( CAMBRIDGE Mass.--(BUSINESS WIRE)--Jun ...)Elixir Pharmaceuticals Presents Additional Preclinical Data,Demonstrating the Potential of Ghrelin Antagonism to Regulate,Metabolism, Body Weight and Glycemic Control,Health

CAMBRIDGE, Mass.--(BUSINESS WIRE)--Jun 5, 2007 - Elixir Pharmaceuticals, Inc., announced today new preclinical data confirming ghrelin antagonism as a potential method for regulating metabolism, decreasing body weight and managing blood glucose. The data were presented in poster sessions during ENDO 07, The Endocrine Society's 89th Annual Meeting, being held in Toronto, Canada. Elixir is focused on the development of drugs to treat and prevent metabolic disease, as well as prevent age-related diseases, based on targets identified in the pathways regulating aging.

Ghrelin is a key metabolic regulator that is known to stimulate appetite and food consumption and is believed to play a key role in metabolism and energy storage. Ghrelin is a naturally occurring hormone secreted by the stomach, which acts primarily at the level of the hypothalamus in the brain.

In the first presentation, Elixir scientists explored whether ghrelin exerts a direct effect on adipocytes (fat cells) and if the effect is mediated through ghrelin receptor (GhrR) mRNA expression in these cells. To assess this, the scientists first examined ghrelin signaling by measuring insulin sensitivity in mouse adipocyte cell lines that were treated with ghrelin for four days. Scientists also assessed the expression of GhrR mRNA in adipose tissue, isolated adipocytes from mice, and the mouse adipocyte cell-line. The results showed GhrR was detected in the isolated adipocytes and mouse adipocyte cell lines, suggesting ghrelin acts directly through its receptor on adipocytes to regulate energy homeostasis. Moreover, the reduction of insulin signaling in adipocytes by chronic ghrelin treatment provides a possible mechanism for increased insulin sensitivity in GhrR knockout mice.

In two additional tandem presentations, Elixir scientists showed that, compared to control mice, GhrR knockout mice resisted the development of diabetes and obesity ass
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