ob gene mutations and human obesity

Abstract

Evidence for a genetic basis to human obesity Whilst recent changes in the prevalence of human obesity point to the importance of environmental determinants, genetic susceptibility has been identified as a major contrib-uting factor (Bouchard, 1996). A number of monogenic and polygenic effects are likely to be involved, with their expres-sion likely to vary with diet and the level of physical activity. These genetic influences are not confined to obesity, but exert their effect across the whole range of body weight, and are consistent with a polygenic inheritance of fat mass. Results from both twin and adoption studies suggest a herita-bility of fat mass of approximately 30-40 %. Data from large twin studies have consistently noted a concordance of 0.74.9 between monozygotic twins and of 0.35-0.45 between dizygotic twins (Borjeson, 1976; Stunkard et al. 1986~). Furthermore, a large Danish study demonstrated a clear relationship between the weight of biological parents (not adoptive parents) and the weight of adoptees (Stunkard et al. 1986b); they found no difference between the intra-pair correlation coefficients of identical twins reared apart com-pared with those reared together, suggesting that sharing the same childhood environment did not contribute to the simi-larity of BMI of twins later on in life.