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Joslin-led study uncovers role of appetite hormone MCH in insulin production

d/or cant use insulin properly (insulin resistance). Both diseases could benefit from treatments that stimulate beta cells in the pancreas to produce insulin.

In the first study, in which mice were genetically engineered to over-express MCH, Dr. Kulkarni and his colleagues observed changes in beta cell mass out of proportion with the degree of obesity, suggesting that MCH had a direct effect on islets. To build on these previous findings, the researchers focused this study on gaining a deeper understanding of how MCH and its receptors influence growth of beta cells.

The investigators first confirmed that MCH and its receptors are indeed expressed in islet cells of mice and humans. They then treated human donor or mouse pancreatic islet cells with MCH and found that it increased insulin secretion, compared to islet cells without MCH, which did not show the same effect.

In the next phase, the researchers examined genetically-engineered mice that did not produce MCH and consequently had abnormally small islets. This indicated to us that MCH is important for growth of islets, says Dr. Kulkarni.

The next step in the research process is to pinpoint exactly how MCH is regulating the growth of beta cells and identify which proteins are involved in this growth process. We know MCH is having an effect on both growth and function likely by recruiting different proteins. It will be worth exploring which proteins are being activated by MCH to cause the growth effect, Dr. Kulkarni explains.

A follow-up study has been designed and is currently awaiting funding. It will look at how MCH interacts with glucagon-like peptide 1 (GLP-1), a hormone involved in beta cell growth. An analogue of GLP-1 hormone has already been approved by the FDA for treating type 2 diabetes. The goal is to understand how GLP-1 and MCH can work together to promote beta cell growth.


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Contact: Marjorie Dwyer
marjorie.dwyer@joslin.harvard.edu
617-732-2415
Joslin Diabetes Center
26-Jan-2007


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