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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 new automated potentiometric method for the determination of colipase was developed, taking advantage of the reactivation of purified lipase, in the presence of bile salt and at pH 6.5. High-fat and high-starch diets induced an opposite regulation of lipase and amylase in the rat pancreas. At the same time, the level of colipase was not influenced by nutrition. During fasting and in alloxan diabetes, the specific activity of lipase almost doubled, that of amylase decreased sharply, and colipase was not affected in the rat pancreas. In obese-hyperglycemic mice, suffering from obesity, hyperinsulinism, and moderate diabetes, there was also no regulation of pancreatic colipase. Thus, at variance with a number of hydrolases, there was no dietary or hormonal adaptation of colipase. However, this was probably without any bearing on intraluminal lipolysis. Indeed, comparison of lipase and colipase activities in pancreas and in small intestine suggests that colipase concentration is not a limiting factor of intraluminal lipolysis. The molecular mechanism of this assumption is discussed on the basis of in vitro studies.
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PMID:Lack of adaptation of pancreatic colipase in rats and mice. 84 20

Cardiovascular risk factors were determined among two similar groups of telephone executives in Tokyo, Japan and New York City, USA. Both historical and electrocardiographic evidence pointed to a marked excess of coronary heart disease among American executives compared with their Japanese counterparts. In keeping with this finding, the Americans ate diets higher in animal fat, were fatter, and had higher serum cholesterol values but lower triglyceride levels. Mean blood pressures were slightly higher among the Japanese, and showed a greater increase with age. Urinary sodium/creatinine ratios were much higher among the Japanese, suggesting a higher salt intake. Cigarette smoking was more common among the Japanese. A review of other comparative studies between Japanese and Americans indicated that the only risk factors uniformly consistent with the frequency of coronary heart disease in the two countries were dietary fat, obesity, and serum cholesterol.
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PMID:Cardiovascular risk factors among Japanese and American telephone executives. 89 71

Using the glycine-l-14C-cholic acid (14C-GCA) test, bile salt deconjugation and excretion were studied in 26 subjects with morbid exogenous obesity before and at selected intervals after jejuno-ileal bypass. In the preoperative group there was no malabsorption or intestinal bacterial deconjugation of the bile salts. In the immediate postoperative period (with relative sterilization of the bowel) there was only a trace of 14C in the breath, but the fecal 14C was highly elevated, indicating severe malabsorption without bacterial activity. In the 8 to 10 day postoperative period both the breath and fecal 14C content were highly elevated, indicating malabsorption and normal bacterial activity. Five to 8 months postoperatively both the breath and fecal 14C content showed only moderate elevation, indicating adaptation. It is suggested that the 14C-GCA test is useful in evaluating the adequacy of small bowel bypass procedures and also in following the adaptive response after the bypass. A significant increase in the breath and fecal 14C soon after surgery followed by rapid decrease suggests an adequate bypass and unusually fast adaptation. If the increase in the breath and fecal 14C soon after the bypass is only moderate, then that suggests an inadequate bypass.
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PMID:Studies on bile salt deconjugation following small bowel bypass procedures. 113 Aug 57

Of 93 patients with small bowel bypass for massive exogenous obesity, three developed calcium oxalate urinary calculi, four stones in their gallbladder, and one developed both gallstones and urinary calculi during a mean follow-up period of 17.6 plus or minus 9.0 months. The urinary oxalate excretion increased from 21.6 to 67.8 mg/24 hours (P smaller than .001); simultaneously, the urinary output decreased from 1,775 to 1,101 ml/24 hours (P smaller than .001). Postoperatively, there was a significant increase in the rate of bile salt synthesis from 1.6 to 4.9 gm/day (P smaller than .02) and in the bile sale glycine/taurine ratio from 4.6 to 6.8 (P smaller than .05). It is suggested that the postbypass increase in the biliary glycine/taurine ratio, with its consequent decrease in the zeta potential of the micelles in bile, is at least partly responsible for the increased incidence of cholelithlasis. The pathogenic basis for the increased incidence of urinary calculi is hyperoxaluria, which is probably related to an increased bile salt and glycine synthesis.
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PMID:Biliary and urinary calculi: pathogenesis following small bowel bypass for obesity. 115 48

Certain aspects of the pathogenesis of the diarrhea after bypass procedures of the small intestine for obesity have been evaluated. In the late postoperative period, a significant increase occurred in fecal weight and in fecal bile salt and free fatty acid output. There was a significant direct correlation between fecal weight and fecal bile salt output. There was no significant correlation between fecal weight and fecal fatty acid output. This suggests that, after bypass procedures of the small intestine, bile salts play a more significant role in the pathogenesis of diarrhea than do free fatty acids.
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PMID:The pathogenesis of diarrhea after bypass of the small intestine. 126 8

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
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PMID:Hypertension and insulin resistance. 128 47

High blood pressure of unknown etiology has been related to many pathogenetic factors, mainly dietary salt intake, mental stress, alcohol consumption, sedentary living and aging. Hypertension is more common in condition such as obesity and diabetes mellitus. Sustained elevation of arterial pressure is mediated by vasoconstriction in response to catecholamine release and activation of the renin-angiotensin-aldosterone system. In obese and diabetic subjects, insulin resistance and hyperinsulinemia have been found to be related to development of hypertension. The hypertension phenotype may correspond to many different genotypes codifying various alterations of hormone and receptor function, as well as inherited diseases linked to hypertension. An outstanding epidemiologic example of how hypertension may appear in a community is found in Easter Island. Hypertension among native adults increased from 3 to 30% in a 10 year period, in relation to influx of tourism and changes in salt intake and diet.
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PMID:[Etiopathogenic factors of arterial hypertension]. 134

We have investigated the cellular basis for the clinical and epidemiologic linkage of hypertension, left ventricular hypertrophy (LVH), obesity, and non-insulin-dependent diabetes mellitus (NIDDM) and have studied cytosolic free calcium and free magnesium levels in these syndromes. Specifically, intracellular free calcium is elevated and free magnesium is deficient in hypertension, and both are related (directly and inversely, respectively) to the ambient level of blood pressure, to LV mass index (and thus to the degree of cardiac hypertrophy), and to the hyperinsulinemia and insulin resistance of essential hypertension. Dynamically, the ability of dietary salt loading to elevate blood pressure corresponds to its ability to elevate cytosolic free calcium and reciprocally to suppress free magnesium levels. Conversely, the ability of calcium channel blockade to reverse salt-induced hypertension is related to its ability to prevent these transmembrane ionic effects. Higher steady-state free calcium or lower free magnesium, or both, are also observed in clinical states linked to hypertension, such as obesity and NIDDM. Oral glucose loading in normal subjects itself elevates free calcium and suppresses free magnesium levels, as does hyperglycemia in vitro. These data suggest an ionic hypothesis of cardiovascular and metabolic disease, in which a generalized defect in cell ion handling is present in all tissues, resulting in higher steady-state free calcium and lower free magnesium levels. In pancreatic beta cells, this would produce hyperinsulinemia; in fat and skeletal muscle, cause peripheral insulin resistance; and in renal tissue, increase proximal sodium resorption and increase urinary calcium excretion--all features of essential hypertension. In vascular smooth muscle, high cytosolic free calcium would increase smooth muscle tone and cause vasoconstriction, and in heart muscle, independent of blood pressure, would increase contractility and predispose to LVH. Therefore, what may appear clinically to be the separate syndromes of hypertension, obesity, and NIDDM may pathophysiologically be different manifestations of the same underlying cellular defect, thus explaining their frequent clinical coexistence. Therapeutically, reversal of this excess free calcium accumulation and/or free magnesium deficit with ion-specific agents, such as calcium channel blocking drugs, may thus ameliorate not only the elevated blood pressure of hypertension but also the concurrent excess morbidity and mortality of the concurrent cardiac, vascular, and metabolic aspects of the hypertensive state.
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PMID:Cellular calcium and magnesium metabolism in the pathophysiology and treatment of hypertension and related metabolic disorders. 138 62

Biliary calcium is believed to be of great importance in gallstone pathogenesis. These studies were therefore performed to determine if quantitative and/or qualitative differences in calcium are present in gallbladder bile from patients with and without gallstones. Bile was obtained by direct gallbladder aspiration from 68 obese patients undergoing elective gastric bypass surgery. Forty-five patients had no evidence of gallstones or sludge, 18 had cholesterol gallstones, and five had black pigment stones. Gallbladder bile was also obtained from 27 nonobese patients undergoing elective cholecystectomy (19 cholesterol; eight black pigment gallstones). For all patients, total calcium ranged from 1.50 to 16.44 mmol/L (mean: 6.05 +/- 0.31 mmol/L); free Ca++ ion ranged from 0.53 to 2.83 mmol/L (mean: 1.28 +/- 0.05 mmol/L). Considerable overlap was observed between obese and nonobese subjects and between patients with and without gallstones. For all patient groups, calcium, Ca++, and bound calcium increased linearly with increasing concentrations of bile salt. No significant differences in the slopes of these relationships were observed with obesity or gallstones. In contrast, free Ca++ ion was greater in gallbladder bile from gallstone patient groups throughout the entire range of bile salt. We hypothesize that this observed increase in Ca++ resulted from increased Gibbs-Donnan forces and excess gallbladder mucin present within the gallbladder bile of patients with gallstones.
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PMID:Calcium in human gallbladder bile. 145


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