bluuebunny/crossref_metadata_2025_split huggingface dataset:
Glucose Intolerance with Hypokalemia: Failure of Short-term Potassium Depletion in Normal Subjects to Reproduce the Glucose and Insulin Abnormalities of Clinical Hypokalemia
Authors: Gorden Phillip 
Published: December 2014

The mechanism by which potassium deficiency per se impairs glucose tolerance was studied in seven subjects who were potassium depleted experimentally (mean depletion = 326 mEq.).
In five subjects studied using the oral glucose tolerance test, all showed impairment during the potassium depletion phase compared to the predepletion control period, and four of five subjects showed improvement with potassium repletion. The four subjects with impaired glucose tolerance compared to both control periods showed a delay in the initial phase of total immunoreactive insulin release. None of the five subjects showed a significant variation in the per cent proinsulin-like component from the potassium depletion phase to either control period. Two subjects studied using the intravenous glucose tolerance test showed no impairment of glucose tolerance with potassium depletion, and no evidence of insulin resistance was found following the injection of 0.05 U. per kilogram of insulin. These two subjects did manifest impaired growth hormone responses to the hypoglycemic stimulus, however.
Potassium depletion per se impairs glucose tolerance. The defect is mild; severe glucose intolerance, alterations in total immunoreactive insulin, and plasma insulin components seen in clinical hypokalemic states involve a complex interplay between potassium deficiency and the primary disease state.
Fetal Rat Pancreas: Differentiation of the Acinar Cell Component in Vivo and in Vitro
Authors: McEvoy Robert C , Hegre Orion D , Leonard Robert J , Lazarow Arnold 
Published: December 2014

Fetal rat pancreases, Day 16 through Day 22 postcoitum, were analyzed biochemically for amylase and chymotrypsinogen to assess acinar cell development in vivo. The interval between -eighteen and twenty days proved to be a critical period in the differentiation of the acinar component. Eighty- and thirtyfold increases in, respectively, amylase and chymotrypsinogen concentration were accompanied by a large increase in the acinar cell percentage of the pancreas.
Explantation of pancreas either before or after this critical period resulted in a developmental pattern which varied from that observed in vivo. The present organ culture system neither supported the differentiated acinar cell nor favored the further development of new acinar cells.
Using the present organ culture system, explants can be produced which are devoid of acinar cells and their exocrine enzymes.
Plasma Norepinephrine and Epinephrine in Untreated Diabetics, During Fasting and After Insulin Administration
Authors: Christensen Niels Juel 
Published: December 2014

Employing a precise and sensitive double-isotope derivative technic, plasma norepinephrine and epinephrine were measured in twenty-three normal subjects and fourteen diabetics during various metabolic conditions. Patients with poorly controlled diabetes showed a rise in norepinephrine, which correlated with the degree of metabolic derangement, during resting conditions. High epinephrine values were seen only in patients with moderate to severe ketoacidosis. During exercise, diabetic patients with ketosis demonstrated large increments in plasma catecholamines as compared to normals. During insulin treatment, when good control had been achieved, plasma catecholaniine levels were similar to those in normal subjects.
During prolonged fasting, plasma norepinephrine rose from 0.18 to 0.40 ng. per milliliter in four normal nonobese subjects. No change was observed in plasma epinephrine.
During insulin hypoglycemia, high plasma epinephrine levels were seen only in subjects in whom the blood glucose concentration declined to values below 20 mg. per 100 ml. Plasma norepinephrine rose as blood glucose concentrations decreased even in diabetics in whom values had not reached hypoglycemic levels. No correlation was observed between plasma epinephrine and increase in pulse rate during hypoglycemia.
Urinary Excretion of n-Hexanedioic and n-Octanedioic Acid in Juvenile Diabetics with Ketonuria
Authors: Pettersen Jon Elling 
Published: December 2014

Urine samples from patients with newly diagnosed juvenile diabetes and predibetic coma or ketonuria, but no acid-base disturbances in the blood, have been analyzed for dicarboxylic acids by combined gas-liquid chromatography and mass spectrometry.
The precomatose patients excreted up to 210 and 38 μg./1 mg. of creatinine, respectively, of n-hexanedioic and n-octanedioic acid. The excretion was almost normalized within a few hours by insulin treatment. Nonacidotic patients with ketonuria excreted 9.2 ± 5.1 mg./24 hr. of n-hexanedioic acid, and some also excreted slightly increased amounts of n-octanedioic acid. All patients excreted normal amounts of 3-methylhexanedioic acid, which was unaffected by insulin treatment.
Our findings direct attention to a metabolic pathway which may be of importance in the pathogenesis of ketosis in diabetes mellitus, namely the formation of short-chain dicarboxylic acids (for instance, intermediates of the tricarboxylic acid cycle) by ω-oxidation of fatty acids followed by β-oxidations of the dicarboxylic acids thus formed.
Diabetes in American Indians and Other Native Populations of the New World
Authors: West Kelly M 
Published: December 2014

This is a review of previous and more recent observations on the prevalence and manifestations of diabetes in aboriginal populations of the New World. Rates of diabetes have now been measured or estimated in more than eighty of these groups in the Americas, Greenland, Polynesia, Micronesia and Melanesia. Diabetes was probably uncommon in all these native populations prior to 1940. It is now rife in many of these groups, but still rare in many. Among certain of these populations, rates of diabetes in adults still differ more than tenfold. Among groups of diabetics there are probably significant intertribal differences in the susceptibility to certain manifestations and complications such as retinopathy and coronary disease. There appear to be peculiarities in the insulin secretion patterns of certain of these tribes.
The available evidence does not rule out the possibility that genetic factors play an important role in determining inter-tribal differences in prevalence and manifestations. But it is also clear that environmental factors exert powerful effects. Low rates of diabetes have been observed in Athapascan tribes and in some Shoshonean tribes. Diabetes was also rare prior to 1940 in Athapascan and Shoshonean Indians of Oklahoma. But diabetes has recently become common in these Oklahoma tribes. They were formerly lean and are now fat. The status of the many Oklahoma tribes is of particular interest because they represent seven of the eight major linguistic groups of North American Indians, having originated in very diverse parts of the Continent. Rates are now high in all Oklahoma tribes for which evidence is adequate to permit an estimate of prevalence. This includes fifteen tribes drawn from seven different linguistic groups. In seven additional Oklahoma tribes preliminary evidence, although less complete, suggests the probability that rates are also high.
Studies of the dramatic emergence of diabetes and its manifestations in these aboriginal groups has considerable potential for gaining a better understanding of the genetic and environmental factors which influence risk and pathophysiology of diabetes and its complications.
Glucose Metabolism and Insulin Secretion in the Newborn Infant: Comparisons Between the Responses Observed the First and Seventh Day of Life to Intravenous and Oral Glucose Tolerance Tests
Authors: Falorni A , Fracassini F , Massi-Benedetti F , Maffei S 
Published: December 2014

Insulin secretion and glucose metabolism were studied during intravenous and oral glucose tolerance tests performed in one day and seven day old full-term and premature infants. Mean glucose disposal during the intravenous tests was more rapid in seven day old than in one day old infants.
Insulin responses after intravenous glucose were characterized by higher insulin levels during the initial phase and lower levels during the second phase in both seven day old premature and full-term groups as compared with the patterns seen in one day old infants. No differences in the mean values for blood glucose and plasma insulin were found among the four groups of infants at any time during the oral tests.
Glycogen Accumulation in Retinal Neurons and Glial Cells of Streptozotocin-diabetic Rats: Quantitative Electron Microscopy
Authors: Sosula Leo , Beaumont Paul , Hollows Frederick C , Jonson Keith M , Regtop Hubert L 
Published: December 2014

The concentration of glycogen β-particles was measured in the inner retinal layers of normal and streptozotocin-diabetic rats with quantitative electron microscopic technics. Diabetes was uncontrolled and of short duration (thirty days). Blood glucose levels in the normal and diabetic animals were 76 ± 8 S.E. and 340 ± 25 S.E. mg./100 ml. Diabetes caused glycogen accumulation in the amacrine, bipolar, ganglionic, Müller and capillary mural cells. Quantitative estimates showed significant increases (p &lt; 0.001) in the glycogen concentrations of cells in the nerve fiber layer (NFL), inner plexiform layer (IPL) and inner nuclear layer (INL) of the diabetic retinas.
The glycogen concentrations increased from 6.4 ± 0.41 β-particles per square micron in the normal to 10.5 ± 0.85 in the diabetic Müller endfeet (NFL); from 12.9 ± 1.5 to 38.6 ± 5.0 in the Müller processes (IPL); from 0.81 ± 0.13 to 3.37 ± 0.49 in the neural processes (IPL); from 2.7 ± 0.66 to 17.3 ± 2.4 in the amacrine cell bodies (INL). Diabetic glycogen accumulation occurred at a greater rate in the neurons than in the Müller cells. The amacrine neurons were the most severely affected and contained massive glycogen deposits in their cytoplasm.
The glycogen concentration in the neurons was less than that of the Müller cells. However, the Müller cells represent only ∼10 per cent of the total cytoplasm of the IPL, whereas the neurons occupy ∼90 per cent of this layer. From the above data, it is evident that the neurons contain about one third of the total glycogen of the normal IPL. In the diabetic IPL, the total glycogen is approximately evenly distributed between the neural and glial compartments.
Sodium Retention Accompanying Insulin Treatment of Diabetes Mellitus
Authors: Saudek Christopher D , Boulter Philip R , Knopp Robert H , Arky Ronald A 
Published: December 2014

Urinary sodium excretion before and during insulin therapy was studied in six patients with poorly controlled diabetes. One subject had ketoacidosis; manifestations in the other five ranged from slight ketoacidosis to hyperglycemia alone. All patients retained sodium when diabetes was controlled by insulin, the mean positive sodium balance being 286 mEq. over three days. The diminished urinary sodium excretion did not correlate with the fall in glucosuria or ketonuria; insulin withdrawal studies in two patients indicated that sodium depletion during insulin lack is not a prerequisite for sodium retention during retreatment Im-munoreactive glucagon fell from elevated levels as control of diabetes was established.
It is concluded that sodium retention occurs regularly during insulin treatment of poorly controlled diabetes, whether ketoacidosis is present or not. The positive sodium balance should be anticipated when insulin therapy is instituted.
Sexual Dysfunction in Diabetic Men
Authors: Kolodny Robert C , Kahn Charles B , Goldstein H Howard , Barnett Donald M 
Published: December 2014

Sexual function was studied in 175 diabetic male outpatients randomly selected. Data collected included medical and sexual histories, physical examination, complete blood count, urinalysis, T4, 12 channel chemistry screening profile and plasma testosterone determination. Eighty-five of the 175 men were impotent (49 per cent), four reported premature ejaculation (2 per cent) and two subjects had retrograde ejaculation (1 per cent). In the group with impotence, the mean age of the subjects and duration of diabetes were respectively fifty-three and six years. In patients without impotence, the comparable values were fortyfive and five years.
Typically, the onset of impotence was gradual, usually progressing over a period of six months to a year with an interval during which firmness of erection was decreased. Levels of sexual interest were sustained in almost all subjects. Over 90 per cent of the males studied gave a pattern of impotence compatible with an organic rather than a psychologic etiology.
Occurrence of impotence'was not definitely correlated with duration of diabetes or with insulin or oral agents. Incidence of peripheral neuropathy was increased in the group with sexual dysfunction.
Plasma testosterone levels were within normal limits in impotent diabetics or in the group without impotence, respectively (mean ± S.E.M.) 627 ±15 and 637 ± 14 ng per cent. It is apparent from these findings that androgen deficiency was not an etiologic factor in this group of diabetic men with impotence.
Clinical Studies of Alcoholic Ketoacidosis
Authors: Cooperman Michael T , Davidoff Frank , Spark Richard , Pallotta Johanna 
Published: December 2014

Seven episodes of severe ketoacidosis in six nondiabetic patients were recognized at this hospital within an eighteen month period. All were women; one pregnant patient experienced two episodes at twenty-eight and thirty-two weeks' gestation. All patients admitted to heavy chronic alcohol intake and drinking binges.
On admission, these patients were conscious and alert. Mean values were 143 mg./100 ml. for plasma glucose and 7.25 for arterial pH. Plasma bicarbonate was depressed with a mean anion gap of 18. Beta-hydroxybutyrate/acetoacetate ratio averaged 5.2. All patients had liver function abnormalities. Mean serum immunoreactive insulin was low, 5μU./ml. (n=2), while cortisol was markedly elevated at 76.5μg. per cent (n=3); mean growth hormone level was 14.1 ng./ml. (n=3). Free fatty acid concentration, measured on admission in one episode, was 1,945 mEq./L. Therapy with glucose, saline, and minimal amounts of alkali led to prompt recovery. Circulating levels of cortisol, insulin and growth hormone were measured serially in one patient during recovery; they quickly returned to normal.
The dissociation of severe ketosis from glycosuria and hyperglycemia in these patients raises important questions concerning coupling of ketogenesis to gluconeogenesis. The striking preponderance of women, including one pregnant patient, reported with this condition also suggests a possible role for ovarian and placental hormones in its pathogenesis; fetal drain on carbohydrate reserves may further contribute to the tendency to ketosis.
Alcoholic ketoacidosis may be relatively common, since we saw one case of this syndrome for about every four of diabetic ketoacidosis during this period.
Purification and Immunologic Identification of Aldose Reductases
Authors: Gabbay Kenneth H , Cathcart Edgar S 
Published: December 2014

A general method for the identification and purification of aldose reductase (alditohNADP oxidoreductase, EC 1.1.1.21) and NADP-L-hexonate dehydrogenase (L-gulonate:NADP oxidoreductase, EC 1.1.1.19) from tissues is described. Two aldose reductase isoenzymes, AR-A and AR-B, were isolated from renal papilla and were characterized. These two forms were also found in brain, retina, pancreas, lens and optic nerve. AR-A and AR-B differed primarily in glucuronate-reducing activity. All tissues, with the exception of lens and optic nerve, also contained NADP-L-hexonate dehydrogenase activity. Human red blood cells contained NADP-L-hexonate dehydrogenase activity but not aldose reductase.
The aldose reductases and the two isoenzyme forms isolated from these tissues were immunologically identical as demonstrated with a specific antiserum prepared in rabbits against papillary AR-B. The antiserum inhibited AR-A and AR-B activity equally in vitro. The extent of enzyme inhibition by the antiserum was similar when glucuronate, glucuronolactone, xylose and glyceraldehyde were used as substrates. The antiserum did not react with NADP-L-hexonate dehydrogenase. Therefore, the method provides a specific means for identifying aldose reductase in crude tissue homogenates.
Acute Metabolic Effects of Human Growth Hormone
Authors: Fineberg S Edwin , Merimee Thomas J 
Published: December 2014

These studies were done to clarify the actions of human growth hormone (HGH) during the two hours after concentrations were increased. These effects cannot be attributed to generation of somatomedin. Mean systemic levels of HGH were increased to 92.6 ng. per milliliter by the intravenous infusion of 4 mg. of HGH over thirty minutes. During the first hour, mean plasma glucose and free fatty acid (FFA) concentrations decreased by 9.5 ± 1.9 per cent and 21.2 ± 3.6 per cent, respectively. After two hours, FFA concentrations rose to 145 per cent of basal.
An identical preparation of HGH was then perfused across forearm tissues at mean forearm venous concentrations of 28.4 ± 1.5 ng. per milliliter or 200.3 ± 7.9 ng. per milliliter. Glucose uptake was acutely decreased (by 30 per cent) by both doses of HGH; neither dose had significant effects upon lipolysis. Therefore, neither physiologic nor supraphysiologic concentrations of HGH had an insulin-like effect upon peripheral muscle or adipose tissue. Small increases in peripheral HGH concentrations had virtually identical effects upon enhancement of potassium uptake and reduction of glucose uptake across muscle as mean concentrations ten times higher.
Cerebral Edema and Depression of Sensorium in Nonketotic Hyperosmolar Coma
Authors: Arieff Allen I , Carroll Hugh J 
Published: December 2014

The influence of body water and solute equilibria between extracellular fluid and cerebrospinal fluid (CSF), both before and during therapy, was studied in fifty-three patients who had hyper-glycemia (blood glucose 600 mg./100 ml.) in the absence of ketoacidosis. Particular attention was directed to both depression of sensorium and the possible production of cerebral edema. Before therapy, depression of sensorium was highly correlated with plasma osmolality (r =.84), but not with glucose concentration or pH of either CSF or plasma. Plasma and CSF were in osmotic equilibrium before therapy (389 mOsm/kg.) but glucose concentration was significantly higher in plasma while Na+ and Cl− were higher in CSF. During treatment with insulin and hypotonic NaCl infusion, the osmolalities of CSF and plasma fell at essentially identical rates. Plasma osmolality fell as a consequence of both a fall in glucose concentration and a gain in free water, but the fall in CSF osmolality was almost entirely due to a gain in water by the CSF. Insulin administration was stopped when plasma glucose was about 250 mg./100 ml., and in all patients there was no increase in CSF pressure or clinical evidence of cerebral edema.
In patients with nonketotic coma, depression of sensorium is highly correlated with the plasma osmolality. During therapy with insulin and hypotonic NaCl infusion, it appears that cerebral edema does not occur if insulin is stopped before plasma glucose falls below 250 mg./100 ml.
Altered Glucoregulatory Hormones During Acute Pneumococcal Sepsis in the Rhesus Monkey
Authors: George David T , Rayfield Elliot J , Wannemacher Robert W 
Published: December 2014

To determine the effects of a Diplococcus pneumoniae infection upon the dynamics of glucose metabolism and the hormones responsible for its control, intravenous glucose tolerance tests (IVGTT's) were performed in monkeys during baseline control conditions and twenty-four hours after initiating infection when the monkeys were febrile. Along with plasma glucose, immunoreactive insulin and glucagon concentrations were measured sequentially through each IVGTT. Furthermore, fasting concentrations of plasma amino acids, immunoreactive growth hormone and cortisol were determined.
These data reveal no differences in the fasting plasma concentrations of growth hormone and glucose, or in the disappearance rates of glucose during the two IVGTT's. There was, however, a mild relative hyperinsulinemia (p &lt; 0.05) (following glucose) along with fasting hyperglucagonemia (p &lt; 0.01) during infection. Of the twenty-one amino acids measured, twenty were depressed during infection; only cysteine was elevated (p &lt; 0.05) in the infected monkeys. Although plasma cortisol levels were significantly (p &lt; 0.05) increased above preinfection values by the stress of infection, they remained within the control range.
The hyperglucagonemia and depression of the mean insulin: glucagon molaf ratio are compatible with the catabolic events occurring during a mild bacterial infection in the monkey.
Characterization of Carbohydrate Metabolism in the Isolated Fetal Rat Heart: Effects of Fasting and Alloxan Diabetes
Authors: Vinicor Frank , Kohalmi Diane , Clark Charles M 
Published: December 2014

Studies have been made on the effects of maternal fasting and alloxan-induced diabetes on fetal and maternal plasma glucose and insulin concentrations, as well as on fetal myocardial and hepatic glycogen concentrations. Maternal fasting for sixteen hours, ending seventy-two hours prior to sacrifice, had no effect on maternal glucose and insulin concentrations. Under these conditions fetal insulin and hepatic and myocardial glycogen concentrations were also unchanged; fetal plasma glucose increased [from 16±2 to 26±3 mg.'100 ml. (p&lt;0.02]. A sixteen-hour maternal fast immediately preceding sacrifice significantly decreased maternal insulin and glucose concentrations. Fetal hepatic and myocardial glycogen levels and insulin concentrations were also decreased; fetal glucose again increased [from 35±1 to 43±1 mg.'100 ml. the fetal rat, and the importance of fetal insulin on fetal glycogen concentrations are discussed.
Maternal alloxan diabetes produced elevated glucose concentrations, unchanged insulin values, decreased hepatic glycogen and increased myocardial glycogen in the fetuses. Possible mechanisms for these findings are discussed. Fetal myocardial glucose uptake in vitro was not affected by either fasting or maternal diabetes.
The data suggest that, whereas near-term fetal rats do possess some ability to control their glucose and glycogen concentrations, manipulation of maternal nutrition by fasting or alloxan diabetes can significantly alter fetal carbohydrate metabolism.
Diet Therapy of Diabetes: Description of a Successful Methodologic Approach to Gaining Diet Adherence
Authors: Weinsier Roland L , Seeman Anne , Herrera M Guillermo , Simmons Jeanette J , Collins Mary E 
Published: December 2014

A multifaceted educational program was designed to maximize dietary adherence of twenty-three diabetic subjects in order to study two experimental diets for forty weeks. The results of the program showed that a high level of diet adherence was achieved in spite of the strict dietary guidelines. The success of the educational approach was also reflected in the high attendance rate (99 per cent of 270 subject visits) and the low voluntary attrition rate (4 per cent).
Five aspects of the over-all design were felt to have been of major importance in gaining subject cooperation: (1) the small, grouporiented learning process; (2) frequent intervals of follow-up; (3) feedback on laboratory data; (4) individualization of diet prescriptions; and (5) family involvement.
Since the majority of diabetics seen in medical clinics fail to follow their prescribed diets, the concepts and approach applied to this study may be applicable to the dietary management of diabetic patients. Such implications and specific recommendations are presented in this report.