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

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
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PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48

A patient with liver dysfunction following small-bowel bypass for obesity was treated successfully with intravenous hyperalimentation. The hepatic steatosis and dysfunction were most likely caused by the preferential absorption of carbohydrate in the remaining small bowel, with resulting relative protein starvation. Routine use of high-protein, low-carbohydrate diets postoperatively until weight stabilization has occurred may prevent this complication.
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PMID:Liver dysfunction following small-bowel bypass for obesity. Nonoperative treatment of fatty metamorphosis with parenteral hyperalimentation. 81 54

In monkeys (Macaca mulatta) without hypothalamic lesions, food intake was found to increase with increasing age and body weight; however, food intake per kilogram body weight showed a decline over the same period of time. As the animals became older, the amount of food intake converted to body weight decreased dramatically (feeding efficiency). Water intake was shown to be closely coupled to food intake. Both daily food and water-intake data were highly reliable over a period of years. Monkeys with ventromedial hypothalamic lesions exhibited hyperphagia and increased feeding-efficiency ratios and eventual obesity. The obese animals developed symptoms of diabetes mellitus. Animals with lesions restricted primarily to the arcuate nucleus showed no hyperphagia but increased feeding efficiency. These animals exhibited decreased growth hormone release and a transitory elevation of serum insulin.
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PMID:Feeding behavior in monkeys with and without lesions of the hypothalamus. 81 9

Adult female rats, depleted of 70 percent of forebrain serotonin by dorsal and median raphe lesions, showed little overeating of food pellets and obesity following medial hypothalamic lesions. However, these rats showed the same reduced acceptance of sucrose solutions, enhanced rejection of quinine solutions, and exaggerated weight gain on a high-fat diet as did other rats made obese by medial hypothalamic lesions alone. Since raphe lesions alone produced none of these effects, the pattern of behaviors observed suggests a hitherto unknown (perhaps secondary) role for brain serotonin metabolism in selective aspects of the medial hypothalamic syndrome.
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PMID:Selective blockade of hypothalamic hyperphagia and obesity in rats by serotonin-depleting midbrain lesions. 83 Dec 88

Modifications in dietary conditions can result in small, but consistent, increases in caloric intake which over time accumulate to substantial increases in body weight. Allowing rats access to either high fat diets or a variety of highly palatable foods can lead to obesity. Recent experiments also have shown that providing access to sweet carbohydrate solutions in addition to the complete diet can cause weight gains in normal neurologically intact adult rats. Although animals increase consumption of carbohydrate on this dietary regime, they continue to maintain minimum requirements for other dietary nutrients. It appears that increasing the palatability of the diet can lead to overeating, but cannot induce the rat to select a diet that is deficient in protein, fat, vitamins, or minerals. Further exploration of the conditions associated with dietary-induced overeating in animals may provide insights into conditions related to obesity in man.
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PMID:Dietary-induced overeating in experimental animals. 83 81

A table of body weight-gain equivalents of selected foods has been developed to illustrate the weight gain to expect when eating single protions of a food above daily maintenance requirements for varying periods. The data were designed to discourage overeating habits, which result in obesity, and may be utilized to reinforce proper dietary habits in counseling of all individuals.
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PMID:Body weight-gain equivalents of selected foods. 84 48

The development of spontaneous activity was studied in obese and lean Zucker rats. Rats were given access to activity wheels for 3 hr/day before weaning and for 24 hr/day after weaning. Zucker obese rats are less active than lean rats. This decreased activity occurs at weaning and follows the onset of hyperphagia and obesity. At 8 wk of age exercised lean and obese rats have less total fat and fewer adipocytes than their appropriate controls. Adipose cell size is decreased only in exercised lean rats. When rats are exercised until 8 wk of age and then confined until 6 mo of age, body weight and fat is elevated in these formerly active rats compared to control rats. Adipose cell number is permanently decreased only in formerly active lean rats. Exercise has no long-term effect in decreasing cell number in obese rats.
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PMID:Spontaneous activity and adipose cellularity in the genetically obese Zucker rat (fafa). 84 5

For many individuals, the practice of overeating is crucial in the development and maintenance of the obese state. Behavior theory views excessive eating leading to obesity as an overlearned habit, strongly conditioned to numerous internal and external cues. A number of studies are reviewed that assess the relationship between emotional arousal and food consumption. Obese persons who successfully lost and maintained a weight loss appeared able to reduce the number of inappropriate stimuli they previously responded to with food intake. The specific behavior modification techniques employed to change eating patterns are discussed, and weight loss maintenance follow-up statistics using these procedures are presented.
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PMID:A behavioral approach to obesity. 85 17

The role of hyperphagia -n the obesity of the diabetic mouse, C57BL/6J db/db, was investigated. Ingestion patterns and the amount of food for diabetic mice were controlled by yoking their food intake to that of nonobese siblings obtaining their food by bar pressing. Over a period of 6 wk, young (initial ages were 28 days) pair-fed diabetic mice accumulated 42% more body weight and approximately five times more extractable carcass lipid than did their siblings. Weight gain and absolute levels of carcass fat were reduced in food-restricted siabetic mice compared with dbs on unrestricted food intake. However, carcass fat as percentage of wet carcass weight was virtually identical in the restricted and unrestricted dbs (47.6% vs. 49.6%). From these results it is concluded that the heightened adiposity of the diabetic mouse does not require hyperphagia for its expression and thus represents a metabolic obesity.
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PMID:Development of obesity in diabetic mice pair-fed with lean siblings. 85 19

Both ovariectomy and hypothalamic knife cuts produced hyperphagia and obesity in adult female rats. The ovarian obesity, however, unlike hypothalamic obesity, was virtually independent of diet palatability. Ovariectomized rats became obese on quinine-adulterated diets, which completely blocked hypothalamic obesity, and they displayed little further weight gain when given a high-fat diet, which greatly potentiated hypothalamic obesity. Ovarian and hypothalamic obesity were also found to be additive irrespective of diet condition when both surgical treatments were combined in the same animal; that is, ovariectomy increased the food intake and body weight of knife-cut animals given the quinine or high-fat diet. In contrast to their dissimilar feeding effects, ovariectomy, hypothalamic cuts, and the combined surgeries, did not differentially alter the aversion to a .01% quinine solution. The results indicate that ovarian obesity and hypothalamic obesity represent two different feeding disorders and are mediated by separate neural mechanisms. The functional nature of these disorders is discussed in light of recent body weight set point interpretations.
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PMID:Comparison of ovarian and hypothalamic obesity syndromes in the female rat: effects of diet palatability on food intake and body weight. 87 May 50


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