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In diabetes sufferers, insulin fails to regulate carbohydrate and lipid metabolism properly. Various factors modify the way that insulin is secreted from pancreatic b cells in response to raised glucose in the blood plasma. Free fatty acids (FFAs) provide an important energy source as nutrients, and act as signalling molecules in various cellular processes including insulin secretion. Although FFAs are thought to promote insulin secretion, this mechanism is not clearly understood.
In a Nature paper published online this week, Shuji Hinuma and colleagues at Takeda Chemical Industries Ltd in Japan, show that a G-protein-coupled receptor, GPR40, which is abundantly expressed in the pancreas, functions as a receptor for long-chain FFAs. Furthermore, the team shows that long-chain FFAs amplify glucose-stimulated insulin secretion from pancreatic b cells by activating GPR40. These results indicate that molecules that block or boost GPR40 could have potential for the development of new anti-diabetic drugs. "We believe that our results will provide new insight into insulin secretion mechanisms and the treatment of diabetes," the researchers conclude. Author contact: Mr Shoji Wakayama
Corporate Communications Department
Takeda Chemical Industries Ltd
Tsukuba, Japan
Tel: +81 6 6204 2412
E-mail: Wakayama_shouji@takeda.co.jp (C) Nature press release.
Message posted by: Trevor M. D'Souza
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