bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nutrition and Somatomedin: II. Serum Somatomedin Activity and Cartilage Growth Activity in Streptozotocin-diabetic Rats
Authors: Phillips Lawrence S , Young Harvey S 
Published: September 2013

Since diabetes mellitus is a condition in which poor growth occurs despite elevation of plasma GH, we have attempted to determine if poor growth in diabetes, as in malnutrition, could be associated with a decrease in somatomedin activity. Young male rats were rendered diabetic with intravenous streptozotocin (STZ). The growth activity of their cartilage was estimated by 35SO4 incorporation in vitro, and somatomedin (SM) activity in their serum was determined by the stimulation of SO4 incorporation by cartilage from hypophysectomized rats or normal young pigs. Cartilage growth activity was significantly decreased 24 hours after STZ and fell to hypopituitary levels after 48 hours. The decreased growth activity could not be attributed to decreased cartilage responsiveness to SM, since incubation of diabetic cartilage with normal rat serum (normal SM) resulted in significant stimulation of cartilage SO4 incorporation. SM in diabetic serum decreased to hypopituitary levels 24 hours after STZ, and decreased further after 48 hours. The decrease in SM and cartilage growth activity was not prevented by the administration of high doses of bovine GH. The fall in bioassayable SM appeared to be due in part to the presence of an SM inhibitor in the diabetic serum, since addition of diabetic serum to normal serum decreased to measurable SM in the normal serum. Administration of insulin to diabetic rats 48 hours after STZ led to significant increases in SM and cartilage growth activity, and insulin therapy 24 hours after STZ prevented the decreases in SM and cartilage growth activity which occurred without insulin.
Thus, acute STZ-induced diabetes in rats was associated with a significant decrease in both serum SM and cartilage growth activity; these changes were not ameliorated by administration of GH, and insulin therapy could both prevent and reverse the fall in SM and cartilage growth activity. From these observations, we conclude that (1) that fall in somatomedin activity and cartilage growth activity associated with STZ-induced diabetes appears to be due to insulin deficiency and (2) growth failure in diabetes, as in malnutrition, may be due to decreased somatomedin activity.
Influence of Fixation and Morphometric Technics on Capillary Basement-membrane Thickening Prevalence Data in Diabetes
Authors: Williamson Joseph R , Rowold Edwin , Hoffman Phyllis , Kilo Charles 
Published: September 2013

Muscle tissue obtained by needle biopsy from 20 diabetic subjects and from 20 age-matched control subjects was divided into two portions, one of which was fixed and processed by our routine procedure (primary glutaraldehyde fixation followed by osmium fixation and embedment in araldite) and the other was fixed initially in osmium tetroxide and embedded in maraglas, the procedure employed by Siperstein et al. Basement-membrane width of capillaries was measured by the 20-point method of Siperstein et al. and by the two-minimum-point technic developed in our own laboratory. Contrary to the experience of Siperstein et al., the prevalence of basement-membrane thickening in diabetic subjects based on mean width values and/or standard deviations in excess of 95 per cent tolerance intervals was highest (65 per cent) in minimum measurements of glutaraldehyde-fixed tissues and lowest (30 per cent) in osmium-fixed tissues (X2 = 4.9123, p &lt; 0.05).
Internal discrepancies in the data of Siperstein et al. indicate that (1) their basement-membrane-width values derived from multiple measurements from control subjects are anomalous (low) and (2) the very high prevalence of basement-membrane thickening they reported in diabetic and in prediabetic subjects and considered as strong support for their conclusion that basement-membrane disease is independent of and precedes glucose intolerance is suspect.
Insulin and Brain Metabolism: Absence of Direct Action of Insulin on K+ and Na+ Transport in Mouse Brain
Authors: Thurston Jean Holowach , Hauhart Richard E , Dirgo John A 
Published: September 2013

This is a study of the effect of insulin on the transport of K+ and Na+ from the blood into the brains of normal mice. Despite profound reductions in plasma and brain glucose levels, reduction of plasma K+ concentration and progressive deterioration of neurologic function 30–120 minutes after insulin injection, in 20–22-day-old animals there was no increase in brain K+ and Na+ concentrations. In fact, at 120 minutes, when the brain water content increased 0.7 per cent, brain K+ concentration was significantly reduced, not elevated.
The effect of insulin on brain electrolyte and water content in adult mice was also studied. Although brain water increased 0.5 per cent at 120 minutes, there was no changes in brain Na+ or K+ concentrations at any time after insulin injection.
The data from mice do not support a role of insulin in electrolyte transport in brain.
Determination of Free and Total Insulin and C-Peptide in Insulin-treated Diabetics
Authors: Kuzuya Hideshi , Blix Petra M , Horwitz David L , Steiner Donald F , Rubenstein Arthur H 
Published: September 2013

Serum levels of free and total insulin as well as total C-peptide immunoreactivity (C-peptide and proinsulin) and C-peptide were measured in insulin-treated diabetics with circulating insulin antibodies by the addition of polyethylene glycol (PEG) before and after acidification. PEG resulted in complete precipitation of insulin antibodies from serum and made it possible to measure free insulin in the supernatant. Incubation of serum at 37δ C. for two hours before addition of PEG resulted in values for free insulin that probably resembled the in-vivo levels most closely. The same method could also be used to remove proinsulin bound to circulating insulin antibodies and permitted the measurement of C-peptide in the supernatant.
Clinical studies using this approach indicate that combined measurements of serum free and total insulin and C-peptide provide information that is helpful in understanding the contribution of endogenous and exogenous insulin to the course and metabolic control of insulin-requiring diabetic patients.
The Roles of Insulin, Glucagon, and Free Fatty Acids in the Regulation of Ketogenesis in Dogs
Authors: Keller Ulrich , Chiasson Jean-Louis , Liljenquist John E , Cherrington Alan D , Jennings Anthony S , Crofford Oscar B 
Published: September 2013

The roles of basal insulin, glucagon, and free fatty acids in the regulation of ketogenesis were studied in three-day-fasted anesthetized dogs. Four protocols were employed: (1) infusion of somatostatin, resulting in combined insulin and glucagon deficiency, (2) somatostatin and intraportal glucagon replacement (1 ng./kg./min.) to produce insulin deficiency, (3) somatostatin combined with intraportal insulin replacement (350 μU./kg./min.) to produce glucagon deficiency, and (4) saline controls. Simultaneous blood sampling from the femoral artery and portal and hepatic veins allowed determination of hepatic uptake or production of free fatty acids, glycerol, ketone bodies, and glucose. When combined deficiency of insulin and glucagon was produced, no significant effect on hepatic ketone production was noted (108 ± 6 per cent of mean basal), whereas the induction of selective Insulin deficiency (basal glucagon level maintained) resulted in a rise of net hepatic ketone production (185 ± 24 per cent of mean basal, P &lt; 0.01). Isolated glucagon lack (basal insulin maintained) did not alter net hepatic ketone production.
To assess the effect of increased substrate supply on ketogenesis, all experiments included a period of acute elevation of free fatty adds (FFA), produced by infusion of Intralipld and heparin. FFA elevation in saline controls caused only a moderate stimulation of ketone production (149 ± 16 per cent of mean basal, P &lt; 0.01) despite a threefold increase in FFA uptake. However, the combination of elevation of FFA and selective insulin deficiency (glucagon maintained) resulted in a greatly increased hepatic ketone production (357 ± 58 per cent of mean basal, P &lt; 0.01 vs. controls), which was also significantly higher than during combined insulin and glucagon deficiency (P &lt; 0.05). Lipolysis, as indicated by arterial glycerol levels, as well as hepatic FFA uptake was not affected by acute suppression of pancreatic hormone levels.
The study demonstrated that basal insulin plays an important role in repressing ketogenesis and that basal amounts of glucagon, while ineffective in the presence of insulin, exert a stimulatory effect on ketogenesis when insulin is deficient. Glucagon's stimulatory effect on ketogenesis was due to an effect in the liver rather than to an increase in lipolysis or in hepatic FFA uptake. Increasing FFA supply per se was associated with only limited stimulation of ketogenesis, whereas the combination of insulin deficiency, basal concentrations of glucagon, and increased FFA load produced a synergistic augmentation of hepatic ketone production.
Diabetes Mellitus in an Urbanized, Isolated Polynesian Population: The Funafuti Survey
Authors: Zimmet Paul , Seluka Alesana , Collins James , Currie Philip , Wicking Julie , DeBoer William 
Published: September 2013

An epidemiologic study of diabetes in the urbanized Polynesian population of Funafuti has established a prevalence of 8 per cent in subjects aged 10 years and over. Of these, only 0.9 per cent were known diabetics, and the remainder were diagnosed on the basis of a plasma glucose level of at least 160 mg/lOO ml. two hours after a 75 gm. glucose load. A further 5.9 per cent had borderline diabetes as judged by a two-hour postload plasma glucose of 140-159 mg./ 100 ml. In those aged 20 years and over, the prevalence of diabetes was 10.1 per cent, similar to that reported in other accuHurated Polynesian groups.
The prevalence of both borderline diabetes and frank diabetes was twice as high in the females as in males. This difference appeared to be related to the greater degree of obesity in the females, but the prevalence was not related to parity. The increase in frequency of diabetes among these islanders coincides with a change of traditional island life style to that of urbanized Western populations. The results suggest that there may be 10 times the actual number of known diabetics in some Pacific populations.
Insulin and Brain Metabolism: Absence of Direct Action of Insulin on K+ and Na+ Transport in Normal Rabbit Brain
Authors: Thurston Jean Holowach , Hauhart Richard E , Dirgo John A , McDougal David B 
Published: September 2013

In fed, unanesthetized rabbits, regular zinc insulin, 50 U./kg. intravenously, decreased plasma glucose levels 52 per cent, p = 0.002, 35 minutes after injection. In 15-hour-fasted, unanesthetized animals, the same dose of insulin decreased plasma glucose levels 68 per cent, p &lt;0.001. Plasma K+ concentration was not affected by insulin injection in the fed animals; in fasted rabbits, plasma K+ levels fell 26 per cent, p = 0.006. Despite this unequivocal evidence of insulin action in both sets of animals, there was no change In the K+, Na+, or H2O content in the brains of the same animals 35 minutes after insulin injection.
These results, which give no evidence of a direct effect of insulin on electrolyte transport in brain, are in sharp contrast with those found in anesthetized rabbits, which suggested that insulin affects brain potassium and water content before any change in plasma glucose occurs.
Bone Mass and Bone Density in Maturity-type Diabetics Measured by the 125I Photon-absorption Technique
Authors: Leeuw I De , Abs R 
Published: September 2013

Bone mineral content (BMC) and bone density (BMC/W) of the radius were measured in 138 maturity-type diabetics with the Norland-Cameron bone mineral analyzer and compared with the results of age- and sex-matched controls. In some age groups the mean cortical and trabecular bone mass and density seemed to be significantly higher among diabetic patients, especially in those treated with oral antidiabetic agents.
Individual analysis reveals the existence of two distinct diabetic populations—a small group with a tendency to bone loss and a large group with bone gain—when compared with nondiabetic subjects. The higher body weight in the second group can be the origin of this difference.
A survey of the already published papers on this subject shows that comparison of the results is impossible because of the heterogeneity in the methodology of material and methods used by the different authors.
Autonomic Neuropathy and Painless Myocardial Infarction in Diabetic Patients: Histologic Evidence of Their Relationship
Authors: Faerman Isaac , Faccio Enrique , Milei José , Nuñez Rodolfo , Jadzinsky Mauricio , Fox Dora , Rapaport Mauricio 
Published: September 2013

Myocardial infarction is considered the prime cause of death among adult diabetic patients. In a great number of cases, during myocardial infarction the patients don't feel pain or it is atypical. Diagnosis can be neglected, and mortality increases.
In search of an explanation for the absence of pain in these patients, the authors studied the autonomie nerve fibers of the heart muscle with argentic and combined techniques, looking for lesions in the sympathetic or parasympathetic nerve fibers that conduct pain.
In the five cases of painless myocardial infarction studied, the nerve fibers showed typical lesions of diabetic neuropathy: beaded thickenings, spindle-shaped thickenings, fragmentation of fibers, and diminution of the number of fibers in the nerves.
The patients in the control group (five diabetics with painful infarction, five diabetics without infarction, five nondiabetics with painful infarction, and five nondiabetics without infarction) had no lesions.
These facts led us to assume that the absence of pain in diabetics with myocardial infarction could be due to a lesion of the afferent nerves that conduct pain.
An Audio Urine-glucose Analyzer for Blind Diabetics
Authors: May Jonathan , Inman Stanford , Wilcox David E , Beckett Ronald S 
Published: September 2013

At the instigation of one of the authors (J. M.)–a young man whose blindness is due to diabetic retinopathy–a urine-glucose analyzer was designed and constructed. Its purpose and function enable him to test his urine himself (free of dependence on others for this service) and, thereby, he can then determine and administer his doses of insulin. He and other young blind diabetics may value the degree of freedom from dependence on others tha the analyzer provides and feel it helps them to be able to work and care for themselves.
A description of the instrument, instructions for its use, and a summary of about 20 months' experience with it are submitted.
Monozygotic Triplets with Discordance for Diabetes Mellitus and Diabetic Microangiopathy
Authors: Ganda Om P , Soeldner J Stuart , Gleason Ray E , Smith Theresa M , Kilo Charles , Williamson Joseph R 
Published: September 2013

A set of monozygotic triplets (PE. K., P. K., S. K.) has been studied. There is no diabetes in first-degree relatives. PE. K. developed insulin-requiring (60 U. NPH) diabetes at the age of 13 years. Over a period of 11 years since that time, numerous studies of insulin and growth-hormone secretion were performed on P. K. and S. K., including multiple oral glucose tolerance tests (OGTTs), cortisone-primed oral glucose tolerance tests (C-OGTTs), intravenous glucose tolerance tests (IVGTTs), and intravenous tolbutamide tests (IVTTs). The results of each test were compared with age- and sex-matched control subjects. P. K. developed insulin-requiring (56 U. NPH) diabetes after remaining discordant for eight years. Glucose, insulin, and growth-hormone responses during all tests were normal except during the IVGTT performed four months prior to the onset of diabetes. This last IVGTT revealed a glucose disappearance rate of 0.98 per cent per minute, and the slope of the regression line of serum-insulin response (IRI) on blood glucose (BG) was markedly decreased to 0.005 μU./ml. IRI/mg./dl. BG (controls, 0.340 ± 0.04; mean ± S. E. M.). The insulin responses in P.K. and S. K. were similar during all OGTTs, C-OGTTs, and IVTTs. S. K. has continued to maintain normal glucose tolerance and normal insulin and growth-hormone responses during all tests.
The histocompatibility antigen studies have revealed HLA-A2, AW24, BW15, and BW40 phenotype in these monozygotic triplets.
Muscle capillary basement membranes of the nondiabetic triplet were normal, whereas both diabetic triplets manifested evidence of capillary basement membrane thickening.
The clinical and biochemical profiles in these triplets and the capillary basement membrane data lend strong credence to the role of “nongenetic” determinants in the development of “genetic” diabetes as well as diabetic microangiopathy in juvenile-onset-type diabetes.
Peripheral and Autonomic Nerve Function in Newly Diagnosed Diabetes Mellitus
Authors: Fraser D M , Campbell I W , Ewing D J , Murray A , Neilson J M M , Clarke B F 
Published: September 2013

Peripheral and autonomic nerve function was assessed in 10 newly diagnosed male diabetics (six insulin-treated and four sulfonylureatreated) with repeated observations over the subsequent six months. There was significant impairment of motor-conduction velocity in the common peroneal nerve at diagnosis in both treatment groups, with improvement following treatment in only the insulin-treated patients.
In contrast, although the blood glucose level fell in both groups, the mean level was significantly lower in the sulfonyhireatreated patients at two months and at each subsequent visit.
In the autonomic function tests significant abnormality was found in the electrocardiographic R-R-interval (beat-to-beat) variation in resting heart rate in two of the insulin-treated patients and all of the sulfonylurea-treated group, with improvement in only one of the latter. One patient in the sulfonylurea-treated group also showed an abnormal response to the Valsalva maneuver (expressed as the Valsalva ratio), and this remained abnormal throughout the period of study. All other patients had normal responses to the Valsalva maneuver and sustained handgrip test. None of the patients had postural hypotension. Abnormalities in autonomic nerve function in diabetics at diagnosis have not been previously reported.
Alteration of Islet Cell Populations in Spontaneously Diabetic Mice
Authors: Baetens D , Stefan Y , Ravazzola M , Malaisse-Lagae F , Coleman D L , Orci L 
Published: September 2013

Endocrine-cell populations in the islets of Langerhans of mutant mice with a severe hypoinsulinemic diabetes (obiob or dbldb on the C57BL/KsJ background) or with a mild hyperinsulinemic diabetes (ob/ob or db/db on the C57BL/6J background) were studied quantitatively by immunofluorescence and morphometry. In severely diabetic mice, islets presented a reduced proportion of insulin-containing cells buf increased glucagon-, somatostatin-, and pancreatic polypeptide (PP)-containing cells, as compared with islets of control (+/+) mice. An inverse change was observed in islets of mildly diabetic mice: islets were hypertrophie and composed mostly of insulin-containing cells, with decreased proportions of glucagon-, somatostatin-, and PP-containing cells.
In both types of diabetic syndromes, the changes in cell populations induced a qualitative alteration of cellular interrelationships in the affected islets.
Hyperchloremic Metabolic Acidosis in Diabetes Mellitus: A Case Report and Discussion of the Pathophysiologic Mechanisms
Authors: Hammeke M , Bear R , Lee R , Goldstein M , Halperin M 
Published: September 2013

A 21-year old woman with poorly controlled diabetes mellitus was examined for persistent hyperchloremic metabolic acidosis. There was no evidence of ingestion of hydrochloric acid or its equivalent. Gastrointestinal loss of bicarbonate was absent. Proximal tubular bicarbonate reabsorption and distal nephron hydrogen-ion secretion were normal. Ammonia and net acid excretions were high, and thus there was no obvious cause for this acidosis.
Further study revealed a very large loss of β-hydroxy-butyrate in the urine that closely approximated net acid excretion. This loss of potential bicarbonate was the principal cause for the hyperchloremic metabolic acidosis. Phosphate, urate, and β-hydroxybutyrate fractional excretions were all abnormally high. Generalized aminoaciduria was also present, but the renal handling of glucose and bicarbonate was normal. With improved control of her diabetes, the generalized aminoaciduria disappeared, the urine β-hydroxybutyrate loss ceased, the fractional excretions of phosphate and urate approached normal, and the acidosis was rapidly corrected.
Comparison and Effects of Natural and Synthetic Glucose Tolerance Factor in Normal and Genetically Diabetic Mice
Authors: Tuman Robert W , Bilbo James T , Doisy Richard J 
Published: September 2013

Glucose tolerance factor (GTF) is thought to be volatile in the dry state at certain temperatures. This property allowed us to measure the stable and the volatile chromium contents of three brewer's yeast GTF preparations and to investigate the possible relationship between the volatile chromium content and its biologic activity. Two forms of chromium were found in brewer's yeast extracts by flameless atomic absorption spectroscopy using two different methods of sample preparation. Three brewer's yeast GTF preparations were found to contain total Cr concentrations ranging from 0.40 to 0.81 μg. per milligram dry weight and volatile Cr concentrations ranging from 0.02 to 0.39 μg. per milligram dry weight. The biologic response obtained with each GTF preparation was linearly related to the concentration of volatile chromium present. These observations suggest that the volatile chromium fraction in brewer's yeast is biologically important, whereas the active component of these yeast preparations is probably a precursor of GTF.
The metabolic effects of synthetic chromium-nicotinic add-ammo acid complexes and a brewer's yeast GTF preparation were compared in normal and genetically diabetic mice. The synthetic preparations mimicked the effects of brewer's yeast GTF by lowering plasma glucose and triglyceride concentrations, although at different time courses. In addition, biologically active synthetic complexes have been synthesized and may contain no volatile chromium. Synthetic complexes of chromium-nicotinic acid-amino acids lowered blood glucose by only IS to 20 per cent in normal mice as against a 36 per cent reduction with brewer's yeast GTF. Further, a synthetic product produced a significant reduction in the elevated plasma concentrations of glucose and triglycerides in genetically diabetic mice (18 and 26 per cent, respectively). This is in contrast to the 29 per cent reduction in plasma glucose and a 56 per cent reduction in plasma triglycerides produced by GTF prepared from brewer's yeast. These findings suggest that the synthetic factors are similar to, but not identical with, the active GTF fraction extracted from brewer's yeast.