Disease relevance of Obesity, Morbid

• Genetic variation in the beta 3-adrenergic receptor and an increased capacity to gain weight in patients with morbid obesity [1].
• Patients with alcoholic liver disease had significantly higher fatty acid levels than did patients with morbid obesity (p less than 0.05), while there was no difference in the triglyceride concentrations between these two groups [2].
• The most common hepatic consequence of jejunoileal bypass for morbid obesity is triglyceride accumulation (steatosis), which usually appears to be maximal during the period of acute weight loss [3].
• Alteration of the leptin network in late morbid obesity induced in mice by brain infection with canine distemper virus [4].
• The relationship between SD score-leptin and GHBP was studied in 128 adults with different nutritional status [8 groups according to body mass index (BMI)], ranging from severely underweight anorexia nervosa to highly morbid obesity [5].

Psychiatry related information on Obesity, Morbid

• Sixteen patients who underwent gastric stapling procedure for morbid obesity were assessed pre- and post-operatively on several psychosocial dimensions using a number of self-report questionnaires including the Eating Disorders Inventory, Locus of Control, and Millon's Clinical Multi-Axial Inventory [6].

High impact information on Obesity, Morbid

• Melanocortin-4 receptor mutations are a frequent and heterogeneous cause of morbid obesity [7].
• Rodents with mutations in the leptin receptor gene develop morbid obesity [8].
• To determine whether genetic variation in PYY and/or Y2R may contribute to morbid obesity in humans, these genes were sequenced in 83 extremely obese Pima Indians (BMI > or = 50 kg/m2) [9].
• Deficiency of either leptin or LRb causes morbid obesity [10].
• The haplotype including wild-type alleles of these SNPs (C/G/G/T/C/G, HAP2) is identified as a risk factor for morbid obesity (P = 0.003) [11].

Chemical compound and disease context of Obesity, Morbid

• CONCLUSIONS/INTERPRETATION: We propose that the significant increase in MFN2 mRNA levels may explain the increase in glucose oxidation observed in morbid obesity following bariatric surgery [12].
• A single-center, randomized, double-blind, prospective trial evaluated 500 mg of ursodeoxycholic acid versus placebo, beginning within 3 days after surgery and continuing for 6 months or until gallstone development, for patients with morbid obesity [13].
• Twelve patients undergoing a 10 to 4 inch end-to-side jejunoileal bypass for morbid obesity were measured pre- and postsurgically for total cholesterol and high-density lipoprotein (HDL) cholesterol levels [14].
• Vitamin A deficiency in a newborn resulting from maternal hypovitaminosis A after biliopancreatic diversion for the treatment of morbid obesity [15].
• Endogenous ethanol production and hepatic disease following jejunoileal bypass for morbid obesity [16].

Biological context of Obesity, Morbid

• A sib-pair analysis study of 15 candidate genes in French families with morbid obesity: indication for linkage with islet 1 locus on chromosome 5q [17].
• The peroxisome proliferator-activated receptor gamma (PPARgamma) gene has been implicated in morbid obesity and is important to lipid and carbohydrate metabolism [18].
• Change in vascular adhesion protein-1 and metabolic phenotypes after vertical banded gastroplasty for morbid obesity [19].
• METHODS: After VBG for morbid obesity, 26 women and four men (mean age = 39.1 years) were weighed and had body composition analysis undertaken at intervals [20].
• CONCLUSION: These findings support the hypothesis that in morbid obesity, weight loss after surgery has positive effects on fibrinolytic function, oxidative stress and antioxidant activity [21].

Anatomical context of Obesity, Morbid

• Plasminogen activator inhibitor 1, transforming growth factor-beta1, and BMI are closely associated in human adipose tissue during morbid obesity [22].
• Gastric acid secretion and vitamin B12 absorption after vertical Roux-en-Y gastric bypass for morbid obesity [23].
• Other factors that may potentially enhance ammonium acid urate stone formation include morbid obesity, recurrent uric acid calculi and recurrent urinary tract infection [24].
• The data obtained here also showed that TNF-alpha and TNFR2 mRNAs were significantly more expressed in subcutaneous adipose tissue of subjects with morbid obesity compared to obese and non-obese subjects [25].
• Gastric acid and serum gastrin secretion before and after bypass of the small intestine for morbid obesity [26].

Gene context of Obesity, Morbid

• Hypoadiponectinaemia and high risk of type 2 diabetes are associated with adiponectin-encoding (ACDC) gene promoter variants in morbid obesity: evidence for a role of ACDC in diabesity [27].
• In summary, our results do not support a major role of the human OBR gene in the development of morbid obesity in our population [28].
• Genetically obese rodents with mutations of leptin or the leptin receptor are defective in leptin signaling and develop morbid obesity and diabetes [29].
• A novel melanocortin 4 receptor (MC4R) gene mutation associated with morbid obesity [30].
• Lepr(db-dmpg) had a deletion in the extracellular domain of LEPR: Lepr(db-rlpy) exhibited a large DNA deletion, leading to a complete lack of LEPR: All three mutations led to morbid obesity and diabetes [31].

Analytical, diagnostic and therapeutic context of Obesity, Morbid

• Other factors, including diabetes, renal failure, smoking, sex, age, reoperation, morbid obesity, and steroid use, were not significant [32].
• A report of reduced serum levels of progestins, following oral administration after jejunoileal bypass, promoted the present investigation of the absorption of D-norgestrel and estradiol following different types of intestinal bypass surgery for morbid obesity [33].
• To study the effects of postoperative chest percussion with postural drainage (CPT), 53 consecutive patients undergoing Roux-en-Y gastric stapling procedures for treatment of morbid obesity were randomized to two groups [34].

References