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

The effect of chronic stress on tissue-type plasminogen activator (TPA) and plasminogen activator inhibitor-1 (PAI-1) antigens was studied in 69 healthy middle-aged men. Chronic stress, defined as feelings of fatigue, lack of energy, increased irritability, and demoralization, was positively associated with plasma concentrations of PAI-1 antigen but was unrelated to TPA. The association remained unaltered after controlling for age, smoking, alcohol consumption, and physical activity but became nonsignificant after further controlling for abdominal obesity, BMI, and serum insulin and triglyceride levels. This attenuated association implies that the relationship between vital exhaustion and PAI-1 may be secondary to the effects of the metabolic variables. Thus, the present study shows that long-term stress affects the fibrinolytic system and suggests that obesity and insulin and triglyceride concentrations, which are closely correlated with the fibrinolytic parameters, may mediate the association. These findings are consistent with the hypothesis that chronic stress causes increased synthesis of PAI-1, thus promoting the risk for atherothrombotic disease by decreasing the likelihood of spontaneous fibrinolysis and increasing the likelihood of fibrin deposition.
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PMID:Association of chronic stress with plasminogen activator inhibitor-1 in healthy middle-aged men. 863 Jun 60

The high incidence of breast cancer in Western women has been linked to nutritional factors such as high-fat/low-fibre diet, obesity and timing of weight gain. A mechanism is postulated through which the Western diet could act in conjunction with inadequate exercise and excessive weight gain at the time of a major change in hormonal balance. All these factors favour the manifestation of insulin resistance, and the concomitants of hyperinsulinaemia might then synergise with oestrogen in promoting the development of breast cancer. The mechanism is compatible with the 'breast tissue age' model of mammary carcinogenesis. The concomitants of hyperinsulinaemia could also influence the growth of established disease subsequent to its promotion, and it is suggested that the hypothesis be tested by an adjuvant randomised trial of a high-fibre/low-fat diet in patients following primary surgery for early breast cancer. It has been suggested that the development of insulin resistance may link the Western lifestyle not only to an increased risk of hypertension and arteriosclerosis, but also to increased breast cancer risk. Large abdominal fat deposits in women are frequently a marker of the presence of insulin resistance and are generally associated with an increased level of bio-available oestrogen. There is evidence that predominantly abdominal distribution of fat in women may be a marker of increased breast cancer risk from puberty onwards. Abdominal obesity may however be hidden, and it is more reliably demonstrated by imaging techniques such as CAT or MRI scans, than by anthropometric measurements such as increased waist-to-hip ratio.
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PMID:Obesity and breast cancer. 869 16

The prevalence of diabetes mellitus and impaired glucose tolerance (IGT) and their relationship to age and obesity was estimated in the rural town of Shikarpur in Sindh Province, Pakistan by a population-based survey in 1994. Oral glucose tolerance tests were performed in a stratified random sample of 967 adults (387 men, 580 women) aged 25 years and above. The diagnoses of diabetes and IGT were made on the basis of WHO criteria. The response rate was 71% for men and 80% for women. The prevalence of diabetes was 16.2% (9.0% known, 7.2% newly diagnosed) in men, and 11.7% (6.3% known, 5.3% newly diagnosed) in women. The prevalence rose with age to a peak of 30% and 21% in 65-74 year-old men and women respectively. IGT was detected in 8.2% of men and 14.3% of women. Thus, total glucose intolerance (diabetes and IGT combined) was present in 25% of subjects examined. These results indicate that glucose intolerance in South Asians can no longer be regarded as a problem confined to migrant communities. Of the 72 subjects previously known to have diabetes, none was using insulin treatment, but 57 (79%) took oral hypoglycaemic agents. Central obesity and positive family history were strongly associated with diabetes, as was prevalence of hypertension. The association with central obesity was greater for women than for men, and suggests important, modifiable risk factor(s) related to lifestyle.
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PMID:Pakistan national diabetes survey: prevalence of glucose intolerance and associated factors in Shikarpur, Sindh Province. 875 Feb 23

Excessive deposition of visceral adipose tissue is known to predispose to cardiovascular diseases. Considerable epidemiological and experimental evidence suggests that many physiological factors are involved in the aetiology of premature atherosclerosis associated with visceral obesity. Insulin resistance is frequently associated with abdominal obesity, and probably plays an important role in the pathophysiology of hypertriglyceridaemia, low levels of plasma high-density lipoprotein (HDL)-cholesterol, hypertension and reduced fibrinolytic activity. Exercise training may counteract the aberrant metabolic profile associated with abdominal obesity both directly and as a consequence of body fat loss. Exercise may increase insulin sensitivity, favourably alter the plasma lipoprotein profile and improve fibrinolytic activity. Changes in the activity of insulin-sensitive glucose transporters and of skeletal muscle lipoprotein lipase are some of the possible explanations for the increased insulin sensitivity and improved blood lipid profile associated with regular exercise. This review presents physical training as a relevant nonpharmacological tool in the treatment of abdominal obesity and associated metabolic disorders. The impact of regular exercise on the different aspects of the insulin resistance syndrome is discussed. The roles of gender, age and the state of insulin resistance on the metabolic effect of physical training are also considered.
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PMID:Effects of exercise training on abdominal obesity and related metabolic complications. 877 9

Certain differences in regional fat distribution might be explicable by subtle hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis. We examined prospectively PA function relative to abdominal obesity defined by waist-to-hip circumference ratio (WHR) in 71 normotensive men aged 30-55 years. Basal PA activity was assessed by measurements of serum cortisol and plasma corticotropin (ACTH) concentrations during the oral glucose tolerance test (OGTT). Functional activity was examined by dexamethasone suppression and ACTH stimulation tests; responses of 17-hydroxyprogesterone (17-OHP), 11-deoxycortisol (S), cortisol, dehydroepiandrosterone (DHEA), and androstenedione were determined. When the subjects were divided into tertiles for the WHR, the ratio of mean ACTH to mean cortisol during the OGTT was increased (p < 0.05), and the ratio of urinary cortisol to body-mass index was decreased (p < 0.01), whilst the net increments of cortisol (p < 0.05) and 17-OHP (p < 0.05) from 0 to 60 min, as well as the ratio of 17-OHP to S increments (p < 0.05) after ACTH were elevated in the highest vs lowest WHR tertile. The ratio of mean ACTH to mean cortisol (r = 0.495; p < 0.001) during the OGTT, the ratio of net 17-OHP to S increments (r = 0.404; p < 0.001), and the net DHEA (r = 0.276; p = 0.020) and 17-OHP (r = 0.336; p = 0.005) responses to ACTH at 60 min correlated with WHR. In multivariate analyses the ratio of mean ACTH to cortisol, cortisol response to ACTH, and the ratio of net 17-OHP to S increments were all significant predictors of WHR independent of smoking, physical activity, and BMI explaining 49.0% of the variance in WHR. Thus, abdominal obesity may be associated with decreased activity of adrenal 21-hydroxylase. Either obesity-related functional alteration of 21-hydroxylase activity or the high carrier prevalence of genetic defects of this enzyme may explain these findings.
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PMID:Pituitary-adrenocortical function in abdominal obesity of males: evidence for decreased 21-hydroxylase activity. 880 94

Increased abdominal obesity has been related to lower insulin sensitivity (SI), independent of overall obesity, but it has been suggested that this relationship may be weaker in non-whites. In the Insulin Resistance and Atherosclerosis Study (IRAS), SI was estimated using a minimal model analysis of the frequently sampled intravenous glucose tolerance test in 1,625 men and women aged 40-69 years. Subjects included African-Americans, Hispanics, and non-Hispanic whites from Oakland and Los Angeles, CA, San Antonio, TX, and the San Luis Valley, CO. Minimum waist circumference was significantly (P = 0.0001) associated with SI after adjusting for age, sex, height, BMI, glucose tolerance status, ethnicity, and clinic. This relationship was significantly (P = 0.0001) stronger in subjects with normal glucose tolerance (NGT) (beta = -0.030, P = 0.0001) than in those with impaired glucose tolerance (IGT) (beta = -0.010, P = 0.02; NIDDM: beta = -0.013, P = 0.0001). There were no significant ethnic differences in effect size across the spectrum of glucose tolerance. Waist circumference was also positively related to fasting insulin, an indirect measure of insulin sensitivity, in NGT (P = 0.0001), IGT (P = 0.0003), and NIDDM (P = 0.0002). The waist-fasting insulin relationship was significantly weaker in African-Americans, relative to non-Hispanic whites, in NGT and IGT (tests of statistical interaction: P = 0.04 and P = 0.02, respectively). In general, these patterns were similar in models specifying waist-to-hip ratio (WHR), rather than waist circumference, as the independent variable. While some ethnic variability exists, a negative relationship between abdominal obesity and insulin sensitivity was confirmed for all three ethnic groups across the spectrum of glucose tolerance.
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PMID:Insulin sensitivity and abdominal obesity in African-American, Hispanic, and non-Hispanic white men and women. The Insulin Resistance and Atherosclerosis Study. 886 60

Obesity is a heterogeneous condition and not every obese patient is at increased risk of cardiovascular diseases (CVD). It is now well established that the regional distribution of body fat is a critical correlate of the metabolic complications of obesity. Studies that have assessed adipose tissue distribution by imaging techniques such as computed tomography have demonstrated the importance of the intra-abdominal (visceral) fat depot as a marker of a cluster of metabolic abnormalities which include glucose intolerance, insulin resistance, hyper-insulinemia, hypertriglyceridemia, elevated number of apo B-carrying lipoproteins as well as hypoalphalipoproteinemia. Although the association between visceral obesity and metabolic complications can hardly be questioned, it has been suggested that it may not necessarily represent a causal relationship. For instance, concomitant alterations in sex steroid levels have been found in both men and women with abdominal (visceral) obesity which have also been reported to be significantly correlated with the insulin resistant-dyslipidemic state found in abdominal obese subjects. In women, abdominal obesity is associated with increased free testosterone concentrations and reduced sex hormone binding globulin (SHBG) levels, whereas in men this condition is associated with reduced testosterone and adrenal C12 steroid (dehydroepiandrosterone, androstenedione, androstene-3 beta, 17 beta-diol) levels as well as decreased SHBG concentrations. These altered steroid and SHBG; levels have been reported to be independent correlates of the metabolic complications of visceral obesity although they cannot solely account for the increased CVD risk found in these patients. In this regard, intervention studies are clearly warranted to better quantity the respective contribution of excess visceral adipose tissue and of the concomitant alterations in sex steroid levels as modulators of metabolic disturbances increasing CVD risk in obesity.
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PMID:Obesity and metabolic complications: contribution of dehydroepiandrosterone and other steroid hormones. 894 99

Obesity, hypertension and hyperinsulinism are frequently related and constitute morbid elements of human athero-thrombogenic syndrom. To elucidate physiopathologic mechanisms linking these symptoms, we have developped an experimental model reproducing the morbid triptyque: obesity-hypertension-insulin resistance were induced by hyperlipidic hypercaloric diet. The aim of this study was to investigate cardiovascular modifications elicited by high fat diet. Four male Beagle-Harrier dogs were used in this preliminary study. We investigated before and 7 weeks after the beginning of the hypercaloric hyperlipidic diet morphologic measures, systemic blood pressure (BP) and heart rate (HR), pulmonary blood pressure, cardiac output (CO), systolic ejection volume (SEV), peripheral arterial resistance (PAR) and HR variability on 24 hours' electrocardiogram obtained by Holter method. Echocardiographic modifications of left ventricule was also studied after 20 weeks. Body weight increased (+15.4%) after 7 weeks and remained stable the whole experimental period. This gain was associated with an increase of thoracic and abdominal circonferences (respectively +5.9% and 14.3% at the 7th week). The abdominal increase was significantly more elevated than the thoracic one. This abdominal obesity was associated with an increase in diastolic (+17.9%) and mean (+16.4%) (but not systolic) BP. High fat diet failed to modify arterial pulmonary blood pressures but induced an increase in both CO (3.0 +/- 5.2 vs 4.3 +/- 0.4 ml/min) and SEV (32.4 +/- 5.2 vs 40.8 +/- 2.7 ml/beat). PAR decreased (43.1 +/- 5.9 vs 33.0 +/- 3.2 UW; p = 0.08). Holter method showed a non significant increase of HR (82.0 +/- 7.8 vs 99.5 +/- 5.6 beat/min; p = 0.1) explained by a significant decrease of parasympathetic HR variability (PNN50: 53.5 +/- 4.1 vs 40.9 +/- 4.1%). No echocardiographic modification of left ventricule was found after 20 weeks of high fat diet. This preliminary study shows that, like in humans, high fat diet in dogs induced abdominal obesity with systemic hypertension but failed to provoke left cardiovascular hypertrophy after 20 weeks. This model will allow to characterize the links between cardiovascular and endocrinometabolic alterations occurring during the development of obesity and hypertension.
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PMID:[Experimental hypertension induced by hypercaloric diet]. 894 71

Evidence for an association between general obesity and risk of stroke is weak. However, abdominal obesity may be more closely related to stroke risk. The association of body mass index and abdominal obesity (waist/hip ratio) with stroke incidence was examined in 28,643 US male health professionals, aged 40-75 years in 1986, who had no history of cardiovascular disease or stroke. In 5 years of follow-up, there were 118 cases of stroke, of which 80 were ischemic. Compared with men in the lowest quintile of body mass index, men in the highest quintile had an age-adjusted relative risk of stroke of 1.29 (95% confidence interval 0.73-2.27). In contrast, the age-adjusted relative risk for extreme quintiles of waist/hip ratio was 2.33 (95% confidence interval 1.25-4.37). This relative risk was not substantially altered in a multivariate model including body mass index, height, and other potential risk factors. There was a weaker relation with waist circumference alone, with men in the highest quintile (> 40.2 inches) having a relative risk of 1.52 (95% confidence interval 0.82-2.82) compared with men in the lowest quintile (< or = 34.5 inches) (1 inch = 2.54 cm). The results suggest that abdominal obesity, but not elevated body mass index, predicts risk of stroke in men.
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PMID:Body size and fat distribution as predictors of stroke among US men. 895 26

The striking geographic differences in colorectal cancer incidence and the changes in disease risk among immigrants suggest an important environmental component to colorectal cancer risk. Table 1 lists risk factors for colorectal cancer. The categories in the table are somewhat arbitrary but are designed to provide an overall semiquantitative summary of the current epidemiologic literature. Certain of the most important risk factors (e.g., age, family history) cannot be modified. Individuals at high risk might benefit from surveillance. Dietary factors appear to be among the most important determinants of colorectal cancer risk. Diet helps to explain geographic variation in disease. A diet that is high in red meat and saturated fat appears to increase risk. Vegetables, fruits, fiber, folate, and calcium may be protective. Obesity, particularly abdominal obesity, and tall stature may be risk factors. Physical activity has been repeatedly shown to reduce the risk of colorectal cancer. Postmenopausal hormone replacement therapy may also be protective. Exciting new data suggest a significantly lower risk of colorectal cancer in regular users of aspirin and NSAIDs. It is important to recognize that the use of these drugs can have adverse as well as beneficial effects, and the appropriate dose and timing are not known. Enough information is available to make recommendations to lower the risk of colorectal cancer. Reducing red meat and fat consumption; increasing fruits, vegetables, and grains; avoiding obesity; and adopting a regular program of physical activity reduce the risk of colorectal cancer. Fortunately, these modifications also decrease the risk of cardiovascular disease, an even more important cause of mortality in Western societies.
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PMID:Epidemiology and risk factors for colorectal cancer. 896 Aug 89


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