Project 184 – Zinc activation of enzymes responsible for insulin signalling and glucose homeostasis in type 2 diabetes

24 Jan 2019

Dr Stephen Myers – $24,138


Type 2 diabetes mellitus(T2DM) is increasing globally and is approaching pandemic levels. T2DM is a debilitating and progressive disease characterised by persistent high blood glucose levels that can lead to kidney failure, blindness, heart disease and stroke.  Preceding the development of T2DM, a patient will experience insulin resistance; a disorder in which tissues such as the liver and muscle do not respond efficiently to insulin, and as a consequence, fail to supply the body with adequate glucose for energy.

A foremost concern for people with insulin resistance is the eventual failure of the pancreas to produce insulin. Thus, these patients will eventually succumb to life-long chronic illness and unfavourable side-effects associated with diabetic treatments. Therefore, prevention strategies that take advantage of the ‘window of opportunity’ (before pancreatic failure) to prevent or lessen disease progression would have an enormous impact on the health and wellbeing of our communities.

The study aims to delineate the molecular mechanism of the insulin- zinc ‘axis’ in regulating glucose metabolism in insulin resistant and type 2 diabetic skeletal muscle cells. Recently, studies on zinc and the proteins that transport this nutrient in cells have shown that it helps allow the entry of glucose into the cell. Understanding the molecular mechanisms of zinc action in controlling glucose metabolism may lead to targeting this nutrient clinically to prevent insulin resistance and the progression to T2DM.