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

Short chain fatty acid absorption from the human rectum has been studied in 46 subjects attending an obesity clinic, using a dialysis bag technique. From a mixed electrolyte solution, acetate concentrations fell from 97.0 to 64.2 mmol/l, and sodium from 97.8 to 85.1 mmol/l with respective net absorption rates of 8.1 and 5.2 mumol/cm2/h. From a solution with mixed short chain fatty acids acetate concentration fell from 62.3 to 37.6 mmol/l, propionate from 20.2 to 11.5 mmol/l, and butyrate from 25.7 to 17.3 mmol/l with absorption rates of 5.2, 1.8, and 1.9 mumol/cm2/h. Lowering pH from 7.2 to 5.5, to test the possibility that absorption occurred by passive non-ionic diffusion, had no effect on absorption rates, although pH rose rapidly in the dialysis fluid. These results are comparable with rates of acetate absorption from the animal large intestine. The hypothesis that short chain fatty acids are not absorbed from the large gut and therefore contribute to faecal bulk by retaining water in the bowel lumen may need revision.
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PMID:Short chain fatty acid absorption by the human large intestine. 3 Jun 83

In five patients in whom a jejuno-ileal by-pass had been previously performed for massive obesity, a relaparotomy was performed because of subjective complaints or unsatisfactory weight reduction. At the reoperation morphometric studies were made of the functioning segments and the by-passed intestine. Length and circumferential measurements were taken, and the villous height and mucosal thickness were measured from histological biopsies. The results were compared with the findings in a control group. After shunt operation adoptive hypertrophy in the functioning remnant, a considerable length growth and dilatation of the gut, as well as a marked increase in villous height and total mucosal thickness, were demonstrated. These adaptive changes seem to be more marked in the distal part of the small intestine. No atrophy of the mucosa could be demonstrated in the excluded intestinal loop.
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PMID:Morphometric studies of the small intestine following jejuno-ileal shunt operation. 126 35

The ester methyl [4-[2-[(2-hydroxy-3-phenoxypropyl)amino]ethoxy]phenoxy]acetate (1) (R1 = OMe) had previously been identified as the most interesting member of a series of selective beta 3-adrenergic agonists of brown adipose tissue and thermogenesis in the rat. In vivo it acts mainly via the related acid 1 (R1 = OH). Amides have been examined to determine whether they have advantages over the ester. In particular, in the rat and dog the half-lives of amides of appropriate potency were no longer than those of the ester. The amide (S)-4-[2-[(2-hydroxy-3-phenoxypropyl)amino]ethoxy]-N-(2- methoxyethyl)phenoxyacetamide [S-27, ICI D7114] was selected as having properties consistent with a sustained-release formulation should that prove necessary. Unlike the ester it is resistant to hydrolysis in the gut lumen. Further testing of ICI D7114 has shown that in the rat, cat, and dog it stimulates the beta 3-adrenergic receptor in brown adipose tissue at doses lower than those at which it affects beta 1- and beta 2-adrenergic receptors in other tissues. Slimming effects were observed in the dog. ICI D7114 may be a selective thermogenic agent in man and may be useful in the treatment of obesity and diabetes.
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PMID:Selective beta 3-adrenergic agonists of brown adipose tissue and thermogenesis. 2. [4-[2-[(2-Hydroxy-3-phenoxypropyl)amino]ethoxy]phenoxy]acetamides. 135 Mar 10

Obesity is a public health issue of major concern for the United States and other developed nations. In the last several decades, bariatric surgery has developed as a means of treating morbid obesity. Vertical banded gastroplasty (VBG) is an attractive procedure because it has fewer side effects than other forms of bariatric surgery and maintains physiological continuity of the gut. VBG was performed in 36 patients at a rural community hospital from 1982-1990. There was only one intraoperative complication necessitating splenectomy and two early postoperative complications--gastric leak and marginal stress ulcer--necessitating reexploration. Twenty-five patients were available for follow-up, at which time they were an average of 6.4 years out of surgery. Two of these patients had died, both from cardiac arrest months or years after VBG. The remainder had gone from a preoperative average of 86.7% over ideal weight according to 1983 Metropolitan Life insurance Tables to 54.5% over ideal weight. Mean BMI for this group had changed from 41.2 preoperatively to 34.7 at follow-up. Success was defined as weight loss to < 60% over ideal or BMI < 35, removing the individual from the morbidly obese category. According to this criteria, VBG provided successful weight loss in 72% of subjects in the follow-up group. Weight loss results may have been biased as a significant number of patients were lost to follow-up and may have constituted failures. In general, most individuals did not make concomitant changes in diet or sedentary life-style which would have supported weight loss effected by VBG. Moreover, regain of weight was progressive and possibly inexorable. Nearly all individuals nonetheless reported great satisfaction with their surgery. VBG is a viable option in the treatment of morbid obesity, but criteria for success needs to be better defined in order to determine whether the procedure is "worth it."
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PMID:Vertical banded gastroplasty: is obesity worth it? 147 72

Cholecystokinin (CCK) is a gut peptide whose proposed effect on satiety is thought to be related to gastric volume and to be signaled through vagal afferent fibers to the medial hypothalamus. To test these hypotheses we infused CCK C-terminal octapeptide (CCK-8) or saline in a random double-blind fashion in three groups of subjects: 17 obese subjects, 6 of whom subsequently received a gastric bubble, and 5 obese subjects whose obesity was due to hypothalamic injury. The number of sandwich canapes eaten after saline or CCK-8 infusion was recorded during three consecutive 10-min eating periods. Each subject served as his/her own control. The prior infusion of CCK-8 significantly decreased the consumption of sandwich canapes in the first eating period in both the control obese subjects and the subjects with obesity due to hypothalamic injury. Insertion of a gastric bubble did not enhance the satiety effect of CCK-8. These studies support the hypothesis that CCK produces satiety in a time-dependent manner that is not enhanced after the insertion of a gastric bubble but is operative in obese subjects with hypothalamic injury.
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PMID:Cholecystokinin and satiety: effect of hypothalamic obesity and gastric bubble insertion. 153 32

Morbid obesity is a major health problem in this country and throughout the world. In addition to its social stigma (in the western world), obesity exacerbates several disease states such as diabetes, hypertension, cardiac disease and restrictive lung disease. When effective medical treatment of obesity becomes available, it will depend in part upon understanding the physiologic factors that control satiety. This review summarizes the information available on brain and gut control mechanisms of satiety. Brain nuclei located in the lateral hypothalamus, ventromedial hypothalamus, and other paraventricular areas are the sites of action for potent neuropeptides, such as cholecystokinin (CCK) and neuropeptide Y, that appear to regulate feeding. Exogenous CCK has been used clinically to decrease meal size in obese patients. The sites of the satiety cascade that are most often manipulated are the gastric and intestinal phases. Physiologic gastric distension is a potent inhibitor of feeding, whereas the intermeal interval may be regulated by intestinal signals released by food in the gut. Jejunal-ileal bypass has fallen from favor and has been replaced by gastric restrictive procedures that create a small proximal gastric pouch that empties into the small bowel (gastric bypass) or the distal stomach (gastroplasty). These operations rely partially on their ability to produce gastric distension in the proximal gastric pouch at an early stage during a meal. Thus, failure results if the pouch compensates by distending or if the stoma widens with subsequent loss of slow emptying. Improved medical and surgical treatment will be designed to intervene at specific sites of the satiety cascade as knowledge of the physiologic control mechanisms of satiety increases.
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PMID:Physiologic approaches to the control of obesity. 229 39

Historically, nutrients and related metabolic signals were considered to control the onset and offset of meals. Recent research has focused upon the roles of peptides found in the gastrointestinal tract and brain as alternate controllers of these processes. During a meal, the gut secretes a variety of peptides as part of the digestive process. Some of these substances, acting as hormonal or as local signals, may also provide information which is relayed to the central nervous system, causing eating to stop and producing the sense of satiety. When administered to animals or people before a meal, exogenous cholecystokinin (CCK), the most studied of the putative satiety peptides, reduces food intake in a dose-dependent manner. Recent findings support the concept that endogenous CCK acts during meals to limit meal size, and evidence is reviewed suggesting a possible pathophysiological role for CCK in bulimia. Adiposity is also regulated via peptide hormones, especially insulin. Insulin is secreted in direct proportion to adiposity, and blood-borne insulin gains access to brain areas important in the regulation of feeding. The administration of insulin into the brain causes reduced eating and weight loss.
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PMID:The regulation of food intake by peptides. 269 89

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

Human gut-associated immunoregulatory events were studied in a pokeweed mitogen (PWM)-stimulated culture system using lymphocytes obtained from the mesenteric lymph nodes (MLN) of female subjects undergoing gastroplasty for obesity. Compared with peripheral blood lymphocytes, lymphocytes obtained from MLN secreted IgG, IgA and IgM isotypes that differ in pattern and distribution despite similar proportions of T cells and B cells expressing isotype-specific surface membrane immunoglobulin (SmIg). Among the isotypes secreted, IgA appeared to be increased relatively to other isotypes in MLN cultures. Crossover coculture experiments using T and B cells isolated from both MLN and blood by E-rosetting and cell panning procedures demonstrated that IgA was particularly sensitive to help and suppression exerted by MLN T cells and T cell subsets defined by monoclonal antibodies OKT4 and OKT8 respectively, when compared with similar subsets isolated from blood. The results presented provide a basis for study of gut handling of ingested antigen in man, and of disturbed immunoregulatory events in inflammatory and neoplastic disease of the human gut.
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PMID:Regulation of IgA secretion in polyclonally induced in vitro human lymphocyte cultures: the function of T and B cells from mesenteric lymph nodes and peripheral blood. 294 20

Technological advances have reduced and refined man's plant food intake and consequently brought about an unprecedented decline in his consumption of dietary fibre (DF). The emergence of certain diseases selectively in regions which have been affected the most by this dietary change has led to an enhanced awareness of the functions of DF. DF is a heterogeneous group of substances which resist digestion by the endogenous enzymes of the human gut, although they are fermented to a substantial extent by the bacterial flora of the large intestine. Chemically, DF essentially consists of nonstarch polysaccharides and lignin, and its major constituents are cellulose, hemicelluose, lignin and pectin. The physiological effects of DF are attributable largely to its physicochemical properties. DF primarily affects gastrointestinal (GI) function; its effects are observable at all stages from ingestion through defaecation. It restricts caloric intake, shows gastric and small intestinal transit, and affects the activity of digestive enzymes and release of GI hormones. Its overall impact is to reduce apparent digestibility of nutrients marginally but consistently. In the large intestine, DF accelerates transit, supports bacterial growth and serves to hold water. As a result, the faecal weight and water content increase, and the transit time generally becomes shorter. Secondary to its GI effects, DF attenuates postprandial glycaemia and has long term effects on glucose tolerance and lipoprotein metabolism. These effects have important implications in the aetiopathogenesis of constipation and its sequelae including diverticulosis, cholesterol gallstones, colorectal cancer, obesity, diabetes mellitus and atherosclerosis. DF has traditionally been used therapeutically for constipation; now its use in diabetes is also well established. Our appreciation of the role of DF in human nutrition has undergone a major change in the last two decades. From a redundant constituent of plant foods, it has now moved to the position of an essential nutrient, the deficiency of which seems to have serious consequences.
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PMID:Dietary fibre: consensus and controversy. 301 Mar 80


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