By Abrams K.
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Additional resources for A Bayesian Approach to Weibull Survival Models - Application to a Cancer Clinical Trial
The identification of true genetic associations in common multifactorial conditions, such as the metabolic syndrome, requires large studies consisting of thousands of subjects. This need is further accentuated by the large number of implicated genetic loci and their potentially small contribution to the phenotype when individually considered. In parallel to linkage and association studies, several studies have evaluated the contribution of specific candidate genes to the metabolic syndrome pathogenesis.
Melanin-concentrating hormone receptor mutations and human obesity: functional analysis. Obes. Res. 2004; 12:743–749. Tao YX. Molecular mechanisms of the neural melanocortin receptor dysfunction in severe early onset obesity. Mol. Cell. Endocrinol. 2005; 239:1–14. Lee YS, Poh LK, Loke KY. A novel melanocortin 3 receptor gene (MC3R) mutation associated with severe obesity. J. Clin. Endocrinol. Metab. 2002; 87:1423–1326. Rached M, Buronfosse A, Begeot M, Penhoat A. Inactivation and intracellular retention of the human I183N mutated melanocortin 3 receptor associated with obesity.
Fatty acid binding protein 2 (FABP2) and apolipoprotein C-III (APOC3) polymorphisms have been directly associated with increased risk for dyslipidemia and the metabolic syndrome in Asian-Indians (132). Other examples include a number of lipidsensitive transcription factors (nuclear receptor subfamily 1, member 4 (FXR), nuclear receptor subfamily 1, member 3 (LXR-a), retinoid X receptor α (RXR-a), PPAR-a, PPAR-d, peroxisome proliferator-activated receptor (PGC1-a), PCG1-b, sterol regulatory element binding transcription factor 1 (SREBP-1c)) that have been implicated in the development of dyslipidemia, one of the very early features of the metabolic syndrome (124).