 Free fatty acids regulate insulin secretion from pancreatic β cells through GPR40Yasuaki Itoh,
Yuji Kawamata,
Masataka Harada,
Makoto Kobayashi,
Ryo Fujii,
Shoji Fukusumi,
Kazuhiro Ogi,
Masaki Hosoya,
Yasuhiro Tanaka,
Hiroshi Uejima,
Hideyuki Tanaka,
Minoru Maruyama,
Rie Satoh,
Shoichi Okubo,
Hideki Kizawa,
Hidetoshi Komatsu,
Fumika Matsumura,
Yuko Noguchi,
Tokuyuki Shinohara,
Shuji Hinuma (),
Yukio Fujisawa and
Masahiko Fujino
Nature, 2003, vol. 422, issue 6928, 173-176 Abstract: Abstract Diabetes, a disease in which carbohydrate and lipid metabolism are regulated improperly by insulin, is a serious worldwide health issue1,2. Insulin is secreted from pancreatic β cells in response to elevated plasma glucose, with various factors modifying its secretion3. Free fatty acids (FFAs) provide an important energy source as nutrients, and they also act as signalling molecules in various cellular processes, including insulin secretion4,5. Although FFAs are thought to promote insulin secretion in an acute phase, this mechanism is not clearly understood6. Here we show that a G-protein-coupled receptor, GPR40, which is abundantly expressed in the pancreas, functions as a receptor for long-chain FFAs. Furthermore, we show that long-chain FFAs amplify glucose-stimulated insulin secretion from pancreatic β cells by activating GPR40. Our results indicate that GPR40 agonists and/or antagonists show potential for the development of new anti-diabetic drugs. Date: 2003 Downloads: (external link) Related works: Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:422:y:2003:i:6928:d:10.1038_nature01478 Ordering information: This journal article can be ordered from DOI: 10.1038/nature01478 Access Statistics for this article Nature is currently edited by Magdalena Skipper More articles in Nature from Nature |
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