Influence of somatostatin on splanchnic glucose metabolism in postabsorptive and 60-hour fasted humans.

Abstract

A B S T R A C T Cyclic somatostatin was administered intravenously (10 ,ug/min for 60 min) to 10 healthy overnight fasted (postabsorptive) subjects and to 5 healthy 60-h fasted subjects. In both groups, arterial insulin and glucagon fell 50%o and splanchnic release of these hormones was inhibited. In the overnight fasted subjects splanchnic glucose output fell 70%, splanchnic uptake of lactate and pyruvate was unchanged, alanine uptake fell by 25%, and glycerol uptake rose more than twofold in parallel with an increase in arterial glycerol.In the 60-h fasted group splanchnic glucose output was less than 40%o of that observed in the overnight fasted subjects. Somatostatin led to a further decrease (-70%) in glucose production. Splanchnic uptake of lactate and pyruvate fell by 30-40%o, amino acid uptake was unchanged, while uptake of glycerol rose fivefold. Total uptake of glucose precursors thus exceeded the simultaneous glucose output by more than 200%o. Splanchnic uptake of FFA rose fourfold during somatostatin while output of beta-hydroxybutyrate increased by 75%. Estimated hepatic blood flow fell 25-35% and returned to base line as soon as the somatostatin infusion ended.It is concluded that (a) somatostatin-induced hypoglucagonemia results in inhibition of splanchnic Dr. Felig is the recipient ofa Research Career Devleopment Award

Quantifying the contribution of gluconeogenesis to glucose production in fasted human subjects using stable isotopes

“…If glucose production was greater during initial period of fasting, the contribution of GNG would be higher. Balance studies do not show sufficient uptake of substrate by the splanchnic bed to account for 64 % production (Wahren et al 1977).…”

“…In the first method concentrations across the liver of blood lactate, pyruvate, glycerol and GNG amino acids, as well as glucose, together with blood flow, are measured. The fractional contribution of GNG to glucose production is then calculated, assuming all the GNG substrates taken up are converted to glucose (Wahren et al 1977). Thus, estimates are maximal, except that a proportion of GNG substrates are produced and converted to glucose within the liver.…”

Metabolic and endocrine response to exercise: sympathoadrenal integration with skeletal muscle

“…The principle organ for regulating blood glucose is the liver, which in the face of increased blood glucose disposal will increase the rate of hepatic glucose production through glycogen catabolism and gluconeogenesis (Ahlborg et al 1974, Wahren et al 1977. Ahlborg & Felig (1982) reported that during prolonged moderate intensity exercise (w60% VO 2max ), the rate of hepatic glucose output barely matched the rate of leg glucose uptake during the first 40 min of exercise.…”

Somatostatin — both hormone and neurotransmitter?

“…10) whereas, in 60 h fasted subjects, the hypoglycaemic effect was also due to suppression of gluconeogenesis [106]. The hyperglycaemia accompanying prolonged infusion of somatostatin was due partially to increased hepatic glucose output, and partially to decreased peripheral uptake of glucose [97].…”