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1. The present study was performed in order to assess the influence of a high-carbohydrate diet on carbohydrate and lipid metabolism in humans. 2. Short-term (3 weeks) and long-term (6 weeks) effects of a high-carbohydrate diet (HCD, 85% carbohydrate) were compared with the effects of 2 weeks on a diet of normal carbohydrate content (ND, 45% carbohydrate). The study was conducted on 4 normal and 11 obese subjects (with normal or impaired glucose tolerance) on a metabolic ward. Fasting blood glucose, insulin and triglyceride levels were measured twice a week. Tolerance to carbohydrates was evaluated by measuring blood glucose and insulin levels after oral and intravenous glucose loads and liquid meals at intervals throughout the 8-week period. 3. Long-term HCD improved the tolerance to oral glucose, i.e., it decreased serum glucose and insulin responses to an oral glucose load. 4. HCD had no effects on fasting levels of glucose or insulin or on the tolerance to an intravenous glucose load. 5. A high-carbohydrate liquid meal induced greater post-prandial glucose and insulin levels than a normal liquid meal. 6. In a second group of 6 normal and 6 obese subjects, efficacy of the liquid meal tests was evaluated. A high-carbohydrate liquid meal induced greater glucose and insulin responses than a normal liquid meal during both dietary periods. 7. Fasting triglyceride levels increased and remained high throughout the HCD period.

The acute and late phases of insulin secretion were studied in mongrel dogs before and after the induction of mild alloxan diabetes. Fasting glucose and insulin levels were unchanged from pretreatment values. The alloxan-diabetic dogs had significantly decreased early-phase insulin responses to glucose pulses (0.5 gm./kg.) and slower plasma glucose disappearance rates. In contrast, these mildly diabetic dogs achieved comparable insulin levels and higher glucose levels during a four-hour 40 mg./min. glucose infusion than pre-alloxan control values. Similar findings in human congenital mild diabetes have been interpreted as beta cell insensitivity or impedance to efficiency of plasma glucose uptake. The present observations in alloxan-induced mild diabetes in dogs suggest that reduced early-phase secretion and intact later phase of insulin secretion are not dependent on genetic determinants and may be induced in a model of acquired diabetes.

Growth hormone (GH) releasing activity of pyroglutamyl-seryl-glycinamide (PSG) and of thyrotropin-releasing hormone (TRH) was assayed on rat pituitaries in vitro, by radioimmunoassay of the GH released into the incubation media. TRH was found to be a partial agonist, producing maximal effects (at ca. 600 ng/ml) that were below the maximum response of the system to hypothalamic extract. The responses to a higher TRH concentration (1500 ng/ml) were smaller than that obtained at 600 ng/ml. PSG also behaved as a partial agonist producing maximum response at 150 ng/ml. The results are discussed in relation to possible structural similarities between the physiological GHRF and the tripeptides TRH, PSG and MIF (MSH release inhibiting hormone).

We describe a girl with the manifestations of geleophysic dwarfism: small stature, a peculiar but pleasant and good-natured facial appearance, a dysostosis-multiplex-like bone dysplasia affecting predominantly hands and feet, hepatomegaly and stenosis, and insufficiency of the aortic valve. The proposita's sister died of heart failure at 3 years and was reported by the mother to have been a tiny child with small hands.

1. Eleven patients with type II diabetes mellitus were studied prior to, and after short- (10 days) and long-term (6 months) glibenclamide treatment. 2. A marked decrease in glucose level was observed after short- and long-term therapy using the oral glucose tolerance test (OGTT) and diet test (DT). 3. After short-term therapy, insulin level increased by 52.5% with the OGTT and by 37.6% with the DT; after long-term therapy, the increases were 78.6% and 69.5%, respectively. 4. Insulin binding to erythrocytes was unchanged by short- or long-term glibenclamide therapy. 5. These data suggest that the hypoglycemic effect of glibenclamide results from an increase in insulin secretion and that extrapancreatic actions at the receptor or post-receptor level are not necessarily involved.

Four rapid glucose injections of 5 g each were administered to normal young adult subjects before, during, and after an infusion of glucose. After the first glucose pulse, insulin responses measured immunologically reached a peak between 3 and 5 min and rapidly returned to base line. A short glucose infusion of 300 mg/min decreased the rapid insulin response to a second glucose pulse (- 58%), but after a longer infusion (20 hr) the acute insulin response to a third pulse was restored to normal. Stopping the infusion was followed by return of glucose and insulin levels to prestudy base line within 1 hr, but a fourth glucose pulse was followed by a supernormal acute insulin response (+ 200%). Other observations during these studies showed that a short glucose infusion of either 100 mg/min or 300 mg/min produced a parallel rise in glucose and insulin, but continuation of the infusion for 20 hr was associated with a "paradoxical" fall in glucose and continued rise in insulin. These observations are considered incompatible with a simple linear model often used to describe the relation between plasma glucose and serum insulin. Instead, a two pool system-one for acute insulin release, and the other a time-dependent compartment for long term insulin responses-is suggested.