bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence of Diabetes and Glucose Intolerance in 199 Offspring of Thirty-seven Conjugal Diabetic Parents
Authors: Tattersall Robert B , Fajans Stefan S 
Published: September 2013

We have studied the prevalence of diabetes and glucose intolerance, both cross-sectionally and longitudinally, in a cohort of 199 offspring of conjugal diabetic parents.
Although the prevalence of already known diabetes was low (11.5 per cent), twenty-eight of 123 tested offspring (23 per cent), ranging in age from ten to sixty (mean 32.6) years had latent diabetes on their initial glucose tolerance test. Eighty of 123 tested offspring had a normal initial glucose tolerance test. Forty-one of those whose first glucose tolerance test was normal were retested after a mean of 9.4 years and showed no significant change in mean glucose tolerance.
On the basis of questionnaire data only, we estimate that cumulatively 36.5 per cent of offspring will have diabetes by the age of sixty years. However, if all offspring are routinely surveyed with glucose tolerance tests, 60 per cent will have abnormal glucose tolerance by the age of sixty years. In view of the high prevalence of asymptomatic latent diabetes, genetic studies of diabetes should not be based on questionnaire data.
In six families all offspring were diabetic; in twenty-one families there was a mixture of diabetic and nondiabetic offspring; and in ten none of the offspring was diabetic. The finding of families with no diabetic offspring suggests the possibility of genetic heterogeneity of diabetes in the parents.
Most of the parents had maturity-onset diabetes with a mean age at diagnosis of 54.5 years of age. Diabetes among their offspring was generally of a mild maturity-onset type. Only 2 per cent of offspring at risk had developed juvenile-onset type diabetes. Thus the prevalence of any metabolic abnormalities in offspring of two maturity-onset type parents cannot be assumed to be relevant to the offspring of parents with juvenile-onset type diabetes.
Effect of Glucose on the Growth Hormone Response to L-dopa in Normal and Diabetic Subjects
Authors: Ajlouni Kamel , Martinson Donald R , Hagen Thad C 
Published: September 2013

The effect of hyperglycemia on the growth hormone response to oral L-dopa (500 mg.) was assessed in eight normal and eight insulin-dependent diabetic subjects. A peak growth hormone response of 21.0 ±4.0 ng./ml. (mean / S.E.M.), significantly above baseline (p &lt;0.01), was achieved in the normal group following oral L-dopa. Glucose concentrations did not change and were approximately 80 mg./100 ml. throughout. Administration of 100 gm. oral glucose with the L-dopa, or thirty minutes thereafter, totally suppressed the growth hormone response in all eight and six of the subjects, respectively.
A peak growth hormone response of 20.0 /1.7 ng./ml. (mean / S.E.M.), significantly above baseline (p &lt;0.001), was obtained in eight nonobese, insulin-dependent diabetics, in spite of prevailing hyperglycemia (mean plasma glucose 243-258 mg./100 ml.) throughout the test. Endogenous hyperglycemia was achieved in these patients by lessening the usual strict adherence to plasma glucose control for the purpose of the study.
These results suggest an abnormality in the hypothalamus or pituitary of diabetic subjects allowing growth hormone responsiveness in spite of hyperglycemia.
Effect of Lectins on Hormone Release from Isolated Rat Islets of Langerhans
Authors: Ewart Robin B L , Kornfeld Stuart , Kipnis David M 
Published: September 2013

Lectins from Agaricus bisporus and Agaricus campestris stimulate insulin and glucagon release from isolated rat islets in the presence of 2 mM glucose. In the case of insulin release, maximal stimulation was observed at lectin concentrations above 58 μg. per milliliter (approximately 1 μM). A. bisporus PHA-B-stimulated insulin release was independent of a source of metabolic energy but was abolished by deuterium oxide. The lectin did not alter islet glucose oxidation to CO2 or incorporation of [3H] leucine into trichloracetic acid-precipitable material nor did it modify rates of insulin secretion induced by 20 mM glucose. None of nine other lectins tested stimulated insulin release, whereas stimulation of fat cell glucose oxidation was a general property of the lectins.
Binding of 125I-Iabeled A. bisporus PHA-B to islets increased with time up to one hour and after attainment of equilibrium was very slowly reversible. Binding was directly proportional to islet number and the estimated Kdiss of the binding reaction was 17 μg per milliliter. The total number of A. bisporus PHA-B binding sites per islet was approximately 2 × 1010.
Binding of A. bisporus PHA-B to the islets and A. bisporus PHA-B-stimulated insulin release were inhibited in parallel by a glycopeptide containing the oligosaccharide receptor for the lectin, suggesting that lectin binding is essential for the expression of insulin-releasing activity.
It is proposed that the specific interaction between mushroom lectin and its receptors may lead to conformational changes in the structure of the membranes of the islet A2- and B-cells that facilitate exocytosis.
Decreased Cyclic AMP and Insulin Response to Glucose in Isolated Islets of Neonatal Rats
Authors: Grill Valdemar , Asplund Kjell , Hellerström Claes , Cerasi Erol 
Published: September 2013

The (3H) cyclic AMP accumulation was measured in incubations of pancreatic islets from one-day, six-day, and thirty-five-day-old rats exposed to a low (0.6 mg./ml.) or a high (3.0 mg.'ml.) glucose concentration with or without the addition of 0.1 mM. of the phosphodiesterase inhibitor 3-isobutyl - 1 -methylxanthine (IBMX). In the thirty-five-day-old rats, (3H) cyclic AMP accumulation was significantly enhanced after sixty minutes' incubation in a high glucose concentration and further increased by IBMX. These changes were paralleled by a stimulated insulin release, measured simultaneously. By contrast,. in the one-day-old rats, no effect of glucose with or without IBMX was seen on (3H) cyclic AMP, while the minor insulin release due to high glucose alone was markedly potentiated by IBMX. Even in the presence of this agent the insulin response to glucose was, however, clearly inferior to that seen in the thirty-five-day-old animals. The stimulatory pattern of glucose-induced insulin release in the six-day-old animals was intermediate between the other two age groups. At this age, stimulation of (3H) cyclic AMP due to glucose was observed only in the presence of IBMX. Measurement of (3H) cyclic AMP after three minutes' incubation confirmed these different stimulatory patterns of glucose in the age groups studied.
It is suggested that the inefficiency of glucose to stimulate theadenyl cyclase-cyclic AMP system of the beta cell from fetal and neonatal animals may be one important factor determining the insensitivity to the insulin-releasing action of glucose that exists at this stage of development.
Studies on the Mechanism of Epinephrine-induced Hyperglycemia in Man: Evidence for Participation of Pancreatic Glucagon Secretion
Authors: Gerich John E , Lorenzi Mara , Tsalikian Eva , Karam John H 
Published: September 2013

In man, epinephrine induces increases in plasma levels of glucagon, a lipolytic and hyperglycemic hormone. To determine glucagon's contribution to this hyperglycemia and lipolysis, the effects of inhibition of pancreatic alpha-cell responses to epinephrine were investigated with somatostatin and adrenergic receptor blockade. To avoid ambiguities that might result from concomitant changes in endogenous insulin secretion, these studies were performed in juvenile-type, insulin-deficient diabetic subjects.
Compared with normal subjects, the diabetics had excessive glucagon responses to epinephrine, which had been infused to attain circulating levels within the range found in man in severe stress. Both somatostatin and propranolol completely prevented glucagon responses and diminished the glycemic response to epinephrine by 40 to 50 per cent. Free fatty acid responses to epinephrine were completely prevented by propranolol but unaffected with somatostatin. Phentolamine had no effect on glucose, free fatty acid, or glucagon responses to epinephrine.
These studies demonstrate that epinephrine, via a betaadrenergic receptor mechanism, causes excessive plasma glucagon elevation in human diabetes mellitus and indicate that this hyperglucagonemia participates in the hyperglycemic, but not the lipolytic, response to epinephrine. Catecholamine-induced hyperglucagonemia may thus provide an additional explanation for the deterioration in carbohydrate tolerance associated with stress.
Insulin Adsorbance to Polyvinylchloride Surfaces with Implications for Constant-infusion Therapy
Authors: Peterson Lance , Caldwell Jeanne , Hoffman James 
Published: September 2013

Because of the current interest in constant intravenous infusions of insulin for hyperglycemic conditions, we have re-examined the problem of insulin adsorption to the solid surfaces of commonly used infusion sets. Using both labeled and unlabeled insulin, we have compared solutions with and without albumin through various methods of delivery. An infusion system incorporating a 50-ml. wash-out with a solution of 25 U. regular insulin in 500 ml. normal saline permits delivery of at least 75 per cent of expected insulin for the first 50 ml. of the infusion and 100 per cent thereafter. After the first 20 ml. of the infusion, the per cent insulin recovered from the system is identical to that observed when albumin was added to the infusion solution at a concentration of 1.25 gm. per cent.
From these data, we conclude that if an insulin concentration of at least 25 U./500 ml. is used, and if 50 cc. is washed through the infusion apparatus before treatment of a hyperglycemic patient is instituted, no extra protein additives are necessary.
Epidemiologic Findings on the Relationship of Time of Day and Time Since Last Meal to Glucose Tolerance
Authors: Mayer Kenneth H , Stamler Jeremiah , Dyer Alan , Freinkel Norbert , Stamler Rose , Berkson David M , Farber Bruce 
Published: September 2013

Data from 10,559 men and women, age 30–64, participating in the morning and afternoon in a Chicago Health Department multiphasic screening project, were used to determine the effects of time of day and time since last meal on the values for plasma glucose one and two hours following oral challenge with 100 gm. of glucose.
Mean plasma glucose values and rates of suspect glucose intolerance (based on several cutpoints) were sizeably higher in the afternoon than in the morning. In addition, plasma glucose values increased with time elapsed since the last meal, up to 10 hours postprandially. Thereafter, both one- and two-hour plasma glucose values tended to exhibit a decline. Analysis of covariance confirmed that fluctuations in glucose tolerance were related to time of day and time since last meal, but the effects of each parameter were exerted independently.
Interaction of Somatostatin, Glucagon, and Insulin on Hepatic Glucose Output in the Normal Dog
Authors: Altszuler Norman , Gottlieb Barbara , Hampshire Jennifer 
Published: September 2013

The interaction of insulin and glucagon during infusion of somatostatin (SRIF), which suppresses secretion of these hormones, was investigated in normal, postabsorptive, concious dogs. Hepatic glucose output (production) and over-all glucose uptake by the tissues was measured with 3-3H-glucose, administered by a priming injection along with a constant infusion. Infusion of SRIF (1.5–5.0 μg/min) for 90 minutes resulted in a moderate hypoglycemia associated with a decrease in glucose production. In some animals glucose production and plasma glucose levels returned to normal before the end of SRIF infusion. Glucose uptake tended to follow plasma glucose levels. Upon termination of SRIF infusion, glucose production and uptake and plasma glucose increased sharply.
Infusion of glucagon (1 μg./kg./hr.) along with SRIF (3.3 μg./min.) caused an exaggerated increase in glucose production and hyperglycemia over that of glucagon infusion alone. Infusion of a smaller dose of glucagon (0.2 μg./kg./hr.) for two hours produced only small increases in plasma glucose and glucose production; addition of SRIF during the third hour caused a significant increase in glucose production and plasma glucose. Addition of insulin (0.03 U./kg./hr.) to the glucagon infusion had little effect. However the further addition of SRIF failed to produce the marked increase in glucose production and hyperglycemia seen with glucagon-SRIF infusion.
It is concluded that acute insulin deficiency produced during SRIF infusion makes the liver more sensitive to the effects of glucagon and that the response of the liver to glucagon and other hyperglycemic agents may be modulated by insulin.
Provocation of Postural Hypotension by Insulin in Diabetic Autonomic Neuropathy
Authors: Page M McB , Watkins P J 
Published: September 2013

The effect of insulin administration on blood pressure has been investigated in eight diabetes with autonomic neuropathy. Systolic and diastolic pressures fell considerably after insulin in all of them. This effect was aggravated by tilting to the vertical position. Five patients fainted when upright with systolic blood pressures less 50 mm. Hg.
This hypotensive effect of insulin occurs whether it is administered intravenously, intramuscularly, or subcutaneously. The onset of the effect is almost immediate after intravenous insulin, is progressive, and may last for several hours. It coincides with a falling blood glucose level and occurs before hypoglycemic levels are reached, and it may be present when the blood glucose level is still elevated. Diurnal variations of postural hypotension have been recorded in some patients, the standing blood pressure falling with the onset of insulin action and rising again as the latter declines.
Some of our patients were unable to differentiate between symptoms of hypoglycemia and hypotension. Postural hypotension may account for some episodes of sudden loss of consciousness without warning, usually attributed to hypoglycemia.
Carbohydrate Metabolism and Capillary Basement-membrane Thickness in Children: I. Cross-sectional Studies
Authors: Sheikholislam Bagher M , Mas Julian J , Lin Hung-Jung , Lowrey George H , Stephenson Steve R , Peterson Gregory E , Devereux Dennis F , Volk Thomas L 
Published: September 2013

Thirty-nine children from three to 16 years of age were included in this study. Nineteen were diabetics, seven were “suspected” diabetics (with evidence of glucose intolerance but without repeated fasting hyperglycemia), and 13 were controls. Mean glucose disappearance rates (K) during intravenous glucose tolerance tests (IVGTTs) were 2.19 for the controls, 1.23 for the suspected diabetics, and 0.70 for 14 diabetics tested; the differences were statistically significant. Diabetics had the smallest and suspected diabetics the greatest plasma insulin responses during IVGTTs. Fasting plasma growth hormone (GH) varied widely. GH generally decreased or remained unchanged during IVGTTs, but two diabetics exhibited slight increases and two suspected diabetics pronounced increases.
Basement-membrane thickness (BMT) was examined in 42 quadriceps femoris needle biopsies. Average BMT (ABMT) and minimum BMT (MBMT) correlated well (r = 0.91). BMT did not correlate well with age or, in the diabetics, with duration of clinical disease. Diabetics had the greatest and controls the least mean ABMT and MBMT, but the differences were not statistically significant. High values (those exceeding mean control values by more than two standard deviations) were much more common among the suspected diabetics and the diabetics. One of 13 controls, three of six suspected diabetics, and six of 19 diabetics had high ABMT values; two suspected diabetics and five diabetics had high MBMT values. Correlations between BMT and K were negative for the most part, but correlation coefficients were small. Serial studies in four of the children suggest that BMT and glucose tolerance tend to change in opposite directions.
Effect of Diabetes Mellitus and Insulin on the Turnover and Metabolic Response to Ketones in Man
Authors: Sherwin Robert S , Hendler Rosa G , Felig Philip 
Published: September 2013

To determine the effect of diabetes mellitus on ketone removal rates, Na DL-β-hydroxybutyrate was administered as a continuous three-hour infusion (3 mg./kg./min.) to healthy volunteers and insulin-dependent diabetics in the postabsorptive state. An additional group of healthy controls received intravenous glucose (50 gm.) or glucose and insulin during the ketone infusion to determine the effect of hyperinsulinemia on ketone removal.
Following ketone infusion, total blood ketone levels in the diabetics were twofold greater than in controls (p &lt; 0.001). The metabolic clearance rate of ketones (MCRk) in the diabetics was reduced by 4per cent from that of controls (p &lt; 0.001). In contrast, the calculated production rate of ketones (PRk) in diabetics was not consistently different from that observed in controls. In diabetics with normal PRk, MCRk remained significantly below control values (p &lt; 0.001).
The ketone infusion resulted in a fall in plasma glucose and alanine levels in the normals as well as diabetics. However, the decline in plasma glucose induced by the ketone infusion was five- to sixfold greater in the diabetics than in controls (p &lt; 0.005) and correlated linearly with the decline in plasma alanine (p &lt; 0.02).
Administration of intravenous glucose during an ongoing ketone infusion in normal subjects resulted in 37 ± 5 per cent reduction in β-hydroxybutyrate, but no change in acetoacetate concentration. The decline in β-hydroxybutyrate was two- to threefold greater than would be expected if glucose had acted solely to inhibit endogenous ketone production. Similar results were observed when hyperinsulinemia without hyperglycemia was produced by simultaneous administration of insulin and glucose.
It is concluded that (1) ketone disposal is reduced in diabetes even when ketone production is normal, suggesting the rate of ketone utilization may be a more sensitive index of insulin deficiency than is ketone production; (2) hyperinsulinemia stimulates β-hydroxybutyrate utilization without influencing acetoacetate concentration; and (3) increased blood ketone levels induced by infusion of Na DL-β-hydroxybutyrate reduce plasma glucose and alanine concentrations in diabetes. These findings thus support a role for insulin in influencing ketone disposal in normal as well as diabetic man and a role for ketones in influencing substrate availability for gluconeogenesis in diabetes.
Quantitation of Human Pancreatic Beta-cell Function by Immunoassay of C-Peptide in Urine
Authors: Horwitz David L , Rubenstein Arthur H , Katz Adrian I 
Published: September 2013

Human proinsulin connecting peptide (C-peptide) was measured by immunoassay in urine from 25 normal subjects, 18 patients with diabetes mellitus, and 34 patients with various degrees of renal insufficiency. Assay validation studies showed that pancreatic C-peptide was quantitatively recovered when added to urine. Fractionation of urine by gel filtration indicated that most endogenous C-peptide eluted in fractions that corresponded to the C-peptide standard.
In 34 nondiabetic subjects with normal kidney function or various renal diseases, C-peptide clearance was independent of creatinine clearance over a range of 6 to 190 ml./min. Urine C-peptide clearance (5.1 ± 0.6 ml./min.) is greater than that of insulin (1.1 ± 0.2 ml./min.), and the total quantity of C-peptide excreted in the urine per day represents 5 per cent of pancreatic secretion, as against only 0.1 per cent of secreted insulin.
Healthy subjects excreted 36 ± 4 μg. C-peptide per 24 hours, while this value in juvenile-onset diabetics was only 1.1 ± 0.5 μg. Adult-onset diabetics excreted 24 ± 7 μg./24 hr., the range overlapping the excretory rates of both normal subjects and juvenileonset diabetics. Two insulin-requiring adult-onset diabetics showed significant beta-cell reserve during the course of acute infections.
These results suggest that urine C-peptide provides a useful means of assessing beta-cell secretory capacity over a period of time and is especially advantageous when frequent blood sampling is not feasible.
On the Mechanism of Diazoxide-induced Hyperglycemia
Authors: Altszuler Norman , Hampshire Jennifer , Moraru Ety 
Published: September 2013

Infusion of diazoxide (16.5 mg./kg. in 10 minutes) into normal unanesthetized dogs resulted in a prompt hyperglycemia due to increased hepatic glucose production as measured with a 3-3H-glucose primer-infusion technique. Plasma insulin and gtucagon were decreased. Glucose uptake failed to increase. Diazoxide administration during period of alpha adrenergic receptor blockade with phentolamine still caused hyperglycemia and increased glucose production. Glucose uptake was inhibited despite adequate plasma insulin. Infusion of somatostatin along with insulin prevented the effects of diazoxide on plasma glucose and glucose production.
It is concluded that diazoxide hyperglycemia is not due solely to decreased insulin secretion or increased epinephrine secretion and that gtucagon is not a contributory factor. Diazoxide may act directly to increase glucose production and inhibit glucose uptake. Somatostatin appears capable of blocking the effect of diazoxide on glucose production by an unknown mechanism.
Oral Contraceptive Use and Other Factors in the Standard Glucose Tolerance Test
Authors: Wingerd John , Duffy Thomas J 
Published: September 2013

Three-hour standard glucose tolerance tests were performed on 2,248 women subjects with a family history of diabetes.
Use of oral contraceptives (OCs) was associated with equal elevations in one- and two-hour values but, surprisingly, lowered fasting blood sugars. A similar but weaker trend was present for other estrogen use.
Increasing age correlated with higher blood glucose values at all time points of the test, most markedly at one hour. Increasing relative weight was also associated with increased values at all hours of the test; here the increase was most marked (and approximately equal) at one and two hours. The rise in glucose, however, remained relatively well sustained at three hours, in contrast to most other variables. Glycosuria in overweight women was accompanied by a greater degree of hyperglycemia than in lean subjects.
A history of first-degree diabetic relatives tended to be associated with elevated values at all time points, but only at the fasting and one-hour points were the values significantly higher than those of women with lesser degrees of diabetic relationship. History of cholecystectomy was also associated with elevated glucose levels.
Heavy drinkers had a high one-hour mean, with normal to low two- and three-hour tests; smoking was not associated with any differences at the fasting or one-hour points, but smokers showed significantly decreased levels at two and three hours.
Principal-components analysis showed that fasting level, the “area under the curve,” and the steepness of descent from the one-hour level were completely independent aspects of the glucose tolerance test curve and could be used to summarize the original four data points of the test.