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

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

There is evidence for involvement of gastrointestinal hormones in pathogenesis of obesity and reports on lipolytic activity in animals. The in vitro lipolytic activity of these hormones was tested in human adipocytes. Vasoactive intestinal polypeptide, glucagon, secretin, human gastrin I, gastrin releasing polypeptide, gastric inhibitory polypeptide, pancreatic polypeptide, motilin, bombesin, neurotensin, C-peptide, as well as cholecystokinin did not stimulate lipolysis significantly above basal. These results indicate that the involvement of these hormones in obesity in man might not be due to a direct lipolytic effect on the human adipocyte.
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PMID:Glycerol release from incubated human adipocytes is not affected by gastrointestinal peptides. 401 16

Early development changes in hormone levels were investigated in strains of pigs with genetic propensities for excessive lipid deposition. Fetal serum growth hormone was lowest in the preobese pigs (Ossabaw and high backfat). Fetal serum triiodothyronine was significantly elevated in the fetal pigs from obese strains. Fetal serum cortisol was highest in the high backfat pigs. There were no statistically significant differences in fetal serum glucagon. Ossabaw (obese) sows have higher serum glucose levels during gestation than low backfat or high backfat sows. This hyperglycemia is reflected in higher serum glucose levels in 110 day old Ossabaw fetal pigs. High backfat sows have higher serum triglyceride levels that low backfat or Ossabaw sows. The Ossabaw fetal pig has lower serum triglycerides than either the high backfat or the low backfat fetuses. These studies characterize early changes in serum metabolites and hormones in pigs which have the genetic propensity for obesity. At 110 days of gestation these pigs are similar in body at content (less than 1%). It is proposed that the lower level of growth hormone in the preobese fetal pig promoted a lower rate of lean body growth and a higher rate of lipid deposition postnatally.
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PMID:Fetal hormone and metabolite levels in lean and obese pigs. 408 6

Plasma concentrations of glucagon, insulin, glucose, and individual plasma amino acids were measured in normal nonobese and obese subjects before and after 3 days of dexamethasone treatment (2 mg/day) and in patients with Cushing's syndrome. The subjects were studied in the basal postabsorptive state and following the infusion of alanine (0.15 g/kg) or ingestion of a protein meal. In nonobese subjects dexamethasone treatment resulted in a 55% increment in basal glucagon levels and in a 60-100% increase in the maximal glucagon response to alanine infusion or protein ingestion. In obese subjects, basal glucagon rose by 110% following dexamethasone, while the response to alanine increased fourfold. In patients with Cushing's syndrome basal glucagon levels were 100% higher and the glucagon response to alanine infusion was 170% greater than in normal controls.Dexamethasone treatment in normal subjects resulted in a 40% rise in plasma alanine concentration which was directly proportional to the rise in basal glucagon. The remaining 14 amino acids were unchanged. In the patients with Cushing's syndrome alanine levels were 40% higher than in normal controls and were directly proportional to basal glucagon concentrations. No other plasma amino acids were significantly altered in the group with Cushing's syndrome. It is concluded that (a) glucocorticoids increase plasma glucagon concentration in the basal state and in response to protein ingestion or aminogenic stimulation; (b) this effect of glucocorticoids occurs in the face of obesity and persists in chronic hypercorticism; (c) hyperalaninemia is a characteristic of acute and chronic glucocorticoid excess, and may in turn contribute to steroid-induced hyperglucagonemia; and (d) increased alpha cell secretion may be a contributory factor in the gluconeogenic and diabetogenic effects of glucocorticoids.
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PMID:Influence of glucocorticoids on glucagon secretion and plasma amino acid concentrations in man. 474 10

We have assessed the presence of VIP/PHI/secretin receptors in heart by: (1) testing the ability of the corresponding peptides to activate adenylate cyclase in cardiac membranes from rat, dog, Cynomolgus monkey and man, and (2) examining the ability of the same peptides to exert inotropic and chronotropic effects on heart preparations from rat and Cynomolgus monkey in vitro. Based on their affinity for natural peptides and synthetic analogs, two types of VIP/PHI/secretin receptors were characterized: the relatively nonspecific "secretin/VIP receptor" of rat heart (that is "secretin-preferring" only in that secretin was more efficient than VIP in stimulating adenylate cyclase), and the "VIP/PHI-preferring" receptor of man, monkey and dog heart. Four physiopathological situations affecting secretin/VIP receptors in rat heart were explored: In male rats from the Okamoto strain and the Lyon strain, two strains presenting spontaneous hypertension, heart membranes exhibited a markedly decreased response of adenylate cyclase to secretin/VIP, with lesser alterations in the responses to isoproterenol and glucagon. This impairment developed in parallel with the occurrence of hypertension and was reproduced in normotensive rats submitted to chronic isoproterenol treatment (but not in Goldblatt hypertensive rats). These findings are consistent with a hyperactivity of norepinephrine pathways in spontaneously hypertensive rats, leading to a reduced number of cardiac post-junctional secretin/VIP receptors bound to adenylate cyclase. Heart membranes from genetically obese (fa/fa) Zucker rats also exhibited severely decreased responses to secretin/VIP with lesser alterations in the responses to glucagon and isoproterenol. These anomalies were specific for the heart, and developed in concomitance with obesity. The first anomaly could not be corrected by severe food restriction. Secretin stimulation of heart adenylate cyclase was also selectively altered in streptozotocin-diabetic rats. Thus, two types of diabetic cardiomyopathy were characterized by a severe local alteration of secretin/VIP receptors coupled to adenylate cyclase. Hypothyroidism, provoked in rat by thyroidectomy or propylthiouracil treatment, again induced a marked decrease in secretin-stimulated cardiac adenylate cyclase activity. In rat papillary muscle electrically stimulated in vitro, secretin exerted a positive inotropic effect. This effect was reduced in obese (fa/fa) Zucker rats. In rat right atrium, secretin also exerted a positive chronotropic effects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Heart receptors for VIP, PHI and secretin are able to activate adenylate cyclase and to mediate inotropic and chronotropic effects. Species variations and physiopathology. 608 34

Hepatic plasma membranes of female obese mice C57 BL-6 orl ob/ob (ob/ob mice) completely lack vasopressin (VP) receptors of the V1 type whereas kidney VP receptors are normally expressed and functionally coupled to adenylate cyclase. To discover if these alterations are linked to a genetic defect of the V1 receptor, we have studied the binding of VP on liver and kidney membranes of two other models, female diabetic mice C57 BL-6 orl db/db (db/db mice) and female Zucker rats Fatty/orl fa/fa (fa/fa rats), which exhibit different temporal pattern of obesity, hyperinsulinemia and insulin resistance. In addition, since VP is known to exert its vascular response through stimulation of V1 receptors, we have studied the reactivity of VP of isolated tail artery in the three different models, ob/ob and db/db mice and fa/fa rats, and in their respective controls. In all cases, VP kidney receptors and VP vascular reactivity are normal. db/db mice exhibit a marked decrease in hepatic VP receptors whereas a 50% decrease was observed in 32 week fa/fa rats. Angiotensin II and prazosin binding sites are still present as well as the adenylate cyclase response to glucagon. These results suggest that the specific alteration in liver VP receptors is not related to a defect in V1 receptor genetic expression but is specific for liver and appears to parallel the level of hyperinsulinemia and/or insulin resistance.
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PMID:Reduction in hepatic but not in renal and vascular vasopressin receptor number in hyperinsulinemic mice and rats. 609 84

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

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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