We utilize a highly translational, non-human primate model to assess how maternal diet and medication consumption during pregnancy influence the embryonic development and postnatal function of pancreatic islets in the offspring. Developmentally programmed changes could alter disease susceptibility later in life. A challenge when working with hard-to-acquire samples such as those from non-human primates is evaluating multiple questions from the same individual efficiently.
Unfortunately, simultaneously extracting information from the metabolome and genome can be difficult due to the incompatibility of assay reagents in time-sensitive degradation of molecules to be quantified. Our protocol allows for extrapolation of metabolite abundance, chromatin accessibility, and differential gene expression from the same starting material. This multi-layered approach provides insight into how metabolism may alter the genome in pancreatic islets.