Hyperinsulinemia and insulin resistance have been reported in patients with liver cirrhosis. Since insulin receptor decrease has been demonstrated in some conditions of insulin resistance, we have studied insulin binding to circulating monocytes in eleven patients with alcoholic liver cirrhosis. Specific insulin binding at tracer concentration was lower in cirrhotics than in control subjects (p < 0.005). Insulin binding to monocytes was correlated with basal plasma insulin level in cirrhotics (r = -0.76; p < 0.01). The inhibiting effect of native insulin on 125I-insulin binding was similar in cirrhotics and controls suggesting that concentration rather than affinity of the binding sites is affected in cirrhosis of the liver. These findings suggest that decrease in insulin receptor concentration exists in liver cirrhosis, probably as a consequence of chronic hyperinsulinemia.
The effect of secretin on insulin release has been studied in normal subjects after prestimulation with arginine. In order to make a comparison a pulse of glucose with arginine prestimulation was given. A pulse of 1 U/kg b.w. of secretin provokes a secretion of insulin that is weak and brief compared to that provoked by glucose; thus secretin fails to potentiate arginine-induced insulin secretion. Such a result does not support the hypothesis of secretin as the central hormone in the enteroinsular axis.
A remission of adrenal adenoma producing aldosterone is described as a consequence of adrenal venous catheterization. The patient did not undergo surgery but she was kept on frequent clinical controls. The complete remission of the syndrome is still persisting three years after the incident. Since adrenal insufficiency is described after adrenal venous catheterization, the authors suggest that this procedure is to be restricted to well selected patients. When this incident occurs in pathological glands, a remission of endocrine syndrome may be expected.
Clonidine, an imidazoline derivative, is an antihypertensive agent which reduces sympathetic tone by acting in the central nervous system to stimulate alpha-2 adrenoceptors. There is evidence that dopamine and norepinephrine modulate the secretion of GH. Stimulation of GH release is a well-known effect of clonidine in man. Obesity is characterized by an impairment of GH release in response to various stimuli. The aim of this work is to study GH release in response to alpha-2 adrenoceptors stimulation by clonidine in obesity. 12 volunteer obese subjects were studied. 10 normal weight subjects, sex and age matched, were controls. The GH responsiveness was tested with a single oral dose of clonidine (0.15 mg). Blood was sampled for GH radioimmunoassay at 0', 30', 60', 90', 120', 150', 180'. Serum GH basal levels were not significant different in obese subjects compared to controls. In obese subjects, no significant changes occurred in blood GH concentration after clonidine. In normal weight controls, instead, a significant increase of GH values was reached at 90' (P less than 0.05) and at 120' (P less than 0.05) after clonidine. The impairment of GH release after clonidine in obese subjects might be in a reduced serotonin release or in a failure of the hypothalamic-pituitary system to stimulate plasma GH caused by a diminished GH releasing factor stimulatory effect or by an excessive endorphin or somatostatin secretion in obesity.
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