Biophysical regulation of thermodynamic effects on type 2 diabetes

Abstract

Regulating cardiovascular stability is important for normal blood flow and heart function as well as for managing protein expression and physiologic workload. In type 2 diabetes (T2DM), cardiovascular instability is common due to an imbalance of proteins, hyperglycemia, and unpaired electrons. Downstream effects of this variability are inflammation, vascular dysfunction, and a greater demand of workload on the body. Because both exercise and temperature variations have shown benefits for T2DM, we hypothesized that a biophysical approach will effectively regulate thermodynamic effects on T2DM. The use of exercise was incorporated by placing T2DM Goto-Kakizaki (GK) and non-diabetic (Wistar) rodents on a treadmill in a heated chamber daily for a two-week period. Body mass was measured daily, and blood glucose and blood pressure were regularly monitored. Through observing energy expenditure, thermal energy was shown to be reduced in the diabetic experimental group. The workload was also lessened due to a decrease in body mass, and power output was affected. Free radical expression was determined through analysis of nitric oxide (NO) bioavailability. As an indication of inflammation, heat shock protein expression was measured. Our results indicate that our thermodynamic process improves vascular dysfunction by limiting the rate of vasoconstriction in GK rodents by nearly 35%, refining diabetic NO concentrations via nitrate by 34% in comparison to the control, and maintaining a physiologic blood pressure. Blood glucose levels also declined, and heat shock protein expression increased, demonstrating an improvement of hyperglycemia and inflammation in the diabetic state. Collectively, these measurements reveal that inducing a thermodynamic approach in T2DM improves cardiovascular stability.