Genetics of fat intake in the determination of body mass

Abstract

Body mass and fat intake are multifactorial traits that have genetic and environmental components. The gene with the greatest effect on body mass is FTO (fat mass and obesity-associated), but several studies have shown that the effect of FTO (and of other genes) on body mass can be modified by the intake of nutrients. The so-called gene-environment interactions may also be important for the effectiveness of weight-loss strategies. Food choices, and thus fat intake, depend to some extent on individual preferences. The most important biological component of food preference is taste, and the role of fat sensitivity in fat intake has recently been pointed out. Relatively few studies have analysed the genetic components of fat intake or fatty acid sensitivity in terms of their relation to obesity. It has been proposed that decreased oral fatty acid sensitivity leads to increased fat intake and thus increased body mass. One of the genes that affect fatty acid sensitivity is CD36 (cluster of differentiation 36). However, little is known so far about the genetic component of fat sensing. We performed a literature review to identify the state of knowledge regarding the genetics of fat intake and its relation to body-mass determination, and to identify the priorities for further investigations.

Keywords: FTO; H 2 heritability; CD36 cluster of differentiation 36; FGF21 fibroblast growth factor 21; FTO fat mass and obesity-associated; GLP-1 glucagon-like-peptide-1; GPR G-protein coupled receptor; GWAS genome-wide association study; G×E gene–environment interaction; IRX3 Iroquois-related homeobox; MC4R melanocortin 4 receptor; OPRM1 opioid receptor mu 1; POMC pro-opiomelanocortin; Body mass; Fat intake; Fat sensitivity; Gene polymorphisms.