Somatostatin, a hypothalamic peptide that inhibits the secretion of pituitary growth hormone, inhibits basal insulin secretion in fasted cats and rats. In fasted baboons both basal and arginine-stimulated secretion of insulin and glucagon are inhibited. Somatostatin appears to act directly on the endocrine pancreas. The action is dose-related, rapid in onset, and readily reversed.
In overnight fasted rhesus monkeys, synchronous, regular oscillations occurred in the plasma concentrations of glucose, insulin, and glucagon. The oscillations displayed a period averaging 9 minutes. The amplitudes for insulin and glucagon were ten and five times greater than for glucose. Insulin cycled in and glucagon out of phase with glucose. In baboons, oscillations of glucose and insulin were smaller than in rhesus monkeys, while in man, regular oscillations were not observed.
A B S T R A C T The nature and extent of somatostatininduced inhibition of pancreatic endocrine secretion were studied by administration of a number of stimuli of either glucagon or insulin to overnight fasted baboons with and without an infusion of linear somatostatin. The stimuli for acute-phase insulin release were intravenous pulses of glucose, tolbutamide, isoproterenol, and secretin. When given 15 min after the start of a somatostatin infusion, these agents were essentially unable to stimulate insulin secretion. Chronic insulin secretion was stimulated by infusions of either glucose or glucagon. Within 10 min of the start of a superimposed infusion of somatostatin, insulin levels fell to less than 40% of prestimulus control and remained suppressed for the duration of the somatostatin infusion. Stimulation of glucagon secretion by insulin-induced hypoglycemia was also blocked by somatostatin.Plasma glucose decreased during somatostatin infusions except when superimposed upon an infusion of glucagon. Somatostatin had no effect on glucose production in a rat liver slice preparation.We conclude: (a) Somatostatin is a potent and so far universally effective inhibitor of both acute and chronic phases of stimulated insulin and glucagon secretion (b) The inhibitory effect is quickly reversible and the pattern of recovery of secretion is appropriate to prevailing signals; (c) Present evidence suggests that the effect of somatostatin on blood glucose is mediated through its effect on blood glucagon; (d) In the overnight-fasted baboon both in the basal state and 45 min into a 4-mg/kg min glucose infusion, a somatostatininduced fall in serum insulin levels appears to be unable to prevent a decrease in hepatic glucose production.
Obesity was studied in a colony of 873 Macaca nemestrina to establish tools for epidemiologic studies, to examine a genetic form of obesity, to document age/sex relationships to obesity, and to compare metabolic profiles of obese and normal monkeys. Age/weight growth curves were analyzed to select the most obese monkeys and age- and sex-matched normal controls. Degree of adiposity was determined using tritiated water for estimation of lean body mass. Body weight, anterior trunk height, and abdominal and triceps skinfolds were measured. Fasting insulin, fasting free fatty acids, and glucose disappearance rate were determined. The results give evidence of similarities between macaque and human obesity.
ExtractPregnant rats during the last 3 days of gestation were fasted 16 hours, anesthetized and infused with glucose-U-C14 for two hours following a loading dose of labeled glucose. Rats infused with tracer only were compared with glucose-loaded rats. The volume of distribution for glucose was 28 % in the fasted rats and increased to 50% of body weight with glucose loading. Hepatic glucose production was 1.2 mg/min/300 g body weight in the fasted rats. This value was depressed to 0.32 with glucose loading. Comparison of maternal and fetal plasma after the two-hour infusion showed that the concentration of glucose in fetal plasma equaled the maternal in fasting rats and paralleled maternal hyperglycemia with a gradient (maternal to fetal) of 1.22 in the glucose-loaded rats. In the fasted rats, the specific activity of fetal plasma glucose was less than half that of maternal plasma glucose, indicating that unlabeled glucose was being produced within the conceptus. By contrast, the specific activities were more nearly equal in the glucose-loaded rats, showing that maternal plasma glucose was the primary source of fetal plasma glucose during hyperglycemia. The glycogen concentrations of fetal liver and placenta were not altered by glucose loading. The degree of labeling of glycogen was very small in fetal liver and placenta in fasting rats, while glucose loading increased the specific activity of glycogen in these two organs but the quantitative change in glycogen remained small compared to the total glycogen stores. However, with glucose loading, the incorporation of radioglucose into maternal liver glycogen reached 31 % of the liver glycogen store.From these data it is concluded that under conditions of fasting, the fetal liver contributes to the fetal plasma glucose through gluconeogenesis in preference to glycogenolysis, while in the presence of maternal hyperglycemia, fetal gluconeogenesis is reduced and glycogen synthesis in fetal liver is accelerated. SpeculationDuring fasting, a competition may develop for gluconeogenetic precursors between the maternal liver, the fetal liver and the growing fetal tissues. Because of such a competition, prolonged fasting or protein malnutrition could result in either reduced availability of fetal glucose or limitation of protein synthesis or both. During short periods of fasting, the store of glycogen in the fetal liver was neither mobilized nor significantly increased by synthesis from glucose, while with glucose loading, net synthesis increased. These data suggest that accumulation of fetal liver glycogen occurs as a stepwise cycle with net synthesis occurring only during feeding and relative retardation of glycogenolysis predominating during fasting.
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