McCurdy, CarrieHetrick, ByronBlaylock, Hunter2021-07-272021-07-272021https://hdl.handle.net/1794/263991 page.Maternal obesity has been shown to negatively impact offspring's metabolic health, leading to a greater and earlier risk for developing metabolic diseases, including type 2 diabetes. This presents a serious concern given that rates of obesity have been steadily increasing over the past four decades. The mechanisms behind the intergenerational effects of obesity are still unknown, however. Using a non-human primate model, the McCurdy lab recently found a large number of genes dysregulated in skeletal muscle of offspring born to a mother fed a western-style, high fat, and high sugar, diet (WSD). Several of the 3089 dysregulated genes have been linked with cellular quality control mechanisms such as autophagy and mitophagy. Disruption in quality control mechanisms in offspring skeletal muscle might result in increased predisposition of the offspring to the development of metabolic disorders as is seen in offspring exposed to maternal obesity during development. To better characterize the cellular effects of this altered gene expression, we developed two novel flow cytometry-based assays to measure the ability of non-human primate myoblasts to effectively clear damaged mitochondria and regulate the biogenesis of lysosomes which are vital to the process of autophagy. Given the gene expression data, it was hypothesized that exposure to maternal western-style diet would result in the impaired ability for these cells to turnover damaged mitochondria and increase lysosome biogenesis in response to autophagic signaling.application/pdfen-USCC BY-NC-ND 4.0obesitymetabolic diseasefetal programmingmaternal dietflow cytometryPresentationhttps://orcid.org/0000-0002-0606-502X