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

Abdominal obesity has emerged as a strong and independent predictor for non-insulin dependent diabetes mellitus (NIDDM). Adiposity located centrally in the abdominal region, and particularly visceral as opposed to subcutaneous fat, is also distinctly associated with hyperlipidemia, compared with generalized distributions of body fat. These lipoprotein abnormalities are characterized by elevated very low density lipoprotein (VLDL) and low density lipoprotein (LDL) levels, small dense LDL with elevated apolipoprotein B levels, and decreased high density lipoprotein2b (HDL2b) levels. This is the same pattern seen in both familial combined hyperlipidemia and NIDDM. The pronounced hyperinsulinemia of upper-body obesity supports the overproduction of VLDL and the increased LDL turnover. We have proposed that an increase in the size of the visceral fat depot is a precursor to the increased lipolysis and elevated free fatty acid (FFA) flux and metabolism and to subsequent overexposure of hepatic and extrahepatic tissues to FFA, which then, in part, promotes aberrations in insulin actions and dynamics. The resultant changes in glucose/insulin homeostasis, lipoprotein metabolism, and vascular events then lead to metabolic morbidities such as glucose intolerance, NIDDM, dyslipidemia, and increased risk for coronary heart disease.
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PMID:Intra-abdominal fat: is it a major factor in developing diabetes and coronary artery disease? 896 90

The present study was undertaken to determine the prevalence of hyperlipidemia and to find out the possible impact of serum lipid profiles on other cardiovascular risk factors in Yonchon County, Korea. Population-based cross-sectional study by random cluster sampling of registered residents over 30 years of age was performed. Out of the 3804 subjects scheduled for the survey, 2520 underwent the actual examination. The prevalence of hypercholesterolemia (serum cholesterol > or = 240 mg/dl) was only 1.2%, whereas that of hypertriglyceridemia (serum triglyceride > or = 250 mg/dl) was as high as 11.3%. The serum levels of cholesterol, triglyceride and HDL cholesterol correlated with anthropometric indices, body mass indices and waist hip ratios. The prevalences of diabetes and/or hypertension increased as either serum cholesterol or triglyceride level increased. In addition, the prevalence rates of obesity, impaired glucose tolerance, hypertriglyceridemia and hypercholesterolemia in its isolated form (free of the others) were much lower than overall prevalence indicating an existence of major overlap among these cardiovascular atherosclerotic risk factors in the form of multiple combinations. Central obesity was found to be an independent associated factor for the aggregation of the conditions related to the increase in cardiovascular risks. The prevalence of hypercholesterolemia in Yonchon County was substantially lower than that previously suggested, albeit that of hypertriglyceridemia was very high. We could also observe a varying degree of transition in cardiovascular risks related to insulin resistance from the rural to the urban area with rapid emergence of non-communicable diseases as a result of modernization.
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PMID:Community-based epidemiologic study on atherosclerotic cardiovascular risk factors. 901 72

A relationship exists between obesity and non-insulin-dependent diabetes mellitus. Central, abdominal obesity carries a particularly high risk that is most likely associated with enlargement of visceral fat deposits. A multiple endocrine perturbation is associated with visceral obesity. This consists of a hypersensitive hypothalamic-pituitary-adrenal (HPA) axis, with resulting excess of cortisol secretion upon stimulation. Growth hormone levels in both sexes are diminished and testosterone concentrations in men are lower than normal. In women a moderate hyperandrogenism is often present. The elevated sensitivity of the HPA axis may be a primary event, followed by adrenal androgen production in women and by interaction at several levels, with inhibition of both the growth hormone and pituitary-gonadal axes. Together, these endocrine perturbations seem to be able to centralize body fat to visceral depots because of a high density of steroid hormone receptors. The endocrine perturbations are most likely followed by insulin resistance. Elevated cortisol levels, deficiencies in sex-specific steroid hormones and excess androgens result in insulin resistance. The endocrine abnormalities in visceral obesity are followed by insulin resistance, both directly and indirectly via contribution of excess free fatty acids from centralized body fat depots. The hyperactivity of the HPA axis may be due to frequent challenges and it is amplified by a deficient feedback inhibition. A depressive, helplessness reaction to stress may be involved. Such stress factors may be found in socioeconomic and psychosocial handicaps, as suggested by results of population studies. This hypothesis is strongly supported by the reproduction of an identical condition in non-human primates that react with a depressive reaction upon psychosocial types of stressors. The perturbations of the HPA axis may thus be in the centre of the syndrome. Studies of this axis in established non-insulin-dependent diabetes mellitus suggest similar perturbations, but the information is not conclusive.
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PMID:The origins and consequences of obesity. Diabetes. 901 75

Prompted by the recent findings that a tryptophan to arginine (Trp64Arg) mutation in the beta3-adrenergic receptor gene was associated with an earlier onset of non-insulin-dependent diabetes mellitus (NIDDM) in Pima Indians, with abdominal obesity and insulin resistance in Finns, and with an increased capacity to gain weight in French whites, we studied the prevalence of this mutation in 231 diabetic and 95 nondiabetic Japanese subjects and assessed its contribution to the development of obesity and NIDDM. The allelic frequencies of the mutation were 0.18 in diabetic and 0.23 in nondiabetic subjects, showing no significant difference between the two groups (P = .067). In nondiabetic subjects, body mass index (BMI) did not differ between those with and without the mutation (22.2 +/- 3.5 v 21.4 +/- 3.2 kg/m2, P = .252). In NIDDM subjects, BMI at the time of study and maximal BMI before the start of treatment did not differ between those with and without the mutation (22.8 +/- 2.6 v 23.2 +/- 3.7 kg/m2, P = .678, and 24.7 +/- 2.6 v 24.9 +/- 3.1 kg/m2, P = .277). Homozygotes for the mutation did not have trends to have increased BMI in either diabetic or nondiabetic subjects. The age at diagnosis of NIDDM also did not differ between the two groups (48.8 +/- 9.9 v 47.8 +/- 12.5 years, P = .796). Fasting serum cholesterol and triglyceride levels and systolic and diastolic blood pressure before the start of treatment did not differ between NIDDM subjects with and without the mutation. In conclusion, although the Trp64Arg mutation is not uncommon in Japanese, it does not appear to be associated with obesity, NIDDM, age at diagnosis of NIDDM, or dyslipidemia. Our results suggest that the mutation has minor effects, if any, on the development of obesity and NIDDM in Japanese.
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PMID:Prevalence of the Trp64Arg missense mutation of the beta3-adrenergic receptor gene in Japanese subjects. 903 Aug 29

The most central findings in both GH deficiency in adults and the metabolic syndrome are abdominal/visceral obesity and insulin resistance. Abdominal obesity is associated with blunted GH secretion and low serum insulin-like growth factor-I concentrations. GH treatment in GH-deficient adults has demonstrated favorable effects on most of the features of GH deficiency in adults, but it is not known whether GH can improve some of the metabolic aberrations observed in abdominal/visceral obesity. Thirty men, 48-66 yr old, with abdominal/visceral obesity were treated with recombinant human GH (rhGH) in a 9-month randomized, double-blind, placebo-controlled trial. The daily dose of rhGH was 9.5 micrograms/kg. Body fat was assessed from total body potassium, and abdominal sc and visceral adipose tissue was measured using computed tomography. The glucose disposal rate (GDR) was measured during an euglycemic, hyperinsulinemic glucose clamp. In response to the rhGH treatment, total body fat and abdominal sc and visceral adipose tissue decreased by 9.2 +/- 2.4%, 6.1 +/- 3.2%, and 18.1 +/- 7.6%, respectively. After an initial decrease in the GDR at 6 weeks, the GDR increased in the rhGH-treated group as compared with the placebo-treated one (P < 0.05). The mean serum concentrations of total cholesterol (P < 0.01) and triglyceride (P < 0.05) decreased, whereas blood glucose and serum insulin concentrations were unaffected by the rhGH treatment. Furthermore, diastolic blood pressure decreased and systolic blood pressure was unchanged in response to rhGH treatment. This trial has demonstrated that GH can favorably affect some of the multiple perturbations associated with abdominal/visceral obesity. This includes a reduction in abdominal/visceral obesity, an improved insulin sensitivity, and favorable effects on lipoprotein metabolism and diastolic blood pressure.
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PMID:Growth hormone treatment of abdominally obese men reduces abdominal fat mass, improves glucose and lipoprotein metabolism, and reduces diastolic blood pressure. 906 72

Coronary heart disease, hypertension, non-insulin-dependent diabetes and obesity are major causes of ill health in industrial societies. Disturbances of carbohydrate and lipid metabolism are a common feature of these disorders. The bases for these disturbances and their roles in disease pathogenesis are poorly understood. The spontaneously hypertensive rat (SHR), a widely used animal model of essential hypertension, has a global defect in insulin action on glucose metabolism and shows reduced catecholamine action on lipolysis in fat cells. In our study we used cellular defects in carbohydrate and lipid metabolism to dissect the genetics of defective insulin and catecholamine action in the SHR strain. In a genome screen for loci linked to insulin and catecholamine action, we identified two quantitative trait loci (QTLs) for defective insulin action, on chromosome 4 and 12. We found that the major (and perhaps only) genetic determinant of defective control of lipolysis in SHR maps to the same region of chromosome 4. These linkage results were ascertained in at least two independent crosses. As the SHR strain manifests many of the defining features of human metabolic Syndrome X, in which hypertension associates with insulin resistance, dyslipidaemia and abdominal obesity, the identification of genes for defective insulin and catecholamine action in SHR may facilitate gene identification in this syndrome and in related human conditions, such as type-2 diabetes and familial combined hyperlipidaemia.
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PMID:Quantitative trait loci for cellular defects in glucose and fatty acid metabolism in hypertensive rats. 917 35

The purpose of the present study was to delineate a health profile of professional Danish army personnel. Two-hundred twenty officers, noncommissioned officers, and gunners on active duty at Varde Barracks, housing the South Jutland Artillery Regiment and the Danish Army Artillery School, were asked about their physical and psychological health, interpersonal relations, and working conditions as well as their dietary, drinking, and smoking habits. Measurements were made of resting pulse rate, blood pressure, height, weight, waist and hip girth, and pulmonary function. The ratio of waist-to-hip girth and body mass index (BMI) were calculated. Psychological well-being was evaluated using the 12-item version of the General Health Questionnaire (GHQ). Psychosomatic symptoms were frequently reported, but very few of those surveyed appeared to have psychiatric disorders as measured by the GHQ. Also, somatic health problems were frequently reported, the most frequent being lower-back pain, mild chest pain, and sensory disorders. Differences in interpretation and reporting of "lasting health problems" may explain the relatively high score for this question. The interpersonal relations, both upward and downward in the hierarchy rank order, received high scores. Compared with the general population, alcohol consumption was very low, whereas smoking-in particular heavy smoking-was much more frequent among professional Danish army personnel. Lung function testing showed significantly poorer mean values of forced expiratory volume in 1st second of expiration and mean forced expiratory flow 25 to 75% of forced vital capacity among smokers compared with nonsmokers, although the mean values for the whole group of both smokers and nonsmokers were well above reference values for all lung function parameters. The frequency of moderately overweight individuals (25 < BMI < or = 30) was significantly higher among the male army personnel than in the general population, whereas this was not the case for obesity (BMI > 30). Abdominal obesity, regarded as an independent risk factor for the development of ischemic heart disease, stroke, diabetes, hypertension, and all-cause mortality, was present in 5%, and 3% belonged to the highest-risk group by having a low BMI as well as abdominal obesity.
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PMID:Health profile of Danish army personnel. 918 68

Circulating (PAI-1) levels are elevated in patients with coronary heart disease and may play an important role in the development of atherothrombosis. Many clinical studies have indicated that the insulin resistance syndrome, which is a situation predisposing to diabetes and ischemic heart disease, may be a major regulator of PAI-1 expression, especially in determining plasma PAI-1 levels. Central obesity is a characteristic of insulin resistance and is a well recognized risk factor for coronary heart disease. Recently the production of PAI-1 by adipose tissue, in particular by tissue from omentum, has been demonstrated and could be an important contributor to the elevated plasma PAI-1 levels observed in insulin resistant patients. Besides the effect of the metabolic status on plasma PAI-1 levels, the role of a genetic control has been emphasized, but according to recent results obtained in a family segregation study, its participation seems limited. Prospective cohort studies of patients with previous myocardial infarction or angina pectoris have underlined the association between increased plasma PAI-1 levels and the risk of coronary events, but the predictive capacity of PAI-1 disappears after insulin resistance marker adjustments. Taken together these results support the notion that PAI-1 can be a link between obesity, insulin resistance and cardiovascular disease.
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PMID:PAI-1, obesity, insulin resistance and risk of cardiovascular events. 919 34

Obesity is associated with increased cardiovascular morbidity and mortality. Individuals who predominantly store fat abdominally (particularly in the visceral area), more often present with an atherogenic lipid profile and are more frequently characterized by hemostatic, metabolic and anatomical abnormalities compatible with insulin resistance and increased atherothrombotic risk. Weight loss improves many of the cardiovascular risk factors associated with abdominal obesity.
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PMID:Obesity and cardiovascular disease: is body structure a factor? 925 35

Obesity has now developed into a world-wide epidemic and is associated with large economic costs and prevalent diseases, particularly with central body fat distribution. Insulin resistance almost invariably occurs, and might be a major trigger for disease-generating mechanisms either directly or via generation of other disease precursors ("risk factors"). The hypothalamo-pituitary-adrenal (HPA) axis seems to be hypersensitive in abdominal obesity, a statement supported by increased responses to challenges from the adrenals to central regulatory centers. Furthermore, the feedback control by central glucocorticoid receptors, probably a secondary, functional consequence of an elevated HPA axis activity, because the receptor gene appears normal. Secretion of sex steroid and growth hormones is diminished, which might be consequence of elevated HPA axis activity. Hyperandrogenicity in women is probably of adrenal origin and another consequence of the sensitivity of the HPA axis. The endocrine abnormalities thus are periodically elevated cortisol and androgen (women) concentrations, as well as low secretions of gender-specific steroid and growth hormones. Since elevated cortisol, and low sex-steroid and growth hormone secretions, probably direct storage fat to visceral depots, the multiple endocrine abnormalities probably cause enlargement of these depots. Furthermore, these hormonal abnormalities most likely at least contribute to the creation of insulin resistance with additional effects of elevated fatty acids from central fat depots, which are sensitive to lipid mobilization agents. This chain of events indicates the central role of the hypersensitive HPA axis. Known causes of sensitization of this axis have been identified in subjects with abdominal obesity, including depression, anxiety, alcohol, and smoking. A common cause of HPA axis activation is perceived stress, with a depressive, defeatist, or "helplessness" reaction. In subjects with abdominal preponderance of body fat stores a number of psychosocial and socioeconomics handicaps have been identified, hypothetically predisposing to such reactions. In a primate model (monkeys), mild psychosocial stress is followed by identical psychological, endocrine, anthropometric, and metabolic abnormalities as in humans with abdominal preponderance of body fat stores, including early signs of diabetes and cardiovascular disease. These findings strongly support the interpretation that a stress reaction activating the HPA axis is involved also in the human syndrome. Interventions with normalization of the endocrine perturbations are followed by clear improvements of the multiple abnormalities in both clinical, experimental, cellular and molecular studies, suggesting that the pathogenesis of abdominal preponderance of body fat and its endocrine, anthropometric and metabolic abnormalities are indeed consequences of the endocrine abnormalities identified.
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PMID:Body fat distribution, insulin resistance, and metabolic diseases. 929 93


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