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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic islet peptides, as well as other gastrointestinal hormones, have been implicated in both the pathogenesis of obesity and the etiology of associated metabolic derangements. This study evaluated the pancreatic islet and gastrointestinal (GI) hormone response to oral glucose in 20 morbidly obese (151% above ideal body weight) patients. Glucose intolerance, hyperinsulinism, and exaggerated gastric inhibitory polypeptide (GIP) release occurred following glucose ingestion. Significant release of PP occurred in 14 patients, while only six patients had release of somatostatin. No significant changes in plasma concentrations of glucagon occurred. Since GIP is insulinotropic in the presence of hyperglycemia, the hyperinsulinism of morbid obesity may be secondary to the abnormally high glucose-stimulated GIP levels in these patients. Failure of glucagon suppression in response to oral glucose many contribute to the hyperglycemia noted. Somatostatin and pancreatic polypeptide may be responsible for some of the metabolic derangements of morbid obesity.
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PMID:Pancreatic islet hormone response to oral glucose in morbidly obese patients. 286 Aug 76

Increased pancreatic somatostatin (somatotrophin release inhibiting factor (SRIF) has been found in hypothyroid rats. Therefore, we wanted to investigate plasma SRIF in patients with hypo- and hyperthyroidism. Two groups of patients, 7 cases with autoimmune hypothyroidism, 31-75 years old, and 7 cases with Graves' disease, 19-43 years old, were compared with regard to plasma SRIF before, during and after an arginine infusion (0.5 g/kg/20 min). None of the patients suffered from diabetes mellitus or obesity. Plasma SRIF was higher in the hypothyroid patients (mean basal value 21.5 +/- 3.9, peak value 28.7 +/- 5.1 pmol/l) compared with the hyperthyroid group (mean basal value 11.6 +/- 3.3, peak value 16.2 +/- 4.0 pmol/l). The hypothyroid group also had significantly higher serum insulin values during arginine stimulation. No difference was found in plasma glucagon, serum growth hormone (GH) or blood glucose. In conclusion, plasma SRIF is elevated in primary hypothyroidism compared with hyperthyroidism. The reason for this finding is uncertain, but a reduced SRIF clearance is a possible explanation. The association of our findings with the reduced glucose tolerance in hyperthyroidism is discussed.
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PMID:Plasma somatostatin is elevated in primary hypothyroidism compared with hyperthyroidism. 287 May 98

This paper presents the first case of extensive, diffuse, somatostatin-immunoreactive D-cell hyperplasia in the human stomach and duodenum. It occurred in a 37-yr-old woman, who showed clinical signs of dwarfism, obesity, dryness of the mouth, and goiter. The density of the distribution of D cells was increased 39-fold in the stomach fundus, 23-fold in the proximal antrum, 25-fold in the distal antrum, and 31-fold in the upper duodenum in comparison with normal values. At the same time, the gastrin-immunoreactive cells were increased 2.3-fold in the antrum. Although the range in size of the D cells was within normal limits in all regions examined, the G cells showed pronounced hypertrophy of up to 127%. A possible relationship between the immuno-histochemical findings and the clinical picture is discussed.
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PMID:Diffuse somatostatin-immunoreactive D-cell hyperplasia in the stomach and duodenum. 287 99

Somatostatin is found in the D-cells of organs that are exclusively responsible for the digestion, absorption, and metabolism of ingested nutrients. D-cells apparently release their secretory products both into the interstitial space (paracrine action) and into the circulation (endocrine action). Ingestion of all three basic nutrients--fat, carbohydrate, and particularly protein--elicits a significant increase in peripheral vein plasma somatostatin levels in dogs and humans. Acidification of a meal stimulates somatostatin release in dogs. Vagal, cholinergic, and adrenergic mechanisms exert a species-dependent effect on somatostatin release. Gut hormones also participate in the regulation of postprandial somatostatin release, and endogenous opioids have an effect that depends on the composition of the meal. Stimulation of postprandial somatostatin release by H2-receptor agonists and prostaglandins has been reported. Insulin inhibits and glucagon stimulates somatostatin release. Elevated levels of circulating glucose reduce the somatostatin response, an effect that cannot be entirely explained by the parallel augmentation of insulin secretion. Circulating nutrients also modify the effect of gut hormones on D-cell function. The physiological action of somatostatin is an inhibitory effect on virtually all gastrointestinal and pancreatic exocrine and endocrine functions. Secretory and/or motor activities are attenuated, thereby preventing an exaggerated and overshooting response. Alterations of tissue somatostatin content and plasma somatostatin levels have been observed in obesity and suggest that somatostatin deficiency may be a pathogenic factor. The observed changes of somatostatin may be secondary to alterations of other functions; nevertheless, hyposomatostatinaemia might facilitate nutrient assimilation.
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PMID:Physiological and pathophysiological aspects of somatostatin. 287 4

GH secretory bursts are due to the combination of a pulsatile GRF release and a decreased Somatostatin secretion in hypophysial portal blood. In the intermediary periods, low plasma GH levels depend on the tonic release of hypothalamic Somatostatin. Experimental studies suggest that alterations in hypothalamic Somatostatin are involved in changes of GH secretion observed under physiological (foetal life, aging, stress), pharmacological (beta-blocking agents) and physiopathological conditions (starvation, obesity, diabetes). The Somatostatin analogue SMS 201-995 induces a long-lasting inhibition of GH secretion and may be useful in the treatment of acromegalic patients.
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PMID:[Somatostatin and regulation of the secretion of growth hormone]. 288 11

A potential role for somatostatin (SRIF) in the pathogenesis of the hyperinsulinemia of obese rats was considered. SRIF like immunoreactivity (ng/mg protein) was therefore measured in hot 2 N acetic acid extracts of pancreas, stomach, pituitary, and hypothalamus in tissues obtained from three models of genetic obesity in rats. These models included the obese and lean controls of LA/N-cp, SHR/N-cp, and Zucker rats. To assess the effects of diet on SRIF levels, mixed diets were provided ad lib which contained a carbohydrate as either sucrose or starch. Some groups were fed chow diets. No significant dietary effects on tissue levels of SRIF were obtained. However, two of the three models (Zucker and SHR/N-cp) showed phenotypic effects on SRIF levels in pancreas; namely, obese rats showed a significantly greater concentration of SRIF (P less than 0.0005 and less than 0.0002, respectively) than did the lean littermates. These findings were confirmed by measurement of total pancreas SRIF content. Gastric levels were significantly altered only in the obese Zucker rats (P less than 0.005) where obese tissues had lower concentrations than those of lean animals. However similar directional changes in pancreas and stomach were observed in all models. It is concluded that the hyperinsulinemia of the obese animals studied is not due to absolute deficiency in pancreatic SRIF content. It is postulated however that decreased pancreatic SRIF secretion (paracrine or otherwise) relative to pancreatic insulin content could still play a role.
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PMID:Tissue somatostatin levels in three models of genetic obesity in rats. 288 60

Somatostatin is present in the gastrointestinal tract in appreciable amounts. The highest concentrations of the polypeptide are found in the stomach, the upper small intestine, and the pancreas. Within the gastrointestinal tract, somatostatin inhibits various functions, including endocrine and exocrine secretion, motility, blood flow, absorption, and growth. The polypeptide regulates these functions by endocrine, paracrine, neurocrine or luminal mechanisms. Abnormalities of endogenous somatostatin have been implicated in several gastrointestinal disorders, including the somatostatinoma syndrome, antroduodenal D-cell hyperplasia, peptic ulcer, obesity, and liver cirrhosis. Because of its potent inhibitory effects, somatostatin or somatostatin-analogues have been used as therapeutic agents in various clinical conditions, such as upper gastrointestinal haemorrhage, endocrine pancreatic tumours, gastrointestinal and pancreatic fistulas, pancreatitis, secretory diarrhoea, and dumping syndrome. The recent availability of the synthetic long-acting somatostatin-analogue SMS 201-995 (Sandostatin) has greatly facilitated the therapeutical application of somatostatin-polypeptides.
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PMID:Clinical and pathophysiological aspects of somatostatin and the gastrointestinal tract. 289 34

In contrast to the United State, type 2 diabetes appears to be a common occurrence in non-obese Asians. In order to evaluate the possibility that this epidemiologic difference was indicative of a basic metabolic phenomenon, estimates of insulin secretion and insulin action were generated in 32 Chinese males, 16 with type 2 diabetes and 16 with normal glucose tolerance. Half of the individuals in each diagnostic category were obese (body mass index greater than 28 kg/m2) and half were non-obese (less than 26 kg/m2). Plasma glucose responses to a 75-g oral glucose challenge were significantly higher in patients with type 2 diabetes, but did not vary significantly within either group as a function of obesity. Plasma insulin concentrations were lower than normal when patients with type 2 diabetes were compared to their weight-matched controls. In addition, the absolute insulin values also varied as a function of body weight, with higher plasma insulin concentrations observed in the obese individuals. Insulin action was estimated by determination of the steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations during the last 60 min of a continuous 180-min intravenous infusion of somatostatin, crystalline insulin, and glucose. Under these conditions endogenous insulin secretion is suppressed, SSPI concentrations are similar in all individuals, and SSPG concentrations provide a quantitative estimate of insulin-stimulated glucose disposal. The results of these studies indicated that patients with type 2 diabetes had significantly elevated SSPG concentrations as compared to normals, and this was true whether the diabetic subjects were obese or non-obese.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin secretion and insulin action in Taiwanese with type 2 diabetes. 289 74

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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PMID:Impaired growth hormone response to clonidine in obesity. 324 43

Diabetes, the most common metabolic disease, is responsible for the deaths of over 300,000 Americans annually. The incidence of the disease increases with age and since the U.S. population is graying, prevalence is also increasing. Obesity and family history are strong predictors of diabetes. The etiology of Type II diabetes is heterogeneous. The hyperglycemia of Type II diabetes can result from a variety of metabolic defects including impaired beta cell secretion, receptor deficiencies, or abnormal hepatic production or uptake of glucose. Other glucoregulatory hormones such as glucagon, growth hormone, cortisol, thyroid hormones, somatostatin, and gastric inhibitory polypeptide may contribute to the aberrations of carbohydrate metabolism. Environmental factors including stress, diet, and exercise may also contribute to the disease. Since most diabetics are obese, weight loss should be the first priority in improving status. A variety of diet and exercise regimens may help achieve this goal or even improve glucose control without weight loss. Due to the heterogeneity of the disease individualized treatment must be used to improve status of patients with the various metabolic defects of Type II diabetes.
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PMID:Dietary sugars and carbohydrate metabolism in type II diabetes. 330 10


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