiency and type 1 diabetes compared with a large cohort of adolescents with type 1 diabetes.

RESULTS: Thirty-seven patients with type 1 diabetes and a diagnosis of idiopathic GH deficiency after onset of diabetes were compared with 48856 patients with type 1 diabetes. After adjustment for age, sex, duration of diabetes, and migration background, a significant difference in mean daily insulin requirement was seen between the 2 groups (1.0 IU/kg/day in subjects with GH deficiency and type 1 diabetes vs 0.85 IU/kg/day in controls; P < .01) and height-SDS (-2.0 in subjects with GH deficiency and diabetes vs +0.03 in controls; P < .0001). There was no significant between-group difference in hemoglobin A1 concentration, however (8.1% ± 1.4% in patients with GH deficiency and type 1 diabetes vs 8.2% ± 1.7% in those with type 1 diabetes only; P > .05). CONCLUSION: An increased daily insulin requirement should be considered in patients with type 1 diabetes treated with GH. With adequate adaptation of insulin dosage, metabolic control is not impaired during GH treatment. Copyright © 2013 Mosby, Inc. All rights reserved.

KEYWORDS: DPV; Diabetes Patienten Verlaufsdocumentationsystem; GH; Growth hormone; H-SDS; HbA1c; Height-SDS; Hemoglobin A1c; IGF; Insulin-like growth factor PMID: The effect of growth hormone (GH) replacement therapy in adult patients with type 1 diabetes mellitus and GH deficiency. - PubMed - NCBI The effect of growth hormone (GH) replacement therapy in adult patients with type 1 diabetes mellitus and GH deficiency. 1Department of Medicine, King's College London, St Thomas' Hospital Campus, London SE1 7EH, UK. emanuel.christ@insel.ch Abstract OBJECTIVES: Specific problems in patients with insulin-dependent diabetes mellitus (IDDM) and GH deficiency are hypoglycaemic attacks, increased insulin sensitivity and loss of energy. These problems may be related to GH deficiency.

PATIENTS: GH replacement was initiated in five patients with type 1 diabetes mellitus and GH deficiency for 6 months [four males and one female, mean age 41.6 +/- 3.8 years, mean +/- standard error of the mean (SEM); body mass index (BMI) 22.3 +/- 1.2 kg/m2]. METHODS: Body composition (bioimpedance), metabolic control [haemoglobin A1C (HbA1C)], insulin requirement and frequency of hypoglycaemia were measured, and quality of life was assessed using validated questionnaires. Monthly eye photographs were taken. RESULTS: IGF-I concentrations were below the age-adjusted range at baseline and increased significantly following GH replacement therapy [analysis of variance (ANOVA), P < 0.05]. Diabetes control as assessed by HbA1C remained stable (8.2 +/- 0.2 vs. 8.0 +/- 0.4), but needed a 1.75-fold increase in insulin dose/day. Lean body mass tended to increase (P = 0.07) and body fat mass decreased significantly (P > 0.01).

Number of severe hypoglycaemic (< 3 mmol/l) attacks decreased significantly (P < 0.04) and quality of life assessed by validated questionnaires improved significantly in all patients [Psychological and General Well-Being Schedule (PGWBS), P < 0.04; Nottingham Health Profile (NHP), P < 0.05]. Monthly eye photographs revealed no changes in the retina in any patients. CONCLUSION: GH replacement therapy has a beneficial effect at the dose used. It restores body composition and decreases frequency and severity of hypoglycaemic episodes, thus improving quality of life. Long-term trials are needed to determine the safety of GH replacement therapy in these patients. PMID: You & Your Hormones | Endocrine conditions | Diabetes mellitus You & Your Hormones Email article to a friend | Last updated: February 19, 2015 Diabetes mellitus is a very common disorder caused by high levels of sugar in the bloodstream. It affects a large number of people, with many more people remaining undiagnosed. Type 1 diabetes: the pancreas (upper centre) cannot make insulin as the insulin-producing cells have been destroyed by the body's immune system.

Therefore, sugar (white) cannot be stored as glycogen in muscle (lower left) and fat cells (lower right). Alternative names for diabetes mellitus Diabetes; type 2 diabetes; type 1 diabetes; sugar diabetes; T2DM, T1DM; insulin -dependent diabetes mellitus; IDDM; juvenile-onset diabetes. What is diabetes mellitus? Diabetes mellitus is a condition in which the body does not produce enough of the hormone insulin, resulting in high levels of sugar in the bloodstream. There are many different types of diabetes; the most common are type 1 and type 2 diabetes which are covered in this article. Gestational diabetes occurs during the second half of pregnancy and is covered in a separate article. Diabetes mellitus is linked with an increased risk of heart attacks, strokes, poor blood circulation to the legs and damage to the eyes, feet and kidneys . Early diagnosis and strict control of blood sugar, blood pressure and cholesterol levels can help to prevent or delay these complications associated with diabetes. Maintaining a healthy lifestyle (regular exercise, not smoking and eating healthily) is important in reducing the risk of developing diabetes. What causes diabetes mellitus?

Insulin is a hormone produced by the beta cells within the pancreas in response to the intake of food. The role of insulin is to lower blood sugar (glucose) levels by allowing cells in the muscle, liver and fat to take up sugar from the bloodstream that has been absorbed from food and store it away as energy. In type 1 diabetes (or insulin-dependent diabetes mellitus), the insulin-producing cells are destroyed and the body is not able to produce insulin naturally. This means that sugar is not stored away but is constantly released from energy stores giving rise to high sugar levels in the blood. This in turn causes dehydration and thirst (because the high glucose ‘spills over’ into the urine and pulls water out of the body at the same time). To exacerbate the problem, because the body is not making insulin it ‘thinks’ that it is starving so does everything it can to release even more stores of energy into the bloodstream. So, if left untreated, patients become increasingly unwell, lose weight, and develop a condition called diabetic ketoacidosis, which is due to the excessive release of acidic energy stores and causes severe changes to how energy is used and stored in the body.

In ‘type 2 diabetes’ (accounting for 90% of all diabetes) the beta cells do not stop making insulin completely, but the insulin produced does not work properly so it struggles to store the sugar found in the blood. As a consequence, the pancreas has to produce more insulin to compensate for this reduction in insulin function. This is called insulin resistance and is commonly linked to obesity . This type of diabetes is seen more commonly over the age of 40 years but can occur at any age. What are the signs and symptoms of diabetes mellitus? There are a range of different symptoms in people with diabetes. They may feel thirsty, pass a large amount of urine, wake up overnight to pass urine, lose weight and have blurred vision. Patients are vulnerable to infections such as thrush and may present with this. Particularly in type 2 diabetes, patients may not be aware of their diabetes for several years and a diagnosis may only be made when they seek treatment for diabetes-related complications such as feet, eye or kidney problems. Some patients may become severely ill and be taken into hospital with an infection and/or very high blood sugar levels. How common is diabetes mellitus? Diabetes mellitus is a public health problem around the world.

As of 2010, it was estimated to affect 285 million (6.4%) of the worldwide population, with this number predicted to rise to 438 million (7.7% ) by 2030. There are a further 344 million people with pre-diabetes (at risk of developing diabetes). This number is projected to increase to 472 million by 2030. In the UK, there is estimated to be between 2 and 3 million people with diabetes. Type 2 diabetes accounts for more than 90% of all patients with diabetes. Is diabetes mellitus inherited? This depends on the type of diabetes. Type 2 diabetes, and to a lesser extent type 1 diabetes, may run in families. If a parent has diabetes, their children will not necessarily get it but they are at an increased risk. In type 2 diabetes, lifestyle factors such as being overweight (obesity) and lack of exercise can significantly increase your risk of developing diabetes. Some rarer types of diabetes mellitus may be inherited. How is diabetes mellitus diagnosed?

A urine sample is taken and tested for sugar; sugar is not normally found in urine but if blood sugar levels are high (as in diabetes), some can spill over through the kidneys and into the urine. If sugar is found in the urine, the diagnosis of diabetes can be confirmed by taking a blood sample after fasting. However, a normal fasting sugar test on its own does not exclude diabetes, as in the early stages of type 2 diabetes fasting sugar may still be normal. In this case, a specialised test called a glucose tolerance test may need to be carried out in which a patient is given a sugary drink with blood samples taken before and two hours after the drink. How is diabetes mellitus treated? The aim of treatment in diabetes is to Reduce circulating glucose to as normal a level as possible, Avoid the acute symptoms of diabetes such as thirst, and Avoid the long-term complications of diabetes such as eye, nerve and kidney damage. While glucose control is the prime aim of treatment, other factors such as blood pressure and blood cholesterol levels are also very important in the management of diabetes and the prevention of long-term health consequences. Type 1 diabetes is always treated with insulin, a life-saving treatment.

Patients will need to take medication several times a day for the rest of their lives. Patients will usually learn how to self-administer this. Insulin is usually given through injections under the skin. Patients normally require two to four injections a day. An increasing number of patients with type 1 diabetes are being treated with ‘insulin pumps’ which provide a continuous supply of insulin. Patients need to ensure that their blood glucose levels are kept as normal as possible so that delicate tissues in the body (especially blood vessels in the eyes, kidneys and peripheral nerves) are not chronically damaged by high glucose levels over a long period of time. To achieve this, patients need to measure their glucose regularly and learn how to adjust their insulin doses in order to optimise their glucose levels (diabetes control). Good diabetes control helps to minimise the risk of long-term diabetes complications, as well as short-term symptoms (such as thirst). Patients with type 2 diabetes can still make insulin, but not enough to control their glucose levels. Type 2 diabetes is therefore initially treated with a combination of lifestyle changes (diet and exercise) which reduce the need for insulin and therefore lower glucose levels.

If this is insufficient to achieve good glucose control, a range of tablets are available such as metformin, which, like diet and exercise, reduces insulin requirements, and sulphonylureas (eg gliclazide) which stimulate insulin secretion. If these measures are not effective, a range of new medications are available such as those raising the levels of incretins, natural hormones, which stimulate insulin production. In many patients, particularly after several years of treatment, insulin production is so low or so insufficient compared with the patient's needs that patients with type 2 diabetes have to be treated with insulin injections, either alone or in combination with tablets. Are there any side-effects to the treatment? Insulin treatment can cause weight gain and low blood sugar. In addition, there may be discomfort at the injection site. There are several types of tablets used to treat diabetes and they have different side-effects. The most common are diarrhoea, nausea, weight-gain and low blood sugar. Some patients may also experience some sexual dysfunction. However, not all patients will experience some or any of these side-effects and patients should discuss any concerns with their doctor. What are the longer-term implications of diabetes mellitus?

Having diabetes requires life-long treatment and follow-up by health professionals. Diabetes can be linked to damage of the eyes, kidneys and feet. It is also associated with increased risk of strokes, heart attacks and poor blood circulation to the legs. Medical care aims to minimise these risks by controlling diabetes, blood pressure and cholesterol and screening for possible complications caused by the diabetes. Maintaining a healthy lifestyle with regular exercise and a healthy diet helps with glucose control and managing diabetes in the long-term. With careful monitoring and appropriate treatment, diabetes patients can lead full and active lives. Women with diabetes who are planning to start a family should discuss this with their doctor as good glucose control is important both prior to conception and throughout pregnancy. Growth Hormone Deficiency and Type 1 Diabetes Growth Hormone Deficiency and Type 1 Diabetes Growth Hormone Deficiency and Type 1 Diabetes Treato found 16 discussions about Type 1 Diabetes and Growth Hormone Deficiency on the web. Symptoms and conditions also mentioned with Growth Hormone Deficiency in patients' discussions 183,930 discussions Diabetes means your blood glucose, or blood sugar, levels are too high. With type 1 diabetes, your pancreas does not make insulin.

Insulin is a hormone that helps glucose get into your cells to give them energy. Without insulin, too much glucose stays in your blood. Over time, high blood glucose can lead to serious problems with your heart, eyes, kidneys, nerves, and gums and teeth. Read more on MedlinePlus.gov. See more about Thank you for sharing your experience! ? Humatrope vs. Genotropin Humatrope vs. Saizen Humatrope vs. Nutropin Humatrope vs. Norditropin Humatrope vs. Tev Tropin Related Hospitals Mayo Clinic Johns Hopkins Hospital University Hospital University Medical Center Middlesex Hospital Massachusetts General Hospital Westchester Medical Center Related Searches Femara Lupron Gonal F Prozac Yasmin Treato does not review third-party posts for accuracy of any kind, including for medical diagnosis or treatments, or events in general. Treato does not provide medical advice, diagnosis or treatment. Usage of the website does not substitute professional medical advice. The side effects featured here are based on those most frequently appearing in user posts on the Internet. The manufacturer's product labeling should always be consulted for a list of side effects most frequently appearing in patients during clinical studies.

Talk to your doctor about which medications may be most appropriate for you. The information reflected here is dependent upon the correct functioning of our algorithm. From time-to-time, our system might experience bugs or glitches that affect the accuracy or correct application of mathematical algorithms. We will do our best to update the site if we are made aware of any malfunctioning or misapplication of these algorithms. We cannot guarantee results and occasional interruptions in updating may occur. Please continue to check the site for updated information. Follow us Testosterone Deficiency, Diabetes and Metabolic Syndrome | myVMC Testosterone Deficiency, Diabetes and Metabolic Syndrome Stress Introduction Testosterone is the key male hormone . It regulates a man’s libido (sex drive) and the development of secondary male sex characteristics, such as facial and body hair, the testes and the penis. Testosterone also protects the health of bone and muscle tissues. Testosterone deficiency is associated with many chronic health conditions, including type 2 diabetes mellitus and other metabolic disorders. Testosterone deficiency has been estimated to affect about 1 in 200 Australian men, although this may under-represent the true number due to not all cases being diagnosed.

In men from Boston, USA, testosterone deficiency was found to affect about 1 in 18 men aged 30–79 years, but in men aged 60–79 this increased to about 1 in 8. Significantly, there is also a strong association between testosterone deficiency and diabetes . A study in the United Kingdom found that 42% of men with type 2 diabetes also had low or borderline levels of testosterone. For more information about testosterone deficiency, see Male Hypogonadism (Primary Hypogonadism and Secondary/Hypogonadotrophic Hypogonadism) . Testosterone deficiency, diabetes and the metabolic syndrome The association between low levels of testosterone (a condition known as hypogonadism) and type 2 diabetes mellitus are well recognised, but it also appears that testosterone deficiency is common in men with diabetes regardless of type. Metabolic syndrome is a condition characterised by several co-occurring metabolic imbalances (e.g. impaired insulin metabolism, obesity , high blood pressure ); it often precedes type 2 diabetes mellitus, and is also associated with testosterone deficiency.

There is considerable evidence that men with metabolic syndrome are more likely to develop hypogonadism and vice versa. There is also a link between low testosterone levels and insulin resistance in men with type 1 diabetes . Testosterone replacement therapy has been shown to improve insulin metabolism. Testosterone and testosterone metabolism In men, testosterone is primarily produced by the Leydig cells of the testes. Testosterone production in the testes is stimulated when a man’s pituitary gland produces a hormone called luteinising hormone (LH). If either the pituitary gland or the testes are dysfunctional, testosterone production may decline or stop, leading to testosterone deficiency or hypogonadism. For more information, see Testosterone . Insulin and insulin metabolism Insulin is a hormone produced by the pancreas and functions to lower levels of glucose in the blood. If the body does not produce enough insulin, or if the insulin produced does not function properly to reduce blood glucose, levels of blood glucose rise and lead to health conditions such as metabolic syndrome and type 1 and type 2 diabetes mellitus. How does insulin resistance affect testosterone levels? Testosterone production is affected in diabetic men because they have higher than normal concentrations of glucose in their blood.

When blood glucose levels are high, the pituitary gland produces less LH than it normally would. As testosterone is only produced when LH is secreted from the pituitary, thisreduces the amount of testosterone produced by a man’s body. The association between diabetes and hypogonadism are interdependent – that is, they work both ways. Low testosterone is a risk factor for diabetes and the metabolic syndrome because testosterone levels affect body fat composition, glucose transport and the ways in which the body’s cells use testosterone. Diabetes is also a risk factor for hypogonadism because it is associated with increased body mass and altered hormone profiles (e.g. reduced LH as a result of high blood glucose levels, which in turn reduces testosterone levels). Evidence of the associations between diabetes, metabolic syndrome and testosterone deficiency Studies have reported that 20–64% of men with testosterone deficiency/hypogonadism also have type 2 diabetes. The proportion of men who have both type 2 diabetes mellitus and hypogonadism increases in older groups of men. Men who have slightly reduced testosterone concentrations (but not low enough to be considered testosterone deficient) are also more likely to have low insulin (and high blood glucose) levels.

Therapies that reduce testosterone levels (e.g. androgen deprivation therapy, which is used by men with prostate cancer because testosterone stimulates the growth of prostate cancer) have also been shown to lower insulin levels. Men with low testosterone concentrations, in addition to having lower insulin levels, are more likely to develop the metabolic syndrome or one of the metabolic imbalances that characterise it (e.g. impaired insulin metabolism, obesity, high blood pressure). Scientists have even suggested that hypogonadism should be considered one of the imbalances that characterise metabolic syndrome. Evidence shows that approximately one third of type 2 diabetics are testosterone deficient. An even greater proportion of men who are both diabetic and obese experience testosterone deficiency, and the likelihood of testosterone deficiency increases as type 2 diabetes progresses or worsens. There is also evidence of an association between insulin resistance, glucose levels, abdominal obesity and free testosterone levels in type 1 diabetic men. Abdominal obesity appears to play a particularly important role in these relationships. Abdominal obesity causes insulin resistance, which in turn reduces testosterone levels because it increases the amount of testosterone converted to oestradiol.

Increasing knowledge about the associations between testosterone deficiency and diabetes have lead to trialling testosterone replacement therapy (TRT) as a treatment for insulin resistance in diabetic men. Evidence to date shows that TRT improves insulin metabolism in hypogonadal diabetic men. For more information on TRT, see Testosterone Replacement Therapy . Diagnosing hypogonadism in men with diabetes and metabolic syndrome Despite mounting evidence of the associations between diabetes, metabolic syndrome and hypogonadism, testosterone deficiency in diabetic men may not always be diagnosed at routine visits to the doctors. There are a number of challenges doctors face when attempting to make such a diagnosis, including: Communication: For example, the man may be embarrassed to discuss symptoms of testosterone deficiency (which include reduced sex drive and loss of masculine characteristics such as a large penis and thick body hair) at a doctor’s consultation for diabetes; Focus on treating erectile dysfunction: For example, men who experience testosterone deficiency may confuse its symptoms (in particular reduced libido) with erectile dysfunction , and seek treatment for erectile dysfunction.

However, the causes of testosterone deficiency and erectile dysfunction are very different and treatment for erectile dysfunction is unlikely to improve symptoms of testosterone deficiency; Education: Men with diabetes are often unaware of the associations between hypogonadism and low testosterone levels and metabolic conditions; Focus on treating diabetes: Doctors may focus on treating diabetes and assessing and managing direct symptoms of diabetes (e.g. blood glucose levels). As consultations are often very short, this may not leave time for testosterone deficiency symptoms to be discussed; Lack of resources: There are few questionnaires available to help doctors assess testosterone deficiency in men with diabetes or metabolic syndrome; and No recommendation for universal screening of testosterone levels in diabetic men. This may mean that low testosterone is not perceived to be as important as other conditions that co-occur with diabetes (e.g. eye diseases) for which universal screening is recommended. Accurate diagnosis is further complicated because many of the symptoms of diabetes are also symptoms of testosterone deficiency. These include: Erectile dysfunction; Reduced sense of wellbeing. Screening for testosterone deficiency in men with diabetes and metabolic syndrome Men with diabetes or metabolic syndrome should therefore openly discuss any symptoms that may reflect testosterone deficiency with their doctor.

They should not be surprised if their doctor provides them with information about the associations between testosterone levels and metabolic conditions. When providing such information, the doctor is not implying that a man has testosterone deficiency or a problem with his sexual functioning. Men should not feel like their doctor is judging them or their manliness if they receive such information. Men with diabetes should also be prepared for the doctor to ask them questions about their sexual functioning. This may include asking if the man has experienced: Reduced libido; Severe hypoglycaemia (low blood sugar) with rapid onset; Papilloedema (swelling of the optic disk); Reduced sense of wellbeing. A doctor may also ask him to complete a questionnaire about testosterone deficiency symptoms to help them assess whether or not the man has testosterone deficiency. If a doctor considers testosterone deficiency to be likely, they will do a blood test to measure testosterone levels. Making such enquiries helps doctors to diagnose testosterone deficiency in a greater number of men with diabetes. This in turn enables the doctor to consider using TRT, which may improve both diabetes and testosterone deficiency.

Diagnosing diabetes and metabolic syndrome in men with symptoms of testosterone deficiency It is also important for men with testosterone deficiency to be aware that this condition often co-occurs with diabetes and metabolic syndrome. Doctors may enquire about metabolic disorders such as diabetes when men present with sexual dysfunctions which may be symptoms of testosterone deficiency. This does not mean that the doctor is not taking the sexual dysfunctions seriously. On the contrary, the doctor recognises that sexual dysfunctions may not improve in men with diabetes, unless their diabetes is also treated. Testosterone replacement therapy for men with diabetes and metabolic syndrome Testosterone is one of the oldest marketed drugs. It has been used in TRT to resolve sexual dysfunctions and other symptoms of hypogonadism in men since the 1930s. While the key goal of TRT is to restore concentrations of testosterone in the blood, there exists considerable evidence that, in addition to resolving symptoms of testosterone deficiency, TRT improves insulin metabolism and other markers of metabolic syndrome.

For example, 83% of hypogonadal men with metabolic syndrome who received combined TRT and diet and exercise intervention reversed symptoms of the condition after one year of treatment, compared to 30% of men who received a diet and exercise intervention alone.Other studies conducted amongst men with metabolic syndrome and testosterone treatment have reported reduced body mass and body fat mass, reduced body mass index (BMI), weight and waist circumference , reduced insulin sensitivity and/or improved glucose control. TRT has also been demonstrated effective in improving characteristics of type 2 diabetes.One study of TRT in hypogonadal men with type 2 diabetes showed significant reductions in fasting blood glucose and insulin sensitivity in the group treated with testosterone. These men also experienced reductions in waist circumference and waist-to-hip ratio and improvements in cholesterol levels. TRT is therefore an effective treatment option for some men with metabolic disorders and testosterone deficiency. It may be an important new avenue for improving insulin resistance and the overall cardiovascular health of these men. However, your doctor will be able to advise if it is a suitable treatment option for you.

Starting testosterone replacement therapy Some men may be reluctant to start TRT because they are afraid the treatment will negatively affect their cardiovascular health, though there is no evidence that TRT induces negative cardiovascular effects. It it is important that men with type 2 diabetes or metabolic syndrome and testosterone deficiency do not treat their testosterone deficiency in isolation. These men should also treat their metabolic disorders, and it is particularly important that they adopt a healthy lifestyle , as both type 2 diabetes and metabolic syndrome are associated with lifestyle factors such as lack of exercise and too much fat in the diet. In some cases, medicine may also be prescribed. Men with type 1 diabetes, a genetic condition which is not associated with lifestyle factors, can also use testosterone replacement therapy. Administering testosterone There are many ways by which testosterone can be administered, including orally (swallowing tablets), intramuscularly (injection into the muscle) and subdermally (absorption through the skin). Each method has its own benefits and limitations; for example, some are easier to administer than others, and some cost less. The most appropriate form of testosterone will depend on the man being treated. Your doctor can discuss suitable options with you if this treatment is applicable.

How will sexual performance change while undergoing testosterone replacement therapy? Most men experience low testosterone in mid or late life (past 40 or 50 years of age). At this point, some may not have been sexually active for a considerable time. Their bodies may have changed markedly in that period (particularly if their blood vessels have become damaged due to diabetes and other metabolic conditions), and their sexual response may also differ. For example, achieving erection or orgasm may be more difficult than at a younger age. As such, it is important for men who commence TRT to have realistic expectations, or they may feel that their treatment is ineffective and stop TRT. It is also important for men to realise that even if rapid improvements to libido and other symptoms of testosterone deficiency are experienced, it is common for men to experience a plateau effect as treatment continues. This means that the improvements will level off soon after starting. Assessing and managing lifestyle risk factors In addition to starting TRT, it is important for hypogonadal men with metabolic conditions to manage modifiable lifestyle factors, as an unhealthy lifestyle may make their metabolic conditions worse and also reduce the effectiveness of their treatment.

Lifestyle factors play an important role in the development of type 2 diabetes mellitus, metabolic syndrome and testosterone deficiency. In particular, low levels of physical activity, unhealthy eating habits (e.g. eating too much, consuming too much fat and sugar), smoking and obesity increase the risk of each of these conditions. The risk of testosterone deficiency in men with diabetes increases further if they are also obese. Men with diabetes who maintain a healthy lifestyle may prevent the onset of testosterone deficiency. Diet and exercise Increasing body mass index ( BMI ) is associated with an increased risk of hypogonadism, and is also an important risk factor for metabolic syndrome. Thus maintaining a healthy BMI is an important component of managing testosterone deficiency. Men should: This information will be collected for educational purposes, however it will remain anonymous. Alcohol, smoking and other recreational drug use Alcohol , smoking and recreational drug use also increase the risk of testosterone deficiency and metabolic disorders. Men should therefore: Reduce alcohol consumption: Both short and long term alcohol consumption has been shown in experiments performed on animals to reduce testosterone levels.

This is because it affects the function of the hypothalamus and pituitary glands, which produce hormones that regulate testosterone production; Quit smoking: Some studies have shown that smoking increases the risk of hypogonadism. Stress Work-related stress was shown in one study to be associated with an increased risk of hypogonadism, and reducing work-related stress (e.g. by finding a healthy balance between work and life ) may therefore reduce the risk of testosterone deficiency. More information For more information on testosterone deficiency in men, including testosterone tests and testosterone replacement therapy, see Testosterone Deficiency . References Allan C. Fact sheet: Diabetes and sexual and reproductive health [online]. Clayton, VIC: Andrology Australia; August 2008 [cited 23 March 2010]. Available from: URL link Rice D, Brannigan RE, Campbell RK, et al. Men’s health, low testosterone and diabetes: Individualized treatment and a multidisciplinary approach [online]. Chicago, IL: American Association of Diabetes Educators; 3 October 2008 [cited 20 March 2010]. Available from: URL link Zitzmann M.

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Testosterone replacement in hypogonadal men with type 2 diabetes and/or metabolic syndrome (the TIMES2 study). Diabetes Care. 2011;34(4):828-37. [ Abstract ] Kalinchenko SY. Tishova YQ, Mskhalaya GJ, et al. Effects of testosterone supplementation on markers of the metabolic syndrome and inflammation in hypogonadal men with the metabolic syndrome: The double-blinded placebo-controlled Moscow study. Clin Endocrinol. 2010;73(5):602-12. [ Abstract ] Handelsman DJ, Zajac JD. 11: Androgen deficiency and replacement therapy in men. Med J Aust. 2004;180(10):529-535. [ Abstract | Full text ] Araujo AB, Esche GR, Kupelian V, et al. Prevalence of symptomatic androgen deficiency in men. J Clin Endocrinol Metab. 2007;92(11):4241-7. [ Abstract | Full text ] Kapoor D, Aldred H, Clark S, et al.

Clinical and biochemical assessment of hypogonadism in men with type 2 diabetes: Correlations with bioavailable testosterone and visceral adiposity. Diabetes Care. 2007;30(4):911-7. [ Abstract | Full text ] Related diseases Growth Hormone Therapy - The Most Common Growth Hormone Deficiency Treatment Growth Hormone Therapy Written by Daniel J. Toft MD, PhD The most common treatment for growth hormone deficiency in both children and adults is growth hormone therapy—injections of growth hormone into the body. Growth hormone—known as somatotropin—can be injected by the patient or a family member (if it's a child with growth hormone deficiency). This hormone, which is normally produced in the pituitary gland , stimulates growth and cell reproduction in the body. Once your doctor prescribes you with growth hormone therapy, you'll typically need daily doses of growth hormone. However, depending on the severity of your condition, you may need growth hormone injections more often. Usually, you'll need to see your doctor every 4 to 8 weeks throughout your treatment so that your doctor can monitor your condition. He or she will test your progress and perform blood tests to help determine whether more growth hormone is needed.

Your doctor will also monitor your cholesterol levels, blood glucose levels, and bone density periodically while you're on growth hormone injections to make sure they're at healthy levels. Taking growth hormone can impact how the body responds to insulin , which controls blood glucose levels. Untreated growth hormone deficiency can lead to high cholesterol and osteoporosis . There are also special considerations for children. Kids who take growth hormone injections typically grow 4 or more inches over the first year of treatment, and over the next 2 years, they can grow 3 or more inches. However, after that, the rate of growth slowly begins to decrease. Is Growth Hormone Therapy Safe? Although growth hormone injections are relatively safe and effective, there are a few side effects. Fortunately, serious side effects are rare. Swelling, numbness, and joint and muscle aches and pains are the most common side effects. You may experience these side effects if you're getting more growth hormone than you need. If you have these symptoms, talk to your doctor immediately. He or she will adjust the amount of growth hormone you're taking. Once your doctor adjusts your dose, the symptoms should go away on their own.

There are some people who shouldn't take growth hormone injections, such as people who have tumors or cancer. People who are seriously ill, have multiple injuries from a trauma, or severe breathing problems should also not take growth hormone injections. Other Treatments for Growth Hormone Deficiency In addition to growth hormone therapy, you may need other treatments for growth hormone deficiency. For example, being very short can affect a child's self-esteem: Classmates can tease a child to the point of tears. That's why mental and emotional therapy is often an important part of treatment. A mental health counselor or psychologist can talk you through your feelings and teach you how to cope with growth hormone deficiency. Getting enough sleep, eating a balanced diet, and regularly exercising are also important parts of an overall growth hormone deficiency treatment plan. Your doctor can teach you how to incorporate growth hormone injections into a healthy lifestyle. Updated on: 02/01/16 Diabetes and Thiamine: A Novel Treatment Opportunity- Hormones Matter Diabetes and Thiamine: A Novel Treatment Opportunity Author: Chandler Marrs, PhD 6 Comments Share: Underlying all diabetic conditions is poor sugar control or hyperglycemia.

Hyperglycemia can be due to a lack of insulin as in Type 1 diabetes or insulin resistance as in Type 2 diabetes. In either case, the corresponding diabetic complications that evolve over time in many diabetics, the cardiovascular disease, retinopathy, peripheral nerve and vascular damage, represent the effects of sustained hyperglycemia. Until recently, the mechanisms by which diabetic vascular damage developed eluded researchers. Although multiple, seemingly discrete biomarkers had been identified, no single, unifying mechanism was understood. It turns out that diabetics, both Type 1 and Type 2, are severely deficient in thiamine or vitamin B1 and that thiamine is required for glucose control at the cell level. Why is thiamine deficient in diabetics and how does thiamine manage glucose control? The answers to those questions highlight the importance of micronutrients in basic cellular functioning, particularly mitochondrial functioning , and the role of excessive sugar in disease . Thiamine Thiamine (thiamin) or vitamin B1 is an essential nutrient for all living organisms. The body cannot synthesize thiamine by itself and so it must be obtained from diet.

Thiamine is present in yeast, pork, fish, various nuts, peas, asparagus, squash and grains (unprocessed) and because of the severity of the illnesses that thiamine deficiency evokes, many processed foods have been fortified with thiamine. Nevertheless, thiamine deficiencies thought resolved by modern nutritional technologies, are emerging once again. Modern thiamine deficits appear to be caused by diets of highly processed, carbohydrate and fat laden foods, exposures to thiamine blocking factors such as alcohol and those found in many medications (fluoroquinolones, possibly others) and vaccines (Gardasil, possibly others), environmental toxicants and some foods . Thiamine deficiency is also common after bariatric surgery and in disease processes like AIDS and cancer. Over the course of our research , thiamine deficiency has been observed in previously healthy, young, non-alcoholic patients, post medication or vaccine, along with symptoms of dysautonomia.

Thiamine Deficiency Symptoms Thiamine deficiency at its worst is linked to severe decrements neurological functioning, like Wernicke’s Encephalopathy that include noticeable ataxic and gait disturbances (loss of voluntary control of muscle movements, balance and walking difficulties), aphasias (language comprehension and/or production difficulties), and if it persists, Korsakoff’s Syndrome (severe memory deficits, confabulations and psychosis). Early on though and as the deficiency is evolving, thiamine deficiency presents much like the mitochondrial disease that it is – with the myriad of seemingly unrelated symptoms, that are not typically attributed to thiamine deficiency, such as fatigue and excessive sleeping , hair loss , cardiac dysregulation , GI disturbances such as gastroparesis and others , autonomic instability , demyelinating syndromes and hormone irregularities, especially thyroid , but also reproductive hormones. In diabetics, thiamine deficiency may present as ketoacidosis, lactic acidosis, hyperglycemia and persistent encephalopathy . Thiamine deficiency attacks the mitochondria . Mitochondrial dysfunction presents diversely. In fact, with mitochondrial dysfunction, symptoms are as varied as the individuals who experience them.

Diabetes, may be just one more phenotype of among many. Thiamine Deficits in Diabetes With diabetes, thiamine deficiencies are common, though likely under-recognized. Diabetics are susceptible to thiamine deficiencies mediated by diet and exposures like most of the Western world, but also have added risk factors associated with the disease itself. In diabetics, kidney function is altered which decreases thiamine reabsorption while increasing thiamine excretion. In some people, diabetic and non-diabetic alike, thiamine deficiency can be exacerbated even further by a mutation in the thiamine transporter protein that brings thiamine into the cells. How thiamine deficient are diabetics? One study found that in comparison to non-diabetics, individuals with Type 1 and Type 2 diabetes had 75% and 64% less thiamine, respectively. Think about this for a moment. If diabetes predisposes individuals to thiamine deficiency without any other intervening factors, imagine what happens when diabetics are nutritionally thiamine deficient, exposed to the myriad of environmentally or medically thiamine-depleting substances currently on the market, or worse yet, carry the thiamine transporter mutation .

Alone, but especially in combination, thiamine deficiency diseases, many of which align with diabetes-related complications, could be magnified exponentially. The remarkable thing about this new research is that treatment is easy, it requires only dietary changes and high dose thiamine therapy alongside normal diabetes interventions. (Although one suspects with Type 2 diabetes at least, dietary changes and thiamine supplements could replace other medications entirely). Backing up a bit though, let us look at the research and mechanisms by which thiamine moderates sugar exposure at the cell level and how thiamine modifies those processes. The Hyperglycemic Cascades Under normal conditions, with appropriate dietary nutrients and physiological concentrations glucose, dietary sugars are converted to ATP in the mitochondria. The byproduct of that reaction is the production of free radicals also known as oxidative stress or reactive oxygen species (ROS). ROS are neither good nor bad, but too much or too little ROS wreaks havoc on cellular functioning. The cells can clear the ROS and manage oxidative stress via activating antioxidizing pathways and shuttling the excess glucose to secondary, even tertiary processing paths.

However, under conditions of chronic hyperglycemia, mediated by diet or diabetes, the conversion of glucose to ATP becomes dysregulated, the production of ROS become insurmountable and a cascade of ill-effects are set in motion. Too much ROS causes the mitochondria to produce high concentrations of an enzyme called superoxide dismutase (SOD) in the endothelial cells of both the small and large blood vessels. SOD is a powerful antioxidant, however, like everything else, too much for too long causes problems. Superoxide then upregulates the five known chemical pathways that alone and together perturb vascular homeostasis and cause the diabetic injuries that have become commonplace. Technically speaking, hyperglycemia causes : Vitamin D Council | Vitamin D and type I diabetes Type I diabetes Summary Type 1 diabetes is an autoimmune disease. It is a condition where your own immune system attacks certain cells called beta-cells. Beta-cells help you produce a hormone called insulin. You need insulin to help your body manage glucose you get from food and turn it into energy for your body to use. Researchers don’t know what increases your chances of developing type 1 diabetes.

Researchers believe that having a family member who has type 1 diabetes might increase your risk of getting type 1 diabetes. Also, viral infections and environmental factors may increase your chances of developing type 1 diabetes, but we need more research to say for sure or understand which factors play a role. Research shows that there is a link between vitamin D and type 1 diabetes. People with high vitamin D intake during their first year of life are less likely to develop type 1 diabetes later in life. Some research also suggests having high vitamin D levels during pregnancy might help prevent type 1 diabetes in their children later in life. However, this research has been observational, meaning we don’t know for sure if getting enough vitamin D prevents type 1 diabetes. Studies have shown that vitamin D supplementation may help improve insulin sensitivity and help control blood glucose levels in those with type 1 diabetes, though research has been small and inconclusive, so we can’t say for sure if vitamin D helps at all in type 1 diabetes.

If you have type 1 diabetes or you are trying to prevent type 1 diabetes and want to take vitamin D, it is unlikely to make your type 1 diabetes worse or cause you any harm, as long as you take less than 10,000 IU per day. However, it’s not proven that it will help your type 1 diabetes. It’s also not proven if taking vitamin D will help you prevent type 1 diabetes. If you have type 1 diabetes, you shouldn’t take vitamin D in place of your treatment medications. Talk to your physician for more advice about taking supplements. What is type 1 diabetes? Type 1 diabetes (T1D) is an autoimmune disease. Autoimmune diseases are conditions where your own immune system attacks your body. Your immune system mistakes healthy parts of your body as dangerous and foreign substances. In T1D, your own immune system attacks certain cells called beta-cells. Beta-cells help you produce a hormone called insulin. You need insulin to help your body manage the glucose you get from food and turn it into energy for your body to use.

Since these beta-cells are under attack, they can’t produce as much insulin as you need, so you have a hard time controlling the glucose in your body. Because of this, people with T1D need to take injections of insulin. Without these injections, people with T1D can have a build-up of glucose and have symptoms like: Excessive thirst Frequent infections Slow-healing wounds In extreme cases, if a person with T1D does not have access to insulin, they can die 1 . How common is type 1 diabetes? T1D is a rare form of diabetes and only about 5% of people with diabetes have T1D. It is usually diagnosed in young children. T1D is a rare form of diabetes and only about 5% of people with diabetes have T1D. It is usually diagnosed in young children. Around 3 million Americans have T1D, and there are an estimated 30,000 people each year diagnosed with T1D. The number of people in the United States with T1D rose by 23% between 2001 and 2009 2 .

It’s important to note that T1D is different than the much more common type 2 diabetes (T2D). You develop T2D gradually overtime, likely due to poor lifestyle and dietary habits. On the other hand, T1D happens much more suddenly and is diagnosed usually during childhood, and it is unclear what causes T1D and why some people get it. There are no obvious risk factors in T1D, like poor dietary habits. What causes type 1 diabetes? Researchers don’t know exactly what causes T1D. They do know that what happens is that cells called T cells, which are the cells that respond to dangerous substances in your body, start attacking your beta cells. Why they do this, researchers don’t know, but this is what leads to the lack of insulin and the buildup of glucose in your body. It is still unclear what can increase your chances of developing type 1 diabetes. Researchers believe that having a family member who has T1D may increase your risk of developing T1D. Also, viral infections and environmental factors may increase your chances of developing T1D, but we need more research to say for sure or understand which factors play a role 1 .

What is the link between type 1 diabetes and vitamin D? The relationship between T1D and vitamin D is still not fully understood and is still being studied. Researchers believe that vitamin D helps make your immune cells act smarter. This may be important in autoimmune diseases, like T1D, where your immune cells are mistakenly attacking your own body. Researchers are wondering if you get enough vitamin D, if it can help make these cells make less mistakes and help prevent or manage autoimmune diseases better. Vitamin D can attach to receptors on your immune cells, and through chemical signals, help direct the cells to communicate and function properly. Vitamin D receptors are present in important areas involved with T1D. Vitamin D binds to these receptors and helps prevent beta cell death, improve insulin production, and reduce inflammation. However, it’s not clear if these receptors and signals are involved in preventing or treating T1D 3 , 4 . What does the research say in general about vitamin D and type 1 diabetes? Preventing type 1 diabetes Researchers are interested if pregnant mothers get enough vitamin D, they can prevent T1D in their children.

Researchers are interested if you get enough vitamin D during early childhood, if you can prevent T1D, or if pregnant mothers get enough vitamin D, they can prevent T1D in their children. Some studies show a link between vitamin D intake and risk of developing T1D. Research has shown that supplementing with vitamin D during the first year of life reduces the risk of developing T1D 3 , 4 . However, most of these studies have been observational, meaning that researchers can’t say for sure whether vitamin D prevents T1D or not. A few studies have looked at the role of vitamin D during different stages of pregnancy and if it might help prevent T1D in children. The results of these studies have been mixed, so researchers can’t say for sure if vitamin D intake during pregnancy can prevent children from developing T1D later in life 5 . Treating type 1 diabetes There have only been a few studies looking at vitamin D in the treatment and management of T1D. None of the studies have found vitamin D to be able to treat T1D, but they do suggest a possible role in helping manage some aspects of the disease.

These studies suggest that vitamin D plays a role in improving the function of the beta cells, improving insulin production, and managing blood glucose levels, all important things in T1D. Vitamin D may have a role in helping the body produce some of its own insulin when alongside standard insulin treatment 6 , 7 . However, these studies looking at treatment of T1D have had inconclusive results, meaning researchers can’t say for sure if vitamin D helps to treat or manage T1D. What does recent research say? Preventing type 1 diabetes A review of many studies in 2013 3 looked at studies on vitamin D and risk of T1D. Out of the studies the researchers reviewed, eight studies looked at vitamin D intake during the first year of life and three studies looked at the effects of vitamin D intake of pregnant women on the risk of T1D in their children years later after they were born. The researchers found: Infants who took vitamin D supplements during their first year of life had a significantly reduced risk of T1D compared to those who did not. There was no relationship between vitamin D intake during pregnancy and risk of T1D in their children.

All of the studies reviewed were observational, meaning that we don’t know for sure if vitamin D intake during early life can help prevent T1D in children. A study in 2012 in Norway 5 looked at a large group of women who had given birth between 1992 and 1994. They wanted to know if low vitamin D levels of the mothers during late pregnancy was related to an increased risk of T1D in their children. They found: The average vitamin D level of mothers with children with T1D had lower levels compared to women with children without T1D. Children born to mothers with vitamin D levels less than 21.6 ng/ml were twice as likely to get T1D compared to women with vitamin D levels above 35.6 ng/ml. This study was observational however, meaning we can’t say for sure if getting vitamin D during pregnancy protects against T1D.

A study done in 2001 in Finland 4 collected data on more than 10,000 children from 1966 and followed them through to 1998 to see if vitamin D supplementation during the first year of life led to a reduced risk of developing T1D in life. The researchers found: Children who took vitamin D supplements, no matter what the dose, had a lower chance of getting T1D compared to those who didn’t take supplements. The children who regularly took vitamin D supplements at the recommended daily dose (at the time) of 2,000 IU/day in the first year of life had an 80% lower risk of developing T1D compared to children who took less. This study was observational, meaning that we can’t say for sure whether vitamin D supplements prevent T1D or not. Treating type 1 diabetes A randomized trial in 2010 6 looked to see if vitamin D has any effect on protecting beta-cell function, a main factor in insulin production and helping manage glucose.

The researchers randomized a group of young adults around the age of 18 years old who had recently been diagnosed with T1D to receive either 1,000 IU of vitamin D or a placebo. The researchers followed them for 2 years and found: Vitamin D supplementation or vitamin D levels did not help how well the beta-cells functioned. This study was small and used a low dose of vitamin D, so researchers can’t say for sure whether or not vitamin D can help with beta-cell function in newly diagnosed T1D patients. An experiment in 2010 in Saudi Arabia 7 looked at a group of teenagers and adults with T1D. They wanted to see if vitamin D and calcium lowered amounts of glycated hemoglobin. High levels of glycated hemoglobin is a common characteristic of T1D and is a sign of poor blood glucose control and higher risk of cardiovascular disease. They looked at 80 vitamin D deficient individuals and gave them 4,000 IU/day of vitamin D and 1,200 mg/day of calcium.

They found: Those who reached vitamin D levels above 30 ng/ml had much lower glycated hemoglobin levels compared to those who remained below 30 ng/ml. This means that the people with high levels of vitamin D displayed better glucose control than those with lower levels of vitamin D. However, the researchers couldn’t say for sure if vitamin D and calcium supplementation and having high vitamin D levels helped, since their findings were observational and not compared to a control group. Key points from the research Research has shown that babies with high vitamin D intake during their first year of life are less likely to develop T1D later in life. Research has shown that pregnant mothers with high vitamin D levels during pregnancy are less likely to have children that get T1D later in life. However, this research is less strong compared to vitamin D intake during early childhood and infancy. Some research has shown that vitamin D may help improve insulin sensitivity and help manage blood glucose in those with T1D, though we can’t say for sure if vitamin D helps at all in T1D. The majority of studies that have been done so far have been observational meaning we cannot say for sure if vitamin D is a main factor in the prevention or treatment of T1D.

More experiments are needed to clearly answer whether vitamin D supplementation can prevent or treat T1D. What does this mean for me? People with high vitamin D intake during their first year of life are less likely to develop T1D later in life. Research shows that there is a link between vitamin D and T1D. People with high vitamin D intake during their first year of life are less likely to develop T1D later in life. Some research also suggests having high vitamin D levels during pregnancy might help prevent T1D in their children later in life. However, this research has been observational, meaning we don’t know for sure if getting enough vitamin D prevents T1D. Studies have shown that vitamin D supplementation may help improve insulin sensitivity and help control blood glucose levels in those with T1D, though research has been small and inconclusive, so we can’t say for sure if vitamin D helps at all in T1D. If you have T1D or you are trying to prevent T1D and want to take vitamin D, it is unlikely to make your T1D worse or cause you any harm, as long as you take less than 10,000 IU per day.

However, it’s not proven that it will help your T1D. It’s also not proven if taking vitamin D will help you prevent T1D. If you have T1D, you shouldn’t take vitamin D in place of your treatment medications. Talk to your physician for more advice about taking supplements. References About Diabetes. International Diabetes Federation, 2013. Web. 12 December 2013. Type 1 Diabetes Facts. JDRF, 2013. Web. 12 December 2013. Dong, J. et al. Vitamin D Intake and Risk of Type 1 Diabetes: A Meta-Analysis of Observational Studies. Nutrients 2013;5;3551-3562. Hyppönen, E. et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. The Lancet 2001;358;1500-1503. Sørensen, I et al. Maternal Serum Levels of 25-Hydroxy-Vitamin D During Pregnancy and Risk of Type 1 Diabetes in the Offspring.

Diabetes 2012;61;175-178. Bizzarri, C. et al. No protective effect of calcitriol on beta-cell function in recent-onset type 1 diabetes: the IMDIAB XIII trial. Diabetes Care 2010;33;1962-1963. Aljabri, K. et al. Glycemic changes after vitamin D supplementation in patients with type 1 diabetes mellitus and vitamin D deficiency. Annals of Saudi Medicine 2010;30;454-458. This page was last updated February 2014. We need your help! Growth Hormone in Kids with Type 1 Diabetes | She Sugar Growth Hormone in Kids with Type 1 Diabetes March 22, 2013 By jewels 1 Comment 0 0 0 Growing children are infamous for the diabetes management challenges they present to both parents and physicians alike. Growth hormone can only be guessed at as a potential irritant to glucose control. As a parent we watch our kids pants legs suddenly grow shorter or visibly see a height change overnight.

If it was only so easy to identify these growth periods as a causation for high blood sugars! What is growth hormone? Growth hormone is released from the pituitary gland which is located at the base of the skull. Like the stress hormone cortisol, growth hormone presents a challenge to insulin in the body. “The cause of insensitivity to insulin during puberty has been under investigation. The major hormonal changes that are associated with the onset of puberty include a two-fold increase in the secretion of growth hormone and an increase in the sex steroids that lead to the development of secondary sexual characteristics, remarkable increase in height, and change in body composition. Thus, both growth hormone and sex steroids are likely hormonal candidates for inducing insensitivity to insulin during puberty.“ ~According to Tfayli and Arslanian in “The challenge of adolescence: hormonal changes and sensitivity to insulin” Does puberty require increased insulin levels? Puberty does require increased insulin levels. As your child grows their insulin needs may surpass that of a grown adult during this period of time. Changes are frequent and unpredictable making puberty a parenting challenge in more ways than one. Maintaining more frequent contact with your child’s health care practitioner is vital.

They have the skills, tips and tricks that will help guide your family through these uncertain changes. Tfayli and Arslanian state “turbulent adolescent years are characterized by important hormonal, metabolic and psychological changes which impact on the management of type 1 diabetes… The decline in insulin sensitivity requires appropriate readjustment of insulin doses in order to prevent deterioration in blood glucose control.” JCI - The relative roles of growth hormone and IGF-1 in controlling insulin sensitivity The relative roles of growth hormone and IGF-1 in controlling insulin sensitivity Find articles by Clemmons, D. in: JCI | PubMed | Google Scholar First published January 1, 2004 - More info Published in Volume 113, Issue 1 (January 1, 2004) J Clin Invest. 2004;113(1):25–27. doi:10.1172/JCI20660. Copyright © 2004, The American Society for Clinical Investigation. Published January 1, 2004 Abstract IGF-1 and growth hormone (GH) interact with insulin to modulate its control of carbohydrate metabolism.

A new study (see the related article beginning on page 96) shows that blocking the effect of GH in the presence of low serum IGF-1 concentrations enhances insulin sensitivity. Understanding the relative roles of peptide hormones in modulating responsiveness to insulin presents a major challenge because of the adaptability of the growth hormone/IGF-1/insulin system. Changes in glucose and insulin secretion result in counter-regulatory responses, and modifications in growth hormone (GH) and IGF-1 function alter insulin’s ability to maintain normal carbohydrate homeostasis. Historically, this problem has been analyzed in both human and rodent hormone-deficiency models (e.g., GH deficiency) in which the hormone of interest is replaced and the metabolic consequences are determined ( 1 ). The recent development of tissue-selective knockout animal models has brought new insights to our understanding of the relative roles of these hormones in carbohydrate homeostasis. In this issue of the JCI, Yakar et al. address the relative roles of GH and IGF-1 in regulating insulin sensitivity in mice ( 2 ).

The authors created an animal model in which IGF-1 synthesis in the liver is eliminated and then crossed these animals with mice that overexpress a mutant form of GH that prevents GH activation of its receptor. The authors conclude that GH is a major determinant of insulin resistance in these IGF-1–deficient animals, since, in the presence of low concentrations of serum IGF-1, blocking the action of GH results in a major improvement in insulin sensitivity. Food intake and GH regulate insulin-like peptide secretion One way to understand the relative roles of IGF-1 in controlling insulin action is from the perspective of primitive organisms. In primitive organisms that do not have a pituitary gland, ligands with structural similarities to both insulin and IGF-1 are synthesized in the olfactory region of the brain and secreted in response to food intake ( 3 ). This results in direct linking of food intake, carbohydrate metabolism, and growth, and a single receptor mediates these responses. In vertebrates, although IGF-1 secretion is primarily regulated by nutrient intake ( 4 ), GH secretion adds an additional layer of complexity (Figure 1 ).

In higher organisms, GH controls growth by regulating IGF-1 concentrations, but another major function of GH is to provide a mechanism for surviving periods of food deprivation. GH stimulates lipolysis, providing FFAs and glycerol as substrates for energy metabolism, and also inhibits insulin-induced suppression of hepatic gluconeogenesis. These effects counteract insulin action and reduce the need for a dietary source of carbohydrate ( 5 ). An important distinction, however, is the relative role of GH in maintaining carbohydrate and lipid homeostasis under normal conditions as compared with conditions in which there is excess GH secretion ( 6 ). When GH is secreted in excess, it acts directly to block insulin signaling by inducing resistance to stimulation of downstream signaling molecules such as insulin receptor substrate-1 and PI3K, which are important for glucose transport in muscle and fat and for inhibiting hepatic gluconeogenesis ( 7 ). This results in elevation of glucose and insulin concentrations. Thus patients with acromegaly often have impaired glucose intolerance and relative hyperinsulinemia ( 8 ).

Similarly, in type 1 diabetes, insulin deficiency leads to impaired hepatic IGF-1 synthesis, and this results in decreased feedback suppression of GH secretion, leading to further impairment of insulin action ( 9 ). Administration of a GH antagonist to diabetics results in relative restoration of normal carbohydrate metabolism but does not completely ameliorate the defect in insulin sensitivity ( 10 ). Similarly, administration of a GH receptor antagonist to acromegalics improves insulin sensitivity but does not restore it to the normal range ( 11 ). Role of IGF-1 in modulating insulin sensitivity IGF-1, which has 48% amino acid sequence identity with proinsulin, enhances insulin sensitivity in both experimental animals and human subjects. IGF-1 binds to insulin receptors with very low affinity; therefore its binding to IGF-1 receptors and/or hybrid insulin/IGF-1 receptors has been postulated to be the mediator of enhanced insulin action ( 12 ). IGF-1 does not bind to hepatocytes or adipocytes, and therefore its primary insulin-sensitizing action is believed to be mediated through skeletal muscle.

Administration of IGF-1 to normal humans results in glucose lowering that is approximately one-twelfth as potent as that induced by insulin ( 13 ), and in patients with extreme insulin resistance it improves insulin sensitivity and carbohydrate homeostasis ( 14 ). One problem in interpreting almost all human studies of IGF-1 has been that, in addition to enhancing insulin action, it also suppresses GH secretion; therefore it has been difficult to determine the relative roles of the direct actions of IGF-1 and those that are mediated by suppression of GH. One exception is the group of individuals with GH receptor mutations who develop insulin resistance as adults. Administration of IGF-1 to these patients, who are unresponsive to GH, results in improvement in insulin sensitivity ( 15 , 16 ). This difficulty in distinguishing between the effects of GH suppression and the direct effects of IGF-1 has been addressed in the studies of Yakar et al. ( 2 ). In an earlier report, they showed that animals in which the liver-specific expression of the IGF-1 gene had been deleted had low serum IGF-1 and increased GH levels ( 17 ). These mice were hyperinsulinemic and resistant to insulin action in skeletal muscle.

The authors extended those findings by overexpressing a dominant negative form of IGF-1 receptor in muscle. This resulted in attenuation of both IGF-1 and hybrid insulin/IGF-1 receptor function. These animals developed severe insulin resistance and diabetes ( 18 ). In contrast, deletion of the insulin receptor in muscle does not result in severe insulin resistance or diabetes ( 19 ). The authors interpreted the difference in the two models to be due to loss of IGF-1’s sensitizing actions in skeletal muscle, leading to the development of insulin resistance. Recently this group has further extended our understanding of this problem by creating a genetic model in which serum total IGF-1 concentrations are lowered by 85% but free IGF-1 concentrations are increased ( 20 ). In this model, animals that do not express IGF-1 in the liver were crossed with animals that do not express the acid-labile subunit, a component of the IGF-1/IGF-binding protein-3/acid-labile subunit complex in plasma, which functions to stabilize the half-life of IGF-1.

In contrast to the animals with liver IGF-1 deletion, these animals showed enhanced insulin sensitivity in both adipose tissue and muscle but no change in liver. When these results are considered together with the current study ( 2 ), they suggest that the major site at which GH blocks insulin action is the liver. Although a secondary role for GH in skeletal muscle cannot be excluded, by this formulation, conditions that lead to increases in GH secretion (whether or not they are associated with lower serum IGF-1) may result in impaired hepatic insulin sensitivity, leading to decreased suppression of gluconeogenesis. Although GH no doubt has an insulin-counter-regulatory role in skeletal muscle, in that tissue the role of IGF-1 may be predominant. An additional issue is that overexpression of the GH antagonist completely eliminates GH action, and therefore this study does not definitively address the role of normal GH secretion and action in mediating insulin resistance. Thus future studies that use tissue-specific gene-deletion animal models and provide different levels of hormone-replacement therapy or that assess the effects of variable doses of the GH antagonist will be necessary to discern the relative roles of IGF-1 and GH in mediating insulin sensitivity in both normal physiologic and pathophysiologic states.

Inhibiting GH action to attain a relatively normal physiologic level rather than a GH-deficient level will be necessary to further understand the contribution of IGF-1 in maintenance of normal glucose homeostasis in these models. Nevertheless, the studies of Yakar et al. highlight the importance of GH antagonism of insulin action in the liver and provide an important step in our understanding of the relative roles of each of these three hormones in maintaining this finely balanced mechanism.

Question: What hormone are Type I diabetics deficient in?
Answer: Insulin