Presenter(s): Maurisa Rapp—Human Physiology
Faculty Mentor(s): Carrie McCurdy, Byron Hetrick
Session: Prerecorded Poster Presentation
Epidemiological studies have shown that offspring from pregnancies complicated by maternal obesity have a 4-fold greater risk for developing childhood obesity and symptoms of metabolic syndrome . The developmental origins of health and disease (DOHaD) hypothesis states that certain environmental exposures during critical windows of development may have consequences for an individuals long term health . DOHaD may explain a portion of the continual increase in obesity rates among children . In a non-human primate model, offspring of obese dams become sensitized to obesity-induced metabolic disruptions, including insulin resistance and mitochondrial disfunction . Increased reactive oxygen species (ROS) production contributes to mitochondrial defects observed in obesity . Oxidative stress, which is caused by overproduction of ROS, can lead to mitochondrial DNA (mtDNA) mutations, decreased copy number, reduced membrane permeability and subsequent suppression of mitochondrial respiratory chain activity . Therefore, I hypothesize that maternal obesity increases offspring mitochondrial ROS production leading to mtDNA damage without loss of mtDNA abundance . To study the effect of maternal obesity, we used a previously established Japanese macaque model of fetal programming . Dams were fed either a control (CON) diet or western style diet (WSD) prior to and during pregnancy and lactation . Offspring were then weaned at 8 months and fed a healthy CON diet . Skeletal muscle biopsies from offspring were collected at 3 years of age and relative mtDNA abundance was measured using quantitative PCR (qPCR) amplification of short regions of mtDNA . No differences were measured in the amount of mtDNA between offspring groups . Moving forward, I will test for elevations in ROS-induced mtDNA damage by qPCR amplification . Overall, these data indicate that exposure to maternal obesity and WSD during fetal development does not reduce mitochondrial abundance in skeletal muscle of adolescent offspring .