Objective Data from animal models show that in utero exposure to a maternal high-fat diet
(HFD) renders susceptibility of these offspring to the adult onset of metabolic syndrome. We
and others have previously shown that epigenetic modifications to histones may serve as a
molecular memory of the in utero exposure, rendering the risk of adult disease. Because
mice heterozygous for the Glut4 gene (insulin sensitive glucose transporter) born to wild-
type (WT) mothers demonstrate exacterbated metabolic syndrome when exposed to an HFD …