Abstract

Background Type 2 diabetes (T2DM) is a disease that affects over 14.5 million Americans, leading to increased morbidity and ultimately mortality. During early stages of the disease, insulin is unable to move glucose into the body’s cells; this results in a buildup of glucose in the blood known as hyperglycemia. These detrimental effects lead to an imbalance of heat shock proteins (Hsps) and nitric oxide (NO), all of which contribute to vascular dysfunction. While both exercise and acute exposure to heat are known to improve the expression of Hsps and the bioavailability of NO, the role of combining the two is unclear during conditions of vascular dysfunction. In this research, we predict that a combination of heat and exercise (heat acclimation) will minimize harmful effects that occur in T2DM. Methods Using a type 2 diabetic rodent model (Goto-Kakizaki (GK)) and corresponding control rodent model (Wistar), animals were subjected to heat acclimation over a period of 14 days. Throughout the study, the animals were pair-fed, and NO availability (by way of plasma nitrite and nitrate) via Nitric Oxide Analyzer (NOA), Hsp expression via ELISA assay, blood glucose, and tail-cuff blood pressure were measured. Results While the blood pressure remained physiological in both the GK and Wistar rats, the GK-heat acclimated blood pressure was stabilized. Furthermore, the blood glucose was reduced. A significant increase in plasma nitrate ( p p Conclusion Heat acclimation has an influential effect on NO availability and Hsp expression in GK type 2 diabetic rodents, potentially improving vascular dysfunction. Disclosure Research supported by Research Initiation Program Grant at Winston Salem State University.

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