Insulin resistance and central adiposity are strong risk indicators for
type 2 diabetes and
coronary heart disease. An important role for adipose tissue in the etiology and progression of these conditions has recently become more evident. A
transcription factor, TFAP2B, has been shown to participate in the regulation of adipocyte metabolism, by facilitating
glucose uptake and
lipid accumulation, while simultaneously reducing
insulin sensitivity, and recently a direct function for TFAP2B as an inhibitor of
adiponectin expression was observed. In this study, we have investigated how
insulin resistance, plasma
adiponectin, and central adiposity, in a normal population of adolescents, are affected by genetic variability in TFAP2B. Our results show that both
insulin sensitivity, as measured from levels of fasting
glucose and
insulin, and central adiposity, estimated by subscapular skinfold thickness, were significantly associated to genetic variability in TFAP2B. This association was restricted to males only, where carriers of the 4-repeat allele of intron 2 had higher
insulin sensitivity and lower subscapular skinfold thickness. Levels of
adiponectin did not show any association to the TFAP2B polymorphism, but was negatively correlated to central adiposity in females. These results suggest that reduction of TFAP2B expression could have a protective effect against future risk of complications associated with decreased
insulin sensitivity and central adiposity, such as
type 2 diabetes and
coronary heart disease.