Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Creatinine-adjusted levels of estrone, estradiol and estriol were determined in overnight urine specimens from 88 postmenopausal women from Athens, Greece, and were correlated with daily nutrient intakes estimated through a semiquantitative food frequency questionnaire. Although obesity was positively and significantly related to all three urinary estrogens and their total, none of the investigated macro- or micronutrients was significantly or suggestively associated to any of these urinary estrogens, after controlling for energy intake, reproductive and biosocial variables. These results suggest that quantitative rather than qualitative aspects of nutrition affect the levels of postmenopausal estrogens, although endogenous factors could also be responsible for the association of these estrogens with obesity. Alcohol intake was also positively associated with urinary estrogens (mainly estrone and estradiol), after controlling for energy intake, obesity and the other indicated variables.
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PMID:Diet and urine estrogens among postmenopausal women. 174 88

The nutritional status of 93 noninstitutionalized elderly of the city of Perugia, mostly of them examined longitudinally, was assessed at the eleventh year follow-up. Diet is still rather rich and unbalanced. Alcohol intake in men is very high. Biological dietary errors have an impact on the nutritional status, particularly for folates, of the individual. But in this regard it is interesting to note that in some cases vitamin and mineral nutriture has improved at this follow-up. In addition the distribution of malnutrition is rather different from that of the previous follow-up. As on previous occasions, no correlation was observed between vitamin intake and corresponding nutritional status (with the exception of riboflavin). Obesity is rather common among women; men present a higher muscular area and hand muscular strength. The clinical evaluation of nutritional status evidences principally changes which are mostly ascribable to old age. Among the pathologies, chronic ischemic heart disease, hypertension, chronic respiratory diseases, osteoarthrosis and diabetes occur most frequently.
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PMID:Nutritional status of the elderly V). Dietary and biochemical data and anthropometry of noninstitutionalized elderly in Perugia at the eleventh year follow-up. 180 40

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome. Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug-induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice-like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease. The clinical syndrome of alcoholic liver disease is the result of three factors--parenchymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension. Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol- or acetaldehyde-altered proteins, and questionably enhanced by viral hepatitis. Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug-induced injuries, jejunoileal bypass, and related "shortcircuiting" of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminophen is the prime example.
Alcohol Clin Exp Res 1991 Feb
PMID:Alcoholic liver disease: pathologic, pathogenetic and clinical aspects. 205 45

Alcohol-like liver disease may be observed in patients with obesity or non insulin-dependent diabetes, or after treatment with such antianginal drugs as amiodarone and perhexiline maleate. In such cases cirrhosis is associated, at histology, with foci of acidophilic necroris, Mallory's bodies and inflammatory neutrophilic infiltrates. Alcohol-like liver disease is rare. It affects mostly women in their fifties and usually is clinically latent. Abnormalities of liver function tests mainly consist of increased serum aminotransferase levels. Complications of portal hypertension are uncommon. The pathogenesis of the disease remains purely hypothetical. In practice, in the absence of antianginal therapy the finding of cirrhosis in an obese and/or diabetic patient should prompt a search for excessive alcohol consumption before ascribing the cirrhosis to obesity and/or diabetes.
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PMID:[Pseudo-alcoholic cirrhosis]. 206 19

Index Medicus was searched to compare the number of articles on treatment trials for alcohol and for non-alcohol drug use disorders (abuse, dependence, withdrawal, intoxication, etc.) to that of two control conditions--anxiety and obesity--for the period 1967-1988. Over the entire 22 years, the number of articles for alcohol use disorders increased an average of 2.7 articles every 2 years and 5.8/2 years for drug use disorders compared to 5.7/2 years for obesity and 5.8/2 years for anxiety disorders. Over the most recent 8 years, articles for alcohol use disorders increased 7.7/2 years and for drug use disorders 7.9/2 years compared to--2.9/2 years and 12.0/2 years for obesity and anxiety disorders. The proportion of articles that cited using only pharmacotherapy decreased over time; however, studies of alcohol and drug withdrawal continue to almost exclusively use pharmacological therapies. We conclude that treatment research in alcohol and drug use disorders is growing as rapidly as that in similar psychological and psychiatric conditions and that such growth is not due to a focus on pharmacological treatments.
Drug Alcohol Depend 1990 Aug
PMID:The growth of treatment research in alcohol and drug use disorders: a computerized literature search. 220 18

In 1214 adult persons, the relationship between alcohol consumption, the "liver enzymes" and other metabolic parameters, including the serum lipids, were investigated. In 798 of the persons, glucose tolerance tests with measurement of plasma insulin were performed (young and old male and female adults, either volunteers or patients without liver-related diseases). There was a high correlation of the three transferases GOT, GPT and GGT not only with the reported alcohol consumption but also with the plasma insulin. Most of the insulin increase, however, occurred in that range of the three transferases which, so far, has erroneously been considered to be the normal one. The C-peptide showed the same behaviour. Plasma insulin was also raised in relation to overweight, but only in persons with the sum of the three transferases over 30 U/l, not in persons who did not drink alcohol and who had really normal transferases (sum of the three transferases below 30 U/l measured at 25 degrees C). The quotient of plasma insulin divided by the relative body weight (Broca Index) was constantly low in the range of really normal transferases (up to 30 U/l), thereafter rising significantly, but only in the range of the transferases so far erroneously considered to be the normal one (GOT to 17, GPT to 22, GGT to 28 U/l, thus sum up to 67). Serum glucose in the tolerance test also rose with the transferases but much less than the plasma insulin. The correlation between both GGT and the sum of the three transferases with the plasma insulin was significantly positive and independent of the relative body weight. It is concluded that overweight (which is generally believed to be the main risk factor for non-insulin-dependent diabetes), and insulin resistance (which leads to hyperinsulinaemia), are largely caused by the toxic effects of "normal" daily alcohol, more in the human male than in the female. Hyperinsulinaemia (which blocks lipolysis) is caused by a toxic effect of ethanol and its metabolites, independent of caloric input and overweight. Hyperinsulinaemia is at least in the human male at present, probably the most important cause of obesity. In obesity, caused by "normal" alcohol consumption, a vicious circle occurs: the enhancement of the triglycerides and, consequently, the free fatty acids leads to a further decrease of glucose utilization by the muscle. A continuously high glucose level has toxic effects: eventually the beta cells of the pancreas are exhausted.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The main cause of diabetes (type II): "normal" alcohol drinking]. 227 72

The nighttime blood oxygen saturation of 35 abstaining chronic alcoholic men was studied. Regression analyses indicated that various measures of alcohol abuse history (r = -.61, p less than .001) account for significant variance in nighttime hypoxemia. Age (r = -.39, p less than .05) and smoking history (r = .45, p less than .01) were less powerful predictors and both obesity and days abstinent from alcohol failed to correlate with hypoxemia. Possible mechanisms to explain the relationship between alcohol abuse history and hypoxemia are discussed. This and previously reported findings indicate that chronic alcohol abuse may predispose an individual to nighttime hypoxemia and be a risk factor for sleep apnea.
J Stud Alcohol 1990 Jan
PMID:Relationship of alcohol abuse history to nighttime hypoxemia in abstaining chronic alcoholic men. 229 46

Low rates of gallbladder disease among blacks have been reported but not systematically studied. The authors investigated the rate of hospitalization with a diagnosis of gallbladder disease in the follow-up in 1982-1984 of the first National Health and Nutrition Examination Survey, a population-based study conducted across the United States in 1971-1975. Based on hospital discharge diagnoses of gallbladder disease, 368 cases were identified for the period 1971-1984 among 10,551 persons, aged 25-74 years, who denied gallbladder disease at the baseline examination. The crude incidence of gallbladder disease per 1,000 person-years was 2.59 for white men, 1.45 for black men, 4.09 for white women, and 2.35 for black women. Controlling for obesity, parity, ethanol consumption, use of diuretics, use of oral contraceptives, and two indicators of socioeconomic status, the authors found that the hazard rate of hospitalization with gallbladder disease increased with age for white women and decreased for black women. The hazard ratio for black women compared with white women at 30 years of age was 0.71 with a 95% confidence interval of 0.52-0.96, but at age 70, it was 0.18 with a 95% confidence interval of 0.09-0.37. For women, obesity and parity were important risk factors for gallbladder disease (p less than or equal to 0.001), and the use of diuretics was marginally associated (p = 0.08). Black men compared with white men had a hazard rate of gallbladder disease of 0.53 with a 95% confidence interval of 0.24-1.16. For men, increasing age was related to gallbladder disease (p less than 0.001), and obesity was weakly related (p = 0.06). The black/white hazard ratios decreased further when controlling for socioeconomic status, persisted if the study population was limited to those hospitalized during follow-up, and increased slightly for cases with an acute complication of gallbladder disease. Thus, differential access to medical care may not explain the lower rate among blacks.
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PMID:Low incidence of hospitalization with gallbladder disease among blacks in the United States. 232 26

The relationships of alcohol intake and corpulence to HDL-cholesterol were studied in 653 women taking medical advice about body weight. The body mass index (BMI) was positively correlated with triglyceride and negatively with HDL-cholesterol. The relation between BMI and HDL-cholesterol was discontinuous. Total cholesterol, triglycerides and diastolic blood pressure were increased for alcohol intakes greater than 10 g/d regardless of body weight. Alcohol intake was associated with higher concentrations of HDL-cholesterol (P = 0.006) in non obese (BMI = 25.2 +/- 1.5 kg/m2) subjects, but not in mildly (27.3 less than or equal to BMI less than 32.3) or massively (BMI greater than or equal to 32.3) obese subjects. The fact that HDL concentrations were not associated with alcohol intake in obese patients suggests that (1) alcohol acts on the HDL pool through one of the pathways which are perturbed in obesity, possibly lipolysis, (2) obesity is one of the reasons for the differences in individual responses of HDL-cholesterol to alcohol, (3) myocardial infarction might not be inversely correlated with alcohol intake in the obese as it is in the non-obese population.
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PMID:Lack of association between dietary alcohol and HDL-cholesterol concentrations in obese women. 232 22

The concentrations and contents of immunoreactive substance P (SP), neurokinin A (NKA), vasoactive intestinal polypeptide (VIP) and gastrin releasing peptide (GRP) were measured in acid-ethanol extracts of intestine (duodenum-jejunum-ileum) and pancreas of C57BL/KsJ diabetes-obese (db/db) mice, Aston obese-hyperglycaemic (ob/ob) mice, and their respective lean controls. The intestinal concentration of GRP and pancreatic concentrations of VIP and GRP were 36-57% lower in lean Aston mice than lean C57BL/KsJ mice, indicating the influence of genetic background in control mice. Intestinal concentrations of SP and NKA were reduced by 19-33% in the db/db and ob/ob mutants compared with their lean controls, but the intestinal contents of these peptides were normal or greater than normal due to intestinal hypertrophy of the mutant mice. The intestinal VIP concentration was not altered, but the content was increased by 87% and 25% respectively in db/db and ob/ob mice, whereas the intestinal GRP concentration was reduced by 51% in ob/ob mice. Pancreatic concentrations and contents of NKA, VIP and GRP were similar in lean and db/db C57BL/KsJ mice. However, pancreatic concentrations and contents of VIP and GRP were reduced by 51-55% in ob/ob mice compared with their lean controls. The sensitivity of the present assay did not permit accurate determination of the low pancreatic concentrations of SP. The results suggest that the spontaneous ob/ob and db/db syndromes of obesity and diabetes in mice are associated with reduced intestinal concentrations of SP and NKA. The ob/ob mouse also exhibited reductions of intestinal GRP and pancreatic GRP and VIP concentrations. These changes in regulatory peptides may relate to abnormalities of intestinal and possibly pancreatic function in obese and diabetic mutant mice.
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PMID:Substance P, neurokinin A, vasoactive intestinal polypeptide and gastrin releasing peptide in the intestine and pancreas of spontaneously obese-diabetic mice. 243 55


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