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

Serum gastric inhibitory polypeptide (GIP), insulin, and glucose responses to either a 75-g oral glucose challenge or a 500-cal liquid test meal were determined in 141 Caucasians and American Indians. The Caucasians were normal weight, averaging 101 +/- 3% (+/-SEM) ideal BW (IBW), or were obese (168 +/- 21% IBW) and had normal glucose tolerance (n = 77), impaired glucose tolerance (IGT; n = 12), or noninsulin-dependent diabetes mellitus (NIDDM; n = 19). The American Indians were all obese (144 +/- 6% IBW) and had either normal glucose tolerance (n = 22) or NIDDM (n = 11). In all study subjects, including obese individuals with and without glucose intolerance, diabetic patients both thin and obese, and lean subjects with impaired glucose tolerance, fasting serum insulin and GIP, and incremental glucose, insulin, and GIP were greater than they were in normal lean subjects, especially during the first hour of the tests. Obese subjects and diabetic patients exceeded lean normal subjects by up to 620% for glucose, up to 640% for insulin, and up to 360% for GIP during the first hour after glucose ingestion or the test meal. Exceptions were two groups with the most severe diabetes in whom incremental insulin values after oral glucose were only 70% (thin Caucasians) and 110% (obese Indians) that of lean normal subjects. The smallest differences in GIP responses occurred between lean normal subjects and obese nondiabetic Caucasians tested with either a meal or oral glucose, whereas American Indians consistently had the greatest insulin and GIP responses to the tests. High fasting GIP and exaggerated GIP increments in response to nutrients could be attributed to neither obesity nor diabetes alone nor to the type of nutrient used to stimulate its release, but, instead, may be genetic or dietary in origin or may be due to other as yet unidentified factors. High basal GIP and exaggerated nutrient-stimulated GIP release were associated with hyperinsulinemia, except in the most severe diabetic patients. These observations suggest that exaggerated GIP release, along with a greater rise in serum glucose in response to nutrients, may play a role in the pathogenesis of the hyperinsulinemia of obesity and early NIDDM.
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PMID:Gastric inhibitory polypeptide responses to nutrients in Caucasians and American Indians with obesity and noninsulin-dependent diabetes mellitus. 400 8

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

The pancreatic islet hormone secretion is modulated by one or more gastrointestinal peptides ("gut-factor") secreted in response to various types of ingested nutrients. Among a number of postulated candidates for the putative "gut-factor", the gastric inhibitory polypeptide (GIP) has recently emerged as a most likely enteric signal of physiologic import, although its precise role in the pathophysiology of diabetes mellitus remains incompletely understood. During the past decade, an avalanche of knowledge has accumulated regarding a number of peptide agents common to the gastro-enteric-pancreatic system and the nervous system. Preliminary evidence indicates a potential role of several of these peptides in the pathophysiology of diabetes. For instance, cholecystokinin and human pancreatic polypeptide (hPP) may be importantly involved in the regulation of appetite and satiety control and the development of obesity whereas somatostatin, "endorphins", and neurotensin may directly or indirectly modulate islet hormone secretion. Finally the significance of the recently demonstrated presence of insulin and glucagon or glicentin-like peptides in the brain requires close scrutiny.
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PMID:The role of gastrointestinal and neuronal peptides in the pathophysiology of diabetes mellitus. 612 74

The gastric inhibitory polypeptide (GIP) is the main hormone of the incretin type acting on the entero-insular axis. It is released after fat, glucose or meal ingestion. The variations of this secretion are described in obesity and in some pancreatic and gastrointestinal diseases: it is increased in maturity onset diabetes mellitus, obesity or duodenal ulcer, variable according to the food taken and the severity of the pancreatic lesion in chronic pancreatitis and cystic fibrosis, normal in insulinoma and decreased in celiac disease. The impaired absorption of the food-stuffs and the defective feed-back regulation of GIP secretion by insulin are the major causes of these variations. To a lesser degree, gastric acid secretion, gastric emptying and vagal control may also influence GIP secretion.
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PMID:Clinical aspects of GIP secretion. 628 Apr 23

Twenty-six patients who were more than 35 per cent above their ideal weight were examined before the introduction of a weight reduction programme. At the end of a three-month period, seven patients had lost more than 10 per cent of their body weight. These patients had significantly lower triglyceride levels, fasting gastric inhibitory polypeptide levels (GIP) and prolactin levels. Fasting vasoactive intestinal polypeptide levels (VIP) before commencing diet were raised in six of the 19 patients who subsequently did not lose weight whereas the seven patients who lost weight had normal VIP levels (X2 = 3.07, P less than 0.05). Patients with high VIP levels had higher triglyceride levels, higher mean C-terminal glucagon-like immunoreactivity (C-GLI) and higher post glucose infusion secretin levels. There was a significant correlation between triglycerides and VIP. The significance of abnormally high VIP levels in obesity and the inability of these patients to lose weight is discussed.
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PMID:Vasoactive intestinal polypeptide in obesity. 634 22

The influence of gastric inhibitory polypeptide (GIP) on fatty acid incorporation into adipose tissue (FIAT) was studied in the rat on epididymal fat pads at concentrations amounting to 1, 2 and 4 ng/ml. Without insulin in the incubation medium, GIP induced a slight though significant FIAT decrease with a maximum of 9% for 2 ng/ml concentration. In the presence of rat insulin (100 microU/ml), it significantly enhanced the insulin-induced FIAT increase, that progressed from 106.4% of the basal value to 110.5% for 1 ng/ml concentration (P less than 0.025) and to 118.2% for 4 ng/ml concentration (P less than 0.0025). The existence of such a phenomenon as well as that of an hyperactive enteroinsular axis in obese subjects could represent two important factors in the development of obesity.
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PMID:Gastric inhibitory polypeptide enhancement of the insulin effect on fatty acid incorporation into adipose tissue in the rat. 635 87

To examine the possibility that the decrease of hyperinsulinemia and blood pressure in obesity associated with physical training is mediated via adaptations in the adrenergic nervous system, a pure beta-adrenergic agonist (isoproterenol) or an alpha-adrenergic antagonist (phentolamine) was infused before and during an oral glucose tolerance test before and after physical training. A number of circulatory, metabolic, and endocrine factors under adrenergic control were followed. Physical training was associated with an augmented beta-agonist response in blood pressure, heart rate, blood glucose, plasma insulin, connecting (C) peptide, and pancreatic polypeptide (PP) but not in plasma glucagon and gastric inhibitory polypeptide. Physical training also resulted in higher values of C-peptide and PP values after alpha-adrenergic blockade. It was concluded that physical training probably is associated with an augmented sensitivity of the beta-adrenergic nervous system. This might also be the case with the alpha-adrenergic system. It was suggested that this in turn might be due to a decreased firing in the adrenergic nervous system leading secondarily to an increased sensitivity in the effector cells. It was hypothesized that such decreased firing could provide a background to explain lower blood pressure and plasma insulin after physical training.
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PMID:Effects of physical training on adrenergic sensitivity in obesity. 636 65

The gastric inhibitory polypeptide (GIP) response to certain stimuli may be exaggerated in patients with obesity and noninsulin-dependent diabetes mellitus. To explore the effects of increased caloric intake and dietary composition on GIP secretion, 20 normal lean volunteers underwent a 4-week ambulatory study. A baseline week (usual diet) was followed by 3 weeks in which the usual diet was supplemented with 45 g fat (diet A), 100 g carbohydrate in the form of sucrose (diet B), or 50 g protein (diet C) for 1 week each. Almost equal numbers of subjects followed sequence ABC, BCA, or CAB in this cross-over study. At the end of the baseline week and each study week, serum glucose, insulin, and GIP were measured in response to a 500-cal liquid test meal. Daily intake of carbohydrate, protein, or fat, as monitored by food records, increased significantly (P less than 0.01) during the appropriate dietary periods, whereas body weight changed slightly, but not significantly, during the 3 study periods. No changes occurred in the total integrated serum glucose concentrations, whereas integrated insulin concentrations changed significantly (P less than 0.05), being 32.5 +/- 3.1 (+/- SEM), 37.2 +/- 4.0, and 30.3 +/- 3.1 microU/ml min-1 during periods A, B, and C, respectively. Insulin secretion was greatest during period B, the carbohydrate week, when insulin concentrations 15-60 min after the test meal were significantly greater (P less than 0.05 to P less than 0.01) than after the baseline period. Total integrated incremental serum GIP concentrations were also significantly different (P less than 0.01) during the 3 study periods, being 1.93 +/- 0.13, 2.53 +/- 0.24, and 1.90 +/- 0.11 ng/ml min-1 during A, B, and C, respectively. Serum GIP was highest during period B (carbohydrate), when average concentrations were significantly higher (P less than 0.01) 15-60 min after the meal compared to those during the baseline study. Similar changes did not occur with the other diets. Thus, GIP and insulin secretion were substantially altered by an acute increase in sucrose intake. The exaggerated GIP response to a meal in some patients with obesity may possibly be the result of adaptation of intestinal GIP cells to diet, particularly one rich in sucrose.
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PMID:Augmented gastric inhibitory polypeptide and insulin responses to a meal after an increase in carbohydrate (sucrose) intake. 636 44

The involvement of the gut hormone GIP (gastric inhibitory polypeptide, glucose-dependent insulinotropic polypeptide) in the hyperinsulinemia of the adult obese Zucker rat was investigated. Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. The sensitivity of the isolated, perfused pancreas to glucose and GIP was studied in basal and hyperglycemic conditions in lean and obese rats. Immunocytochemical studies of the gut and pancreas were also carried out. The glucose and GIP responses to oral glucose were similar in lean and obese rats, but obese animals were hyperinsulinemic compared with lean controls under fasting conditions and after oral glucose. The isolated, perfused pancreas of obese Zucker rats had an elevated insulin response to 300 mg/dl glucose. GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. Immunocytochemical studies demonstrated the presence of enlarged islets in obese rats due to an increase in the B-cell mass. A-, D-, and PP-cells appeared normal. Obese and lean rats had similar numbers of GIP-containing cells in the gut. This study suggests that GIP may contribute to the fasting hyperinsulinemia characteristic of adult obese Zucker rats. GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals.
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PMID:Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat. 637 59

An 18-year-old man had cystic fibrosis (CF) and insulin-resistant carbohydrate intolerance characterized by (1) obesity, basal hyperinsulinemia, and hyperglucagonemia; (2) impaired oral glucose tolerance; (3) hyperinsulinemia in response to oral and intravenous (IV) administration of glucose and to IV administration of tolbutamide; (4) exaggerated gastric inhibitory polypeptide secretion following orally administered glucose; and (5) diminished sensitivity to insulin administered IV compared with other patients with CF. Both parents also demonstrate basal and stimulated hyperinsulinemia in response to orally administered glucose. The long-term outlook for patients with CF is improving, and more patients are surviving childhood. Thus, it should be recognized that an insulin-resistant form of carbohydrate intolerance may develop in patients with CF with obesity and/or genetic risk factors.
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PMID:Insulin resistance in a young man with cystic fibrosis. 637 49


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