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

Obesity can be reversed in ob/ob mice by parabiosis to lean littermates, by islet transplantation, and by injection of pancreatic polypeptide. These observations suggest that obese mice have functioning satiety centers but lack a circulating satiety factor of pancreatic origin which could be pancreatic polypeptide. This hypothesis has been difficult to test because antisera currently available do not cross-react with rodent pancreatic polypeptide. We have raised an antiserum against the biologically active carboxyl-terminal hexapeptide that measures mouse pancreatic polypeptide specifically. This antiserum has been used to compare circulating and tissue concentrations of pancreatic polypeptide in obese and lean mice. Although pancreatic contents were significantly (p less than 0.01) increased in obese mice (237 +/- 34 pmol/g) compared with lean littermates (107 +/- 20 pmol/g), no postprandial increase in circulating concentrations was observed in obese mice. The hypothesis that obese mice lack a satiety factor of pancreatic origin could be explained by the failure of release of pancreatic polypeptide.
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PMID:Failure of pancreatic polypeptide release in congenitally obese mice. 637 66

Ten severely obese women were subjected to physical training for three months on ad libitum diet. Under metabolic ward conditions oral glucose tolerance test was performed before and after the training period with the same energy intake quantitatively and qualitatively, and glucose, insulin, connecting (C)-peptide, gastric inhibitory polypeptide (GIP) and pancreatic polypeptide (PP) were determined. In confirmation of previous work, physical training caused no decrease in body fat in these severely obese subjects, and no change in body cell mass or glucose tolerance, while insulin and blood pressure decreased. The control of dietary conditions demonstrated that the latter phenomena were not due to quantitative or qualitative changes in the diet. C-peptide concentrations decreased also, indicating effects of physical training in obesity on insulin production. GIP is believed to be a gastrointestinal factor facilitating insulin secretion (Incretin). Previous work has indicated that gastrointestinal factor(s) are involved in the insulin lowering effect seen after physical training. It is possible that GIP is contributing to this phenomenon.
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PMID:Effects of physical training on insulin, connecting peptide (C-peptide), gastric inhibitory polypeptide (GIP) and pancreatic polypeptide (PP) levels in obese subjects. 637 15

Twenty-three morbidly obese and 17 control subjects were studied with a breakfast meal. Neither fasting nor postprandial plasma pancreatic polypeptide (PP) levels differed significantly between the two groups, whereas postprandial serum insulin and blood glucose were significantly higher in the obese subjects. Our results do not support the suggestion that PP participates in the appetite regulation or the development of obesity.
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PMID:Fasting and postprandial plasma pancreatic polypeptide (PP) levels in obesity. 639 20

Serum pancreatic polypeptide (PP), gastric inhibitory polypeptide (GIP), insulin and glucose responses to meal stimulation were studied in 10 normal weight patients, 13 normal obese patients and 7 patients with Prader-Willi syndrome (PWS) associated obesity. Serum and plasma concentrations of PP, glucose, insulin and GIP were obtained at 15 min intervals from 0-180 min. after a 275 K calorie meal. Basal and peak responses of glucose, for patients with PWS were significantly lower when compared to normal or obese controls. Basal and peak insulin responses in PWS were significantly greater than those of the normal controls but still less than those of the obese controls. Basal GIP concentrations in the patients with PWS were significantly less than normals and their peak response was less than the obese control group. No significant differences in basal or peak PP responses were noted between normal and obese controls. All 7 patients with PWS had abnormal PP responses. Five failed to show significant PP release after the stimulation; one had a peak response to 130 pg/ml while the 7th patient (PB) had an exaggerated response to 2000 pg/ml. The 6 patients with low or no response had basal PP values of 62 +/- 12 pg/ml and a mean PP peak response of 78 +/- 15 pg/ml. This observation of blunted PP response in a human model of hyperphagia and obesity parallels the animal models and suggests PP may have a significant role in appetite control.
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PMID:Blunted pancreatic polypeptide responses in children with obesity of Prader-Willi syndrome. 701 2

Pancreatic polypeptide was infused into obese-hyperglycemic (ob/ob) mice and lean littermates to determine its effect on weight gain. Obese mice continuously infused with 30, 60, or 100 micrograms/day for 7 days developed both diarrhea and weight loss in a dose dependent fashion. Lean littermates infused with 100 micrograms/day developed neither diarrhea nor weight loss. Light microscopic study of ileum and colon revealed no abnormalities. These studies indicate that the effects of pancreatic polypeptide are in part genetically determined since the obese and non-obese mice differ at only one gene locus.
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PMID:Pancreatic polypeptide causes diarrhea and weight loss in obese mice but not in lean littermates. 717 27

Plasma levels of pancreatic polypeptide (PP) were studied in a group of 22 normal and 22 obese subjects after an overnight fast. In a second group of 10 normal and 13 obese adults, PP secretion was stimulated by a protein-rich meal. The results indicate lower fasting PP values in the obese subjects and a decreased response during the second phase of the meal-induced secretion. This could suggest a possible role of PP in obesity.
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PMID:Low plasma levels of pancreatic polypeptide in obesity. 738 Jan 12

Biliopancreatic bypass for obesity entails a 2/3 distal gastrectomy with Roux-en-y reconstruction, being the small bowel transected at its midpoint and the enteroenteroanastomosis placed 50 cm proximal to the ileocecal value. Pancreatic polypeptide (PP) and motilin fasting and meal-stimulated plasma concentrations were determined in 13 nonobese healthy volunteers, in 13 nonoperated obese patients, in 9 subjects within two months, in 12 subjects four to twelve months, and in 7 subjects fifteen to twenty months after operation. There were no significant differences in PP fasting levels between either the obese and control groups or between the postoperative groups and the preoperative group. Both meal-stimulated peak and integrated response values were similar in the obese and control groups, and were strikingly and progressively reduced postoperatively, with statistically significant difference between all postoperative groups and preoperative group. Mean plasma motilin fasting and peak values were higher in the obese group than in the control group, and significantly reduced in the 4-12 and 15-20 month group. Despite the huge variability among data, the integrated response in the 0-2 month group was significantly decreased in comparison with the preoperative group, while a subsequent progressive increase was shown by the 4-12 and 15-20 month groups.
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PMID:[Behavior of plasma pancreatic polypeptides and motilin in obese patients subjected to biliopancreatic bypass]. 745 3

Previous studies showed that in hamsters the 139H, but not the 263K, scrapie strain caused a marked increase in pancreatic size and led to obesity, hypoglycaemia and striking hyperinsulinaemia. In the preceding paper (Ye et al., 1994), the islets of Langerhans in 139H-affected hamsters showed cellular atrophy, fibrosis, cytoplasmic vesicles and nuclear pathological changes. In the present study, the profiles of pancreatic islets were classified into three sizes with an image analyzer. The number and total area covered by "small" islet profiles were less in 139H-affected than in normal hamsters. In contrast, the number and the area of "medium" and "large" islet profiles were significantly greater in 139H than in normal hamsters. With antibodies to insulin, glucagon, somatostatin and pancreatic polypeptide, the proportions of B, A, D and F cells were determined. With somatostatin-positive cells arbitrarily given a value of 1, the ratio of B:A:D:F cells in the islets was 27:5:1:0.04 in normal hamsters and 122:7:1:0.04 in 139H-affected hamsters. The increase in B cells would account for the islet enlargement and the hypoglycaemia-hyperinsulinaemia seen in 139H-affected hamsters.
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PMID:Hyperplasia and hypertrophy of B cells in the islets of Langerhans in hamsters infected with the 139H strain of scrapie. 804 Mar 83

The neural regulation of food intake seems to be quite similar in birds and mammals. The ventromedial hypothalamic syndrome produced by lesions within the mediobasal hypothalamus of both birds and mammals is composed of several independent physiological and behavioral changes. Other neural sites known to be important in mammals for regulating food intake need to be examined in birds including the paraventricular nucleus, nucleus tractus solitarius and parabrachial nucleus. Members of the opioid and pancreatic polypeptide families are effective in stimulating food intake in avian species. Both prolactin and growth hormone are also efficacious in stimulating food intake. In contrast, cholecystokinin inhibits food intake when administered intracerebroventricularly. The autonomic and endocrine hypothesis developed to explain obesity in mammals appears to be quite applicable to genetic strains of commercial birds selected for meat production. Specifically the commercial broiler appears to display an imbalance of the autonomic nervous system. The parasympathetic nervous system dominates as a consequence of intense genetic selection for growth rate.
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PMID:Central neuroanatomical systems involved in the regulation of food intake in birds and mammals. 806 84

Disturbed satiety mechanisms may contribute to obesity. There has been speculation that cholecystokinin (CCK) and pancreatic polypeptide (PP) are involved in the regulation of satiety. We have therefore investigated whether there are differences between healthy lean and healthy non-diabetic obese volunteers in plasma CCK or PP release after a neuropeptidergic stimulation with bombesin and after infusion of a mixed meal. There were no differences in plasma CCK between groups either basally or in response to either form of stimulation. However, the plasma PP concentrations after the meal were significantly less in obese (2845 +/- 404 pM.min) than in lean subjects (5569 +/- 997 pM.min), whereas the plasma PP concentrations during bombesin were similar in both groups. We tested two other groups of nine obese and lean subjects to determine whether a disturbed vagal function could be the cause of the diminished plasma PP in obese persons, by studying the effect of modified sham feeding (MSF) on plasma PP. However, there were no significant differences in the plasma PP response to MSF between lean and obese subjects. We conclude that there are no differences between lean and obese persons in plasma CCK secretion in response to infusion of the neuropeptide bombesin or to ingestion of a mixed meal. However, the plasma PP after a mixed meal, is markedly diminished in obese subjects. This could not be attributed to a disturbed vagal cephalic stimulation.
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PMID:Plasma cholecystokinin and pancreatic polypeptide secretion in response to bombesin, meal ingestion and modified sham feeding in lean and obese persons. 814 26


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