Figure 5.

Relationship between maternal outcomes on the HF diet with juvenile offspring hepatic triglycerides and gene expression. Correlations between (A) juvenile offspring liver triglycerides and maternal insulin AUC (log transformed) during GTT, pregnancy body weight, and plasma triglycerides and (B) offspring inflammation and lipogenic gene expression with maternal insulin AUC. Open circles represent HF+IS (n = 9) and closed circles represent HF+IR (n = 25) maternal–offspring pairs. C: Mechanisms for NAFLD in HF+IR offspring. HF+IR placentas have increased transplacental lipids, decreased uterine and fetal blood flow, and increased placental inflammation, which increases fetal cytokine exposure. We speculate that this combination of lipid, cytokine, and hypoxia exposure in utero produced by the HF+IR mother programs the offspring liver for increased NAFLD at 1 year of age.