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Database: PubMed
Entry: 20102775
LinkDB: 20102775
Original site: 20102775 
PMID:
     20102775
Authors:
     Deluis DA, Sagrado MG, Aller R, Izaola O, Conde R.
Title:
     Effects of C358A missense polymorphism of the degrading enzyme fatty acid amide 
     hydrolase on weight loss, adipocytokines, and insulin resistance after 2 
     hypocaloric diets.
Journal:
     Metabolism. 2010 Sep;59(9):1387-92. doi: 10.1016/j.metabol.2009.12.029. Epub 2010 
Abstract:
     It has been demonstrated that the polymorphism 385 C/A of fatty acid amide 
     hydrolase was associated with obesity. We decided to investigate the role of a 
     polymorphism (cDNA 385 C->A) on insulin resistance and weight loss secondary to a 
     low-fat vs a low-carbohydrate diet. A population of 248 patients with obesity was 
     analyzed. Basal measurements were performed, and values were compared to those at 
     the end of a 3-month period in which subjects received either diet I (low fat) or 
     diet II (low carbohydrate). One hundred seventy-eight patients (71.8%) had the 
     genotype C358C (wild-type group), and 70 (28.2%) patients had the genotype C358A 
     (62 patients, 25%) or A358A (8 patients, 3.2%) (mutant-type group). With diet I, 
     body mass index, weight, fat mass, waist circumference, and systolic blood 
     pressures decreased in the wild-type and mutant-type groups. With diet II, body 
     mass index, weight, fat mass, waist circumference, and systolic blood pressures 
     decreased in both genotypes. With diet I, leptin, glucose, total cholesterol, 
     triglyceride, insulin, and homeostasis model assessment for insulin sensitivity 
     (HOMA) decreased in the wild-type group. In the mutant-type group, only 
     cholesterol decreased in a significant way. With diet II, leptin, interleukin-6, 
     glucose, total cholesterol, low-density lipoprotein cholesterol, insulin, HOMA, 
     and C-reactive protein decreased in the wild-type genotype. The allele A358 of 
     fatty acid amide hydrolase was associated with a lack of improvement on glucose 
     insulin, HOMA, and leptin levels in both diets after weight loss.

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