Meeting Abstract

P2-20   -   The Effect of Cold Exposure on Obesity Induced Pathological Hypertrophy Burns, MPA*; Barnhill, S; Schaeffer, PJ; Miami University, Oxford, OH burnsmp3@miamioh.edu

Cardiac hypertrophy can be both physiological and pathological in nature. In the case of pregnancy or exercise, we see hypertrophy marked by eccentricity (normal wall thickness) and reversibility. Pathological hypertrophy associated with pressure overload, such as the case of obesity leads to heart disease and heart failure. In mouse models, obese mice are often exercise resistant. During cold exposure, however, organisms must defend body temperature in order to maintain homeostasis regardless of body condition. We show that metabolic rate in cold exposed mice (4℃) is double that of control mice. Does increased cardiac load through cold exposure reduce the pathological markers of hypertrophy in obese mice? In order to test this, we conducted a four-way factorial design using obese mice and wild type mice held at either room temperature or 4℃. Obesity was induced by feeding a high fat (58% calories by lipids) western diet to UCP-DTA transgenic mice which have deficient brown adipose tissue. Following cold exposure, mRNA was extracted from the left ventricles of the mice (n=16) and sent for sequencing. Differential gene expression was determined using CLC Genomics Workbench. Gene ontology and enrichment of the differentially expressed genes was conducted using AMIGO2. Of the differentially expressed genes identified between warm and cold exposed obese mice, evidence of a reduction in pathology was observed. Our preliminary results show that six of the genes upregulated in cold-exposed mice are mitochondrial respiratory genes, the downregulation of which is associated with pathological hypertrophy.