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

The authors have studied insulin receptors on peripheral blood monocytes and insulin sensitivity, evaluated by simultaneous infusion of glucose, insulin and somatostatin in 10 control subjects and in 20 obese patients with normal glucose tolerance. The obese patients have been divided into two groups, normo (NO) and hyperinsulinemic (HO), according to the total insulin response during OGTT. We considered HO patients with insulin response higher than M + 2DS of controls. Obese patients showed, in comparison to the controls, a lower specific binding and higher degree of insulin resistance. The subdivision of obese patients allowed us to distinguish two groups. The first was characterized by basal hyperinsulinemia, normal insulin response to the stimulus, reduced number of insulin receptors and normal or slightly reduced sensitivity. The second group showed high basal and after stimulus insulinemic values, reduced number of insulin receptors and high level of insulin resistance. When we compared the two groups of obeses we found that the first has a shorter duration of obesity and lower blood glucose values after OGTT. However both groups show the same reduction of insulin bound and the same degree of basal hyperinsulinemia. These data suggest that a reduction of insulin receptors is not the main factor responsible for insulin resistance in obesity. Furthermore, the presence of basal hyperinsulinemia and normal insulin sensitivity in our first group suggests that the modification of basal insulin concentrations is not dependent on the presence of insulin resistance.
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PMID:Insulin receptors and insulin sensitivity in normo and hyperinsulinemic obese patients. 389 56

A study was made of change in hormone secretion in 243 patients with alimentary-constitutional and hypothalamic obesity. Activation of the somatostatin mechanism, a decrease in somatotropic and thyrotropic function of the hypophysis, an increment of corticotropin, beta-lipotropin and vasopressin levels in the blood, disturbance of circadian fluctuations of hormone secretion, an increase in insulin and C-peptide secretion, a decrease in glucagon secretion and triiodothyronine and cortisol levels in the blood, activation of the renin-aldosterone system and cortisol secretion rate were equally expressed both in alimentary-constitutional and primary hypothalamic obesity. The central mechanisms of the regulation of endocrine functions were incorporated in a pathological process even in alimentary-constitutional obesity. Disorders of the hypothalamic regulation lay in the basis of both types of obesity.
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PMID:[Comparative evaluation of the hormonal changes in alimentaro-constitutional and hypothalamic obesity]. 395 72

Increased in vivo resistance to insulin-mediated glucose disposal has been observed in obese subjects with normal glucose tolerance and in nonobese subjects with glucose intolerance. To determine whether the insulin resistance of glucose-intolerant obese subjects can be accounted for by obesity alone, insulin-mediated glucose disposal was measured in 14 glucose-intolerant and 21 nondiabetic. Southwestern American Indians with similar degrees of obesity. A mixture of insulin, glucose, and somatostatin was infused which delivered the same quantity of glucose and achieved similar plasma insulin concentrations in all subjects. Despite similar steady state plasma insulin levels, the mean steady state plasma glucose concentration was higher in the glucose-intolerant subjects than in weight-matched subjects with normal glucose tolerance (226 +/- 10 vs. 136 +/- 13 mg/dl; P < 0.0001). This increased resistance to insulin action was found in the presence of similar insulin binding to mononuclear cells (measured in 8 glucose-intolerant subjects and 9 subjects with normal glucose tolerance). In obese Southwestern American Indians with glucose intolerance, abnormalities beyond the site of insulin binding to its receptor may explain the observed increase in in vivo insulin resistance.
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PMID:Increased insulin resistance in obese, glucose-intolerant Southwestern American Indians: evidence for a defect not explained by obesity. 610 47

Islets of 5-mo-old obese Zucker rats secreted 50% more somatostatin (SRIF) in response to 8.3 mM or 16.7 mM glucose than did islets from lean controls; the islet SRIF contents of obese and lean rats were similar. As expected, islets of obese rats demonstrated a greater basal and a fivefold greater glucose-induced insulin release and also a twofold greater insulin content than did islets from lean rats. Obese rats were pair fed with lean animals from the age of 9 wk until killed, when 5 mo old. While this curtailed the weight gain of obese rats to that of lean controls, it caused no reduction in the percent body weight found in the form of lipid. The responses of the pancreatic delta and beta cells to pair feeding were markedly different. Pair feeding caused no alteration in either SRIF content or glucose-induced SRIF release, while the expected reductions in both islet insulin content and glucose-induced insulin secretion were observed. Islets from older obese Zucker rats (15--18 mo old) had four to five times greater contents of both SRIF and insulin than did islets from age-matched lean controls. The obese rats of this age had a moderate glucose intolerance. SRIF secretion from the islets of such rats was distinctly greater than from those of lean controls at all glucose concentrations tested (range, 1.0--16.7 mM). The delta cells of the older obese rats had lost their sensitivity to glucose, while those of lean controls remained sensitive. Beta cells of islets from both obese and lean 15-mo-old rats remained glucose sensitive. Under all conditions tested, secretion of SRIF and insulin was greater from islets of obese than lean rats. The results demonstrate a marked difference in pancreatic delta and beta cell responses to pair feeding in the obese Zucker rat. At present, the role played by hypersecretion of pancreatic SRIF in the obesity syndrome of the Zucker rat remains obscure.
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PMID:Hypersection of pancreatic somatostatin in the obese Zucker rat: effects of food restriction and age. 610 55

Somatostatin-like immunoreactivity (SRIF-LI) content in 2 N acetic acid extracts of hypothalamus, gastric antrum, and pancreas was measured in genetically obese (C57BL/6J ob/ob and db/db) and diabetic (C57BL/KsJ db/db and ob/ob) mice and normal littermate controls from 5 to 24 wk to determine the relationship of previously reported changes to the development of metabolic abnormalities. Hypothalamic SRIF-L concentration was similar in control, diabetic, and obese mice at all ages and increased progressively with age in all groups. Gastric antrum SRIF-LI was similar in all groups of mice at all ages. Obese mice gained weight progressively and showed moderate hyperglycemia and marked hyperinsulinemia from 5 wk of age. Pancreatic SRIF-LI content in obese (C57BL/6J) animals was similar to that in lean littermate controls, but pancreatic SRIF-LI concentration (expressed by weight or protein content) was decreased until 8 (6J ob/ob) and 10 (6J db/db) wk. Diabetic (C57BL/KsJ) mice showed a similar metabolic pattern until 10 wk with no change in pancreatic SRIF-LI content or concentration. Thereafter a progressive fall in serum insulin and a marked rise in serum glucose was associated with increasing pancreatic SRIF-LI content and concentration. These studies suggest that the genetically hyperphagic syndromes are unassociated with any change in hypothalamic or gastric SRIF-LI; that pancreatic SRIF-LI increases occur in response to, rather than as the cause of, relative hypoinsulinemia; and that the genetic background of the mice (KsJ or 6J) rather than the mutant gene (db or ob) determines the defect in carbohydrate metabolism and the pancreatic SRIF-LI response.
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PMID:Temporal relationship of tissue somatostatin-like immunoreactivity to metabolic changes in genetically obese and diabetic mice. 610 73

Somatostatin content in the blood of healthy persons, of patients with cerebral nanism, diabetes mellitus, Icenko-Cushing's disease, and obesity, was studied by radioimmuno--assay. Comparative analysis of somatostatin, somatotropin, glucagon and immunoreactive insulin content in the blood of patients with different endocrine disturbances was carried out. Significant elevation of somatostatin level was revealed in cerebral nanism. An increase in the blood somatostatin concentration of patients with diabetes mellitus, Icenko-Cushing's disease and obesity was accompanied by a fall in somatotropin and glucagon secretion and a rise in the blood insulin level.
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PMID:[Relation between blood somatostatin concentration and somatotropin, insulin and glucagon secretion in endocrine diseases]. 611 41

A comparison of the somatostatin with the insulin and glucagon secretions in hypothalamic obesity and genetic obesity was made using the isolated perfused pancreas of rats. In our perfusion experiment, the somatostatin response to 19 mM arginine in the presence of 4.4 mM glucose was significantly greater in both ventromedial hypothalamus (VMH)-lesioned and Zucker fa/fa rats than in their controls, as was the perfusate insulin. The perfusate arginine-stimulated glucagon secretion appeared no different in obese and control rats. Because hyperinsulinemia in vivo and hyperresponses to arginine of perfusate insulin and somatostatin were observed in both VMH-lesioned and Zucker fa/fa rats, whereas the perfusate glucagon secretion in the presence of 4.4 mM glucose was unchanged by obesity, the secretory behavior of some pancreatic hormones seems similar in VMH-lesioned and Zucker fa/fa rats in certain conditions. These results suggest that some abnormalities of pancreatic hormone secretion may be caused by a mechanism common to obesity, whether caused experimentally or genetically.
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PMID:Somatostatin, insulin, and glucagon secretion from isolated perfused pancreas of obese rats. 611 83

We have studied the effects of starvation and of obesity on somatostatin, insulin, and glucagon release from an isolated perfused organ system in fed and 3- and 5-day fasted Holtzman rats and in obese (fa/fa) and lean (Fa/?) Zucker rats. Fasting for 3 days significantly decreased basal (-71%) and amino acid-stimulated (-62%) somatostatin output. After 5 days of starvation, there was a significant increase over the 3-day level in somatostatin output stimulated by amino acid plus glucose (+540%) and by amino acids plus tolbutamide (+238%). Three and five days of starvation severely depressed insulin output while having no statistically significant effects on glucagon secretion. Somatostatin output from obese Zucker rats was significantly greater than that from lean controls in response to amino acids (41.2 +/- 13.2 vs. 16.3 +/- 10.3 ng/25 min, P less than 0.05). Insulin output was greatly increased from obese compared to lean Zucker rats, whereas there were no statistically significant differences in glucagon output. These data show that fasting decreases and obesity increases both somatostatin and insulin release. They suggest that altered stimulation by nutrients was primarily responsible for changes in somatostatin and insulin release observed in starving and obese rats.
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PMID:Effects of starvation and obesity on somatostatin, insulin, and glucagon release from an isolated perfused organ system. 611 33

Immunocytochemical analysis using antisera generated against the brain peptide somatostatin (SRIF) was examined in the brain of normal mice and in mice with chemical lesions of the arcuate nucleus produced neonatally by the administration of monosodium glutamate (MSG). In the normal mouse brain, SRIF immunoreactivity was seen in perikarya of the preoptic and hypothalamic periventricular nuclei. The normal distribution of SRIF fibers was apparent in several hypothalamic nuclei including the arcuate nucleus and in the internal and external zones of the median eminence. Extrahypothalamic sites of SRIF immunoreactive neurons and fibers were also observed throughout the telencephalon. At 60 days of age, certain neuroendocrine deficiencies, including growth parameters and obesity, were apparent in MSG-treated newborn mice. Analysis of SRIF projections in the brain of MSG-treated mice demonstrated a neurotoxic effect on arcuate neurons and a loss of SRIF projections to this region as well. Other components of the SRIF system in brain appeared unaffected. SRIF fibers of the arcuate region seem to originate from neuronal perikarya of the periventricular nucleus suggesting that MSG-induced endocrine deficiencies may be due to SRIF interactions at the level of the arcuate nucleus.
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PMID:Distribution of somatostatin in the mouse brain: effects of neonatal MSG treatment. 612 Jul 49

Glucose, somatostatin-like immunoreactivity (SLI), and glucagon were measured in the portal vein during a glucose infusion (0.5 mg/kg) in 9 diabetic and 7 normal rabbits. The diabetic animals were from a colony of New Zealand white rabbits which develop spontaneous hyperglycemia characterized by low basal and stimulated serum insulin levels and lack of obesity. SLI and insulin were also extracted from pancreatic islets isolated from the diabetic and normal animals. The concentrations of SLI and glucagon, although quite variable, were similar in the portal and peripheral plasma in diabetic and control animals. The insulin content/islet was moderately decreased in the diabetic rabbits, however the content of insulin/microgram protein was similar to the controls. In contrast, SLI content/islet was no different than controls, but was increased when expressed/microgram of protein. Thus, this rabbit colony develops diabetes characterized by some decrease in beta cell mass. The remaining beta cells appear to have a severe defect in the release of insulin.
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PMID:Somatostatin secretion in diabetic rabbits. 612 63


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