Title page for ETD etd-11082010-104150


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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