Effect of somatostatin on metabolic and hormonal changes induced by nicotinic acid in insulin-dependent diabetics

Abstract

Summary. The study investigated the respective influences of nicotinic acid and somatostatin on plasma concentrations of blood glucose, free fatty acids, glucagon, growth hormone and cortisol in insulin-dependent diabetic subjects. After administration of nicotinic acid alone, marked depression of plasma FFA was accompanied by significant increases of plasma glucagon, growth hormone and cortisol. The glucagon and growth hormone responses to nicotinic acid were significantly reduced when plasma FFA were raised by intravenous administration of heparin and triglycefides. Somatostatin alone induced a significant decrease in blood glucose, plasma g!ucagon and growth hormone concentrations. Plasma FFA remained unchanged. Somatostatin did not modify the nicotinic acid-induced fall in plasma FFA, but completely blocked the corresponding increments in glucagon and growth hormone. The cortisol rise was not altered by soma~ostatin. Rebound of glucagon and growth hormone levels were seen upon discontinuation of the somatostatin administration. These results demonstrate that the plasma FFA concentration plays a role in the regulation of glucagon and growth hormone secretion in insulin-dependent diabetics. Furthermore, they indicate that somatostatin, previously shown to be capable of negating the stimulatory effect of various factors on glucagon and growth hormone secretion, also affects the response of these hormones to FFA depression.

A 6-hour nocturnal interruption of a continuous subcutaneous insulin infusion: 2. Marked attenuation of the metabolic deterioration by somatostatin

“…In agreement with previous studies, somatostatin depressed basal levels of growth hormone by more than 50% [7,17] and remarkably suppressed its nocturnal peaks [18,19]. The studies of Gerich et al [8], in which an infusion of growth hormone during suppression of its endogenous secretion reproduced physiological hormone levels, demonstrates the absence of significant metabolic changes in presence of insulin.…”

“…As expected, somatostatin induced a significant decrease in plasma glucagon levels [7,14,17]. This inhibition which was already detectable on the basal glucagon levels from 23.00 until 03.00 h became more obvious from 04.00 to 07.00 h when the late and significant glucagon rise observed in the control test was completely suppressed by somatostatin.…”

Comparison of the Lipid‐lowering Effects of Nicotinic Acid and 2,5‐dimethylpyrazine in Rats

“…While the former functions through GPR109A in peripheral adipose tissues, the latter remains to be investigated (Karpe and Frayn 2004), except that both the pituitary and adrenal functions are required for the rebound after NA administration (Pereira 1967). Thus, the rebound phenomenon may be derived via activation of the hypothalamus-pituitary-adrenal (HPA) axis that results in an elevation of cortisol in systemic circulation (Luyckx and Lefebvre 1976), stimulating HSL activity in adipocytes to secrete NEFA (Björntorp 1991). Accordingly, the difference between NA and 2,5-DMP may be attributed to inquiry about the possible effect on the HPA axis.…”

Somatostatin — A Regulatory Peptide of Clinical Importance

“…Influence in pathogenesis After discovering the inhibitory effect of Somatostatin on glucose and insulin, clinical 1 studies were performed in order to evaluate the importance of this peptide in diabetes mellitus. Somatostatin lowers blopd glucose levels in patients with diabetes mellitus and in normal subjects (121)(122)(123). Via the artificial pancreas somatostatin is able to reduce the requirement of insulin in more than 70% öf patients with juvenüe diabetes (124 analogue, without the general inhibiting potency of somatostatin, could play a role in diabetes treatment (125).…”