High-fat diet consumption during pregnancy and the early post-natal period leads to decreased α cell plasticity in the nonhuman primate.

We investigated the impact of poor maternal nutrition and metabolic health on the development of islets of the nonhuman primate (NHP). Interestingly, fetal offspring of high fat diet (HFD) fed animals had normal total islet and β cell mass; however, there was a significant reduction in α cell mass, and decreased expression of transcription factors involved in α cell differentiation. In juvenile animals all offspring maintained on a HFD during the postweaning period demonstrated increases in total islet mass, however, the control offspring displaying increased islet number, and HFD offspring displayed increased islet size.

Maternal high-fat diet triggers lipotoxicity in the fetal livers of nonhuman primates.

Maternal obesity is thought to increase the offspring's risk of juvenile obesity and metabolic diseases; however, the mechanism(s) whereby excess maternal nutrition affects fetal development remain poorly understood. Here, we investigated in nonhuman primates the effect of chronic high-fat diet (HFD) on the development of fetal metabolic systems. We found that fetal offspring from both lean and obese mothers chronically consuming a HFD had a 3-fold increase in liver triglycerides (TGs).

Developmental origins of disease and determinants of chromatin structure: maternal diet modifies the primate fetal epigenome.

Chromatin structure is epigenetically altered via covalent modifications of histones to allow for heritable gene regulation without altering the nucleotide sequence. Multiple lines of evidence from rodents have established a role for epigenetic remodeling in regulating gene transcription in response to an altered gestational milieu. However, to date, it is unknown whether variations in the intrauterine environment in primates similarly induce changes in key determinants of hepatic chromatin structure.