Volume 28, Issue S1 1086.5
Physiology
Free Access

Effects of epicatechin on glucose transporters in cardiac tissue and peripheral nerves in type 2 diabetes (1086.5)

Nelson Gonzalez

Nelson Gonzalez

Biological Sciences California State University Los Angeles, Los Angeles, CA, United States

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Abstract

An abnormally high level of blood glucose is the key characteristic of type 2 diabetes (T2D). Studies have established that this results from decreased translocation of glucose transporters. Due to the consequences of T2D, i.e. cardiovascular disease and diabetic neuropathy, two glucose transporters of interest are the type 4 (GLUT4) and the glucose transporter type 3 (GLUT3). T2D has been linked to energy deficiency leading to cardiovascular disease. A key protein in an insulin independent pathway is 5' adenosine monophosphate-activated protein kinase (AMPK), which is directly involved with the translocation of GLUT4. Thus, one of the main objectives of this study is to investigate the translocation of GLUT4 and relative AMPK expression in T2D. Moreover, studies have shown that hyperglycemia can cause peripheral nerve damage. GLUT3 translocation is independent of insulin signaling and can lead to an accumulation of glucose resulting in damage to the nerves. Peripheral nerve damage triggers the innate immune response which exacerbates the degeneration of peripheral nerves. In particular, the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) has been observed to play a role. Therefore, another objective of this study is to investigate the expression of GLUT3 and TNF-α in T2D to evaluate the progression of diabetic neuropathy. Using an in vivo high fat, streptozotocin (STZ) induced T2D model, we will inspect whether (-)-epicatechin (EPI), a naturally occurring flavonoid with demonstrated anti-diabetic properties, alters the relative expression of the aforementioned proteins. Using samples collected from the heart and sciatic nerves of these animals, biochemical and immunohistological analysis will be performed to evaluate the expression and location of the proteins of interest. Ultimately, these results will further validate the anti-diabetic properties of EPI and provide crucial data on its relatively elusive mechanism.

Grant Funding Source: Supporter by Dr. Katrina Yamazaki and IMPACT LA