Disease relevance of Obesity

• 9. The association was not explained by confounding due to the indications for thiazide use, such as hypertension, or other factors, such as obesity or the use of other drugs [1].
• To investigate whether mutations in the gene for the beta 3-adrenergic receptor predispose patients to obesity and non-insulin-dependent diabetes mellitus (NIDDM), we studied this gene in 10 Pima Indians by analysis of single-stranded conformational polymorphisms and dideoxy sequence analysis [2].
• Leptin-null (Lep(ob/ob)) mice exhibit obesity, decreased energy expenditure and hyperphagia [3].
• Increased FOXC2 levels, induced by high fat diet, seem to counteract most of the symptoms associated with obesity, including hypertriglyceridemia and diet-induced insulin resistance--a likely consequence hereof would be protection against type 2 diabetes [4].
• The inverse relation of alpha cholesterol of prevalence of coronary heart disease was independent of beta cholesterol, obesity, and other factors [5].

Psychiatry related information on Obesity

• Bardet-Biedl syndrome is an autosomal recessive disorder characterized by mental retardation, obesity, retinitis pigmentosa, polydactyly and hypogonadism [6].
• Our data support the idea that the Y5 receptor is the postulated 'feeding' receptor, and may provide a new method for the study and treatment of obesity and eating disorders [7].
• Behavior therapy and sibutramine for the treatment of adolescent obesity: a randomized controlled trial [8].
• Genetic ablation of orexin neurons in mice results in narcolepsy, hypophagia, and obesity [9].
• INTERPRETATION: Smoking cessation, treatment of hypertension, and reduction in blood glucose and central obesity (perhaps through dietary modification) may be important in preventing IHD in Asian Indians [10].

High impact information on Obesity

• Insulin resistance plays a key role in the pathogenesis of several human diseases, including diabetes, obesity, hypertension, and cardiovascular diseases [11].
• Lymphatic vascular defects promoted by Prox1 haploinsufficiency cause adult-onset obesity [12].
• Variants of ENPP1 are associated with childhood and adult obesity and increase the risk of glucose intolerance and type 2 diabetes [13].
• In an era marked by the increasing prevalence of obesity, diabetes, and cardiovascular disease, the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma) has emerged as a transcriptional regulator of metabolism whose activity can be modulated by direct binding of small molecules [14].
• Integrating genotypic and expression data in a segregating mouse population to identify 5-lipoxygenase as a susceptibility gene for obesity and bone traits [15].

Chemical compound and disease context of Obesity

• To investigate whether abnormal insulin oscillations are an early feature of diabetes, we studied 10 minimally glucose-intolerant first-degree relatives of patients with non-insulin-dependent diabetes and 10 controls matched for age and obesity [16].
• Bile cholesterol saturation correlated with obesity (r = 0.41; P less than 0.001) and urinary estrogen excretion (r = 0.44; P less than 0.001) [17].
• Obesity resistance and multiple mechanisms of triglyceride synthesis in mice lacking Dgat [18].
• The increases may be explained by dysregulation of 11 beta-hydroxysteroid dehydrogenase causing increased oxidation of cortisol to cortisone, which cannot be accounted for by obesity [19].
• We studied the relation in Pima Indians between obesity in children and diabetes during pregnancy in their mothers [20].

Biological context of Obesity

• Cidea-deficient mice have lean phenotype and are resistant to obesity [21].
• As Ucp2 is widely expressed in mammalian tissues, uncouples respiration and resides within a region of genetic linkage to obesity, a role in energy dissipation has been proposed [22].
• In the future, however, it may be possible to stimulate or inhibit the activity of lipoprotein lipase in specific tissues and to alter metabolic processes so as to improve the quality and length of life in patients with metabolic diseases such as hypertriglyceridemia, HDL2 deficiency, and obesity [23].
• As deficiency of a single component of the pathway that limits food intake (such as leptin or receptors for melanocortin-4) causes obesity, it has been suggested that orexigenic signals are more redundant than those limiting food intake [24].
• Because GLUT4 has been shown to be dysregulated in pathological states such as diabetes and obesity, it was expected that genetic ablation of GLUT4 would result in abnormal glucose homeostasis [25].

Anatomical context of Obesity

• Our studies implicate a role for HMGIC in fat-cell proliferation, indicating that it may be an adipose-specific target for the treatment of obesity [26].
• Because visceral obesity predicts insulin resistance, we studied whether alterations in the gene encoding for the beta 3-adrenergic receptor in visceral fat are associated with insulin resistance [27].
• In insulin-resistant states such as obesity and type 2 diabetes, GLUT4 expression is decreased in adipose tissue but preserved in muscle [28].
• To determine whether uncoupling respiration from oxidative phosphorylation in skeletal muscle is a suitable treatment for obesity and type 2 diabetes, we generated transgenic mice expressing the mitochondrial uncoupling protein (Ucp) in skeletal muscle [29].
• In animal models of obesity with disrupted leptin signalling, CART mRNA is almost absent from the arcuate nucleus [30].

Gene context of Obesity

• These data demonstrate that melanocortin signalling transduced by Mc4r is not an exclusive target of leptin action and that factors resulting from obesity contribute to leptin resistance [31].
• A biochemical function for attractin in agouti-induced pigmentation and obesity [32].
• Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans [33].
• Like its close relatives UCP1 and UCP3, UCP2 uncouples proton entry in the mitochondrial matrix from ATP synthesis and is therefore a candidate gene for obesity [34].
• Identification of the gene (BBS1) most commonly involved in Bardet-Biedl syndrome, a complex human obesity syndrome [35].

Analytical, diagnostic and therapeutic context of Obesity

• Oral administration of a mimetic in a mouse model of high-fat diet-induced obesity reduced body weight gain, adiposity and insulin resistance [36].
• These data demonstrate the feasibility of gentle manipulation of adiposity and allow a functional dissection of obesity and its metabolic sequelae [37].
• MAIN OUTCOME MEASURES: Statistically significant changes (P<.01) in state prevalences of cigarette smoking, binge alcohol use, physical inactivity, obesity, safety belt use, and mammography; screening for cervical cancer, colorectal cancer, and cholesterol levels; and receipt of influenza and pneumococcal disease vaccination [38].
• This discovery reveals how mutations in CBS sequences in these proteins cause hereditary diseases and provides a rich vista of conceptual opportunities for therapies in energy metabolism, obesity, diabetes, cancer, antivirals, and immunosuppression [39].
• Biliary lipid secretion in cholesterol gallstone disease. The effect of cholecystectomy and obesity [40].

References