A lack of differential effect between fat types on insulin sensitivity accords with our findings in lean individuals, and may be explained by the fact that the majority of subjects had a nonfatty liver (<5%) also after the intervention; i.e., the absolute amount of liver fat accumulation may have been too small to impair insulin action also in the current metabolically healthy, overweight population, as supported by findings in obesity-matched subjects with and without NAFLD (44). The gene discussed is INS; the disease is obesity disorder.