Type of Document	Dissertation
Author	Suagee, Jessica Kanekakenre
Author's Email Address	jksuagee@vt.edu
URN	etd-11082010-104150
Title	Regulation of Nutrient Metabolism in Equine Skeletal Muscle and Adipose Tissue
Degree	PhD
Department	Animal and Poultry Sciences
Advisory Committee	Advisor Name Title Corl, Benjamin A. Committee Co-Chair Wong, Eric A. Committee Co-Chair Crisman, Mark Virgil Committee Member Geor, Ray Committee Member Hulver, Matthew W. Committee Member McCutcheon, L. Jill Committee Member
Keywords	glucose horse insulin laminitis obesity
Date of Defense	2010-10-25
Availability	restricted
Abstract Glucose and lipid metabolism are dysregulated in obese horses. Altered glucose metabolism is evidenced by the development of insulin resistance and increased fasting plasma insulin concentrations (hyperinsulinemia) while altered lipid metabolism is evidenced by increased plasma lipid concentrations. Obesity in horses also increases the risk of the painful hoof disease, laminitis. Three experiments were performed to investigate the regulation of nutrient metabolism in skeletal muscle and adipose tissue of lean, healthy horses. Adipose tissue was found to be the primary lipogenic tissue of horses, with acetate being the primary lipogenic substrate. Secondly, ten, lean horses were used to investigate the effects of acute hyperinsulinemia on nutrient metabolism. Increasing plasma insulin concentrations to >1,000 mIU/L for six hours decreased transcript abundance of glucose transporters and the insulin receptor in adipose tissue, and decreased protein abundance of the insulin receptor in skeletal muscle, potentially indicating that hyperinsulinemia potentiates insulin resistance. Insulin infusion also reduced mRNA abundance of lipid transporters in adipose tissue while increasing them in skeletal muscle. The final experiment investigated the influence of the insulin-sensitizing drug, pioglitazone, and lipopolysaccharide, on nutrient metabolism in skeletal muscle and adipose tissue, and their association with insulin sensitivity. Pioglitazone treatment did not increase insulin sensitivity; however it did increase skeletal muscle transcript abundance of the insulin receptor and the non-insulin sensitive glucose transporter and adipose tissue protein abundance of the insulin-sensitive glucose transporter (GLUT4). Lipopolysaccharide decreased insulin sensitivity regardless of pioglitazone pre-treatment, which was associated with decreased transcript abundance of GLUT4 in skeletal muscle and adipose tissue of untreated horses, but not adipose tissue of pioglitazone treated horses.
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