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Query: UMLS:C0028754 (obesity)
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The National Heart, Lung, and Blood Institute (NHLBI) Twin Study provided longitudinal data on a cohort of 514 pairs of adult male twin pairs who were examined at approximate ages of 48, 57, and 63 years. Because the sample was selected from military veterans, height and weight data were also available from their induction physical examinations when they were approximately 20 years of age. From the total NHLBI Twin Study cohort, 124 monozygotic and 119 dizygotic male twin pairs had complete data available for both members of the pair at induction and three examinations spanning 43 years of adult life. Using these data, the contributions of genetics and shared and non-shared environmental factors to BMI over the 43 year period were estimated by model fitting procedures. Model fitting included both a factor decomposition of these effects as well as a developmental path model. Results from the decomposition procedure indicate significant genetic effects at each examination cycle. Fitting a developmental path model, two independent genetic contributions to the variability of BMI were found: one at, or prior to, the induction examination about age 20, and a second between ages 20 and 48. Significant non-shared environmental contributions at each examination were also indicated, but shared environmental effects were not significant. We conclude that cumulative genetic effects explain most of the tracking in obesity over time; non-shared environmental effects, although significant at each age, are relatively short-lived and make only a minor contribution to tracking.
Int J Obes Relat Metab Disord 1992 Sep
PMID:Evidence for independent genetic influences on obesity in middle age. 132 90

The association of obesity and fat distribution with glucose tolerance and cardiovascular risk factor levels were investigated in a population-based study in East Finland including 396 non-diabetic men and 673 women aged from 65 to 74 years. Obese men and women (BMI greater than 27 kg/m2) had higher levels (P less than 0.001) of fasting and 2 h plasma glucose and insulin as well as total triglycerides and diastolic blood pressure, and lower levels of HDL cholesterol than normal weight men and women. Central fat distribution (the highest vs. the lowest tertile of waist-hip ratio) was associated independently of obesity with high fasting glucose (5.7 vs. 5.5 mmol/l in non-obese subjects, 5.9 vs. 5.7 mmol/l in obese subjects, P less than 0.05) and insulin levels (13.7 vs. 10.6 mU/l in non-obese subjects, 18.4 vs. 15.6 mU/l in obese subjects, P less than 0.01) and with adverse changes (P less than 0.05) in lipid and lipoprotein levels (triglycerides: 1.59 vs. 1.41 mmol/l in non-obese subjects, 1.92 vs. 1.69 mmol/l in obese subjects; HDL cholesterol: 1.33 vs. 1.43 mmol/l in non-obese subjects, 1.20 vs. 1.32 mmol/l in obese subjects). There were no marked differences in metabolic aberrations related to obesity between men and women. However, the association between waist-hip ratio and risk factors was non-linear in men whereas it was linear in women. In conclusion, obesity per se rather than its distribution was a more significant determinant of glucose and insulin as well as total triglyceride and HDL cholesterol levels in elderly subjects.
Int J Obes Relat Metab Disord 1992 Sep
PMID:Association of obesity and distribution of obesity with glucose tolerance and cardiovascular risk factors in the elderly. 132 93

Of all cancers in the United States, 35% are estimated to be caused by dietary factors and may be preventable. Diets high in fat or calories, for example, are said to be associated with five of the six most common cancers: breast, colorectal, pancreatic, prostatic, and uterine. Conversely, some dietary components such as vitamin A, in fruits and vegetables, and fiber may help protect against certain cancers. Obesity may confer a small risk of breast cancer on a woman, but women with upper body fat localization are at significantly higher risk of developing breast cancer and endometrial cancer.
Prim Care 1992 Sep
PMID:Nutrition and cancer prevention. 132 28

A high plasma insulin concentration in the presence of a normal or high plasma glucose level appears to be a common feature of glucose intolerance, obesity, and hypertension. Hyperinsulinemia has been recognized as a major risk factor for the development of coronary artery disease independent of blood pressure and plasma lipid levels. All these conditions are frequently associated, particularly in aging, a state itself characterized by hyperinsulinemia. This common association has prompted the hypothesis that hyperinsulinemia may be a causative factor rather than the consequence of obesity, diabetes, hypertension, and hyperlipidemia. If that is the case, defining the nature and mechanisms of hyperinsulinemia becomes of primary interest. Insulin resistance is also a striking feature of all of the above mentioned pathologic states. In the presence of a preserved B-cell function, hyperinsulinemia can represent the mechanism designed to overcome the defect in the biological action of the hormone. For instance, there is a clear-cut age-related decline in the body's sensitivity to insulin. In order to compensate for this defect in insulin-mediated glucose metabolism, the B-cell must increase its secretion. On the other hand, a certain degree of insulin resistance can be induced both in animals and man by prolonged euglycemic hyperinsulinemia. Little is known regarding possible primary defects of the B-cell leading to uncontrolled oversecretion of insulin and subsequent insulin resistance. The primary defect, more probably, resides in an alteration of one or more of the steps whereby insulin exerts it own action. In favor of this hypothesis are the observations that insulin resistance segregates in familial clusters and that the first defect found in normoglycemic relatives of insulin-resistant diabetic patients is a reduced transformation of glucose into glycogen. Whatever is the primary defect, it is likely that a correction of insulin resistance might reduce the circulating levels of plasma insulin, possibly playing a beneficial effect on glucose tolerance, body weight, blood pressure and plasma lipid concentration.
Presse Med 1992 Sep 09
PMID:[Hyperinsulinism. Causes and mechanisms]. 133 21

Open cholecystectomy causes changes in pulmonary function test volumes; such changes can be related to respiratory complications of hypoxemia and atelectasis. Little data is available on lung volume changes after laparoscopic cholecystectomy. We measured preoperative and postoperative vital capacity (VC), functional residual capacity (FRC), arterial PO2, and chest X-ray atelectasis in 31 patients undergoing laparoscopic cholecystectomy and found small but significant decreases (p < 0.01) in VC (13 +/- 19%) and FRC (7 +/- 17%). The PO2 decreased from 89 +/- 11 mm Hg to 82 +/- 14 mm Hg, with only one patient's PO2 less than 60 mm Hg. Three patients demonstrated new segmental lobar collapse on postoperative chest X-ray. The postoperative changes in FRC (R2 = 0.40, p < 0.04) and atelectasis (R2 = 0.46, p < 0.03) could be predicted by multiple regression of risk factors, including obesity, smoking, use of narcotics, age, and symptoms of prior respiratory disease. We conclude that the respiratory changes after laparoscopic surgery are small in comparison to those expected after open cholecystectomy.
Surg Laparosc Endosc 1992 Sep
PMID:Postoperative respiratory function after laparoscopic cholecystectomy. 134 35

Central adiposity, sometimes described as male pattern fat distribution, is adversely related to cardiovascular risk and mortality independent of other measures of obesity. In a cohort of 511 men aged 30 to 79 years in 1972 to 1974, levels of androstenedione, testosterone, and sex hormone-binding globulin measured at baseline were inversely related to subsequent central adiposity, estimated 12 years later using the waist-hip circumference ratio. The observed differences in waist-hip ratio between top and bottom tertiles of these hormones and sex hormone-binding globulin were similar to mean waist-hip ratio differences between men with stroke or ischemic heart disease and those without in another prospective study. These findings, consistent with studies suggesting that testosterone seems to mobilize the abdominal depot on males, suggest that "male pattern" fat distribution may be a misleading description for central adiposity, at least, in men. Degree of maleness as indicated by total androgen levels is, in fact, negatively associated with central adiposity. However, the role of sex hormone-binding globulin in regulating androgenic activity warrants further investigation.
Ann Epidemiol 1992 Sep
PMID:Lower endogenous androgens predict central adiposity in men. 134 19

The specific binding of [3H]YM-09151-2 was used to investigate the possible differences in age-associated changes in striatal D2 dopamine (DA) receptor properties in genetically obese (fa/fa) Zucker rats and their lean (Fa/?) littermates. The maximal binding sites (Bmax) of D2 DA receptors was found to decline with age in both obese and lean rats; the rate of decline in receptor Bmax was slightly higher in lean than obese rats. However, the Bmax of D2 DA receptor in 6-, 12- and 18-month-old obese rats was significantly lower compared to the age-matched lean rats. These data indicate that obesity decreases the number of striatal D2 DA receptors without affecting the rate at which receptor number decreases with age.
Brain Res 1992 Sep 04
PMID:Decreased striatal D2 dopamine receptors in obese Zucker rats: changes during aging. 135 96

BRL 26830A is a thermogenic beta-adrenergic agonist drug which has an anti-obesity effect in animals and diet-restricted obese man. This study was undertaken in obese subjects who were not calorie restricted to assess the effect of three weeks drug administration on energy expenditure and glucose, amino acid and fatty acid metabolism in the post-absorptive and fed states. Stable isotope tracers were employed to determine kinetic data both at baseline and during adrenaline infusion. There was no evidence of BRL 26830A causing a major shift in fuel metabolism or having an anabolic effect. Baseline plasma concentrations of glycerol (P less than 0.01) and palmitate (P less than 0.01) were reduced, glucose remained within the normal range, whereas insulin decreased after BRL 26830A. The hypoaminoacidaemic effect of adrenaline was attenuated by BRL 26830A (P less than 0.01 for branched-chain amino acids, P less than 0.05 for total amino acids). The results suggest that BRL 26830A improves insulin sensitivity and causes selective down-regulation of adrenergic receptors. The increased insulin sensitivity may be a useful therapeutic effect for this class of drug and suggests a possible role in the treatment of obese non-insulin dependent diabetic patients.
Int J Obes Relat Metab Disord 1992 Sep
PMID:Metabolic effects of three weeks administration of the beta-adrenoceptor agonist BRL 26830A. 135 39

A male case of Prader-Willi syndrome (2.8 years in age) with an interstitial deletion of a chromosome affecting 15q 11-12 region is reported. The chief complaints were hypoplastic scrotum and defect of bilateral scrotal content. The clinical features were short stature, obesity, delayed mental development, bilateral cryptorchidism, hypogenitalism, hypopigmentation, and bilateral moderate vesicoureteral reflux with a history of muscular hypotonia. Bilateral orchidopexy was done. Endocrinologically both base values of luteinizing hormone (LH) and follicle stimulating hormone (FSH) were normal although LH reserve function was impaired on gonadotropin releasing hormone (GnRH) test. Testosterone response was normal by the stimulation of human chorionic gonadotropin. An interstitial deletion of proximal 15q, and pituitary-gonadal axis in Prader-Willi syndrome are discussed in relation to the clinical features and therapy.
Hinyokika Kiyo 1992 Sep
PMID:[Prader-Willi syndrome associated with chromosomal aberration: report of a case]. 135 45

A DNA mapping panel derived from an interspecific backcross was used to position the mouse insulin-2 locus (Ins-2) on Chromosome 7, near H19 (0/114 recombinants) and Th (1/114 recombinants). Ins-2 is part of a human-mouse conserved linkage group that includes Th, H19, and Igf-2. Analysis of segregation in the F2 generation from the cross C57BL/6J-tub/tub x CAST/Ei demonstrated that Ins-2 and the obesity mutant tubby (tub) are distinct loci, thus eliminating Ins-2 as a candidate gene for tub. These results also refine the estimated genetic distance between tub and Hbb to 2.4 +/- 1.4 cM. The predicted location for a human homolog of tubby is HSA 11p15.
Genomics 1992 Sep
PMID:Localization of insulin-2 (Ins-2) and the obesity mutant tubby (tub) to distinct regions of mouse chromosome 7. 135 94


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