Poster abstracts
Poster number 24 submitted by Jacob Longenecker
Cardiac methyltransferase-like 3 (METTL3) is a novel regulator of whole-body metabolism during Western diet challenge.
Jacob Longenecker (Department of Physiology & Cell Biology, College of Medicine, The Ohio State University), Federica Accornero (Department of Physiology & Cell Biology, College of Medicine, The Ohio State University)
Abstract:
Obesity has become a worldwide epidemic in recent years, with the rate of obesity nearly quadrupling since 1990. Occurring predominately in industrialized nations, this increase has resulted largely from excessive caloric intake and has contributed to reduced life expectancies and quality of life around the globe. The ability of the heart to maintain its own metabolic homeostasis in response to challenges such as exercise and excessive caloric intake is critical to the maintenance of proper cardiac function. Perturbations to this aspect of the heart can have far reaching effects, including dysregulation of systemic metabolic homeostasis. Of note, post transcriptional modification of cardiac RNAs have become increasingly accepted as important modulators of dysregulated processes within the stressed myocardium. One modification of interest is N6-methyladenosine (m6A), which is the most abundant mRNA modification known and has been shown to regulate a wide variety of cellular processes. Added to mRNAs by the enzyme methyltransferase-like 3 (METTL3), the role of m6A in the heart during diet induced obesity (DIO) remains unknown. We have used mouse models with cardiac-restricted METTL3 loss of function (LOF) or gain of function (GOF) in combination with consumption of a Western diet (42% kcal fat/45% kcal carbohydrate) to assess the role of METTL3 and m6A in the heart in modulating the response to DIO.
Keywords: Obesity, m6A, Heart