Michael Cowley

Professor Cowley returned to Melbourne after ten years in the US, more recently as Associate Professor in the Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton US where he specialised in research into obesity.

Michael has established his laboratory at Monash University as part of the Monash Obesity Initiative.

Research project: Re-establishing glucose sensing in α-MSH cells to treat diabetes

Michael and his team recently discovered that a specific group of neurons in the brain detects blood sugar levels and these are probably master cells regulating metabolism (Parton et al., 2007). These cells produce a transmitter (that can also act as a hormone) called melanocyte stimulating hormone (α-MSH) and this regulates the production of glucose by the liver and the use of glucose by tissues in the body. How α-MSH does this is unknown, but the researchers do know stimulation of α-MSH secretion in response to glucose normalizes blood sugar levels in obese diabetic mice. They have recently uncovered evidence in human liver transplant patients that the brain regulates glucose secretion from the liver in humans too.

Unfortunately in diabetic mice glucose is unable to stimulate α-MSH secretion in response to glucose, so the feedback loop fails, and blood glucose levels rise catastrophically. They have developed two therapeutic interventions, the first is a molecule called genipin that reactivates α-MSH in response to glucose in diabetics.

The second intervention is to develop long acting analogues of α-MSH for acute treatment of diabetes. These new therapies would complement existing diabetes treatments. The overall strategy will be to confirm and refine treatment with genipin and α-MSH and conduct trials in non-human primates. Optimal doses would be determined and the development of pharmaceutical products would be progressed with a pharmaceutical company partner (Orexigen Therapeutics) and the objective would be clinical trials within 3 years.