The relationship between GPR40 and lipotoxicity of the pancreatic β-cells as well as the effect of pioglitazone

Biochemical and Biophysical Research Communications

Volumn 403, Issue 1, 2010, Pages 36-39

  Wu, Peiwen ^a   Yang, Liyong ^a   Shen, Ximei ^a  

^a FUJIAN MEDICAL UNIVERSITY   (China)

Author keywords

TC6 cells; Free fatty acids; GPR40; Insulin secretion; Short hairpin RNA

Indexed keywords

FATTY ACID; G PROTEIN COUPLED RECEPTOR 40; GLUCOSE; GLUCOSE TRANSPORTER 2; INSULIN; PIOGLITAZONE; SHORT HAIRPIN RNA; TRANSCRIPTION FACTOR PDX 1;

ANIMAL CELL; ARTICLE; CHRONIC TOXICITY; CYTOTOXICITY; GENE EXPRESSION; GENETIC TRANSFECTION; INSULIN RELEASE; MOUSE; NONHUMAN; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL;

ANIMALS; CELL LINE, TUMOR; FATTY ACIDS, NONESTERIFIED; GENE KNOCKDOWN TECHNIQUES; GLUCOSE; HYPOGLYCEMIC AGENTS; INSULIN; INSULIN-SECRETING CELLS; MICE; PLASMIDS; RECEPTORS, G-PROTEIN-COUPLED; THIAZOLIDINEDIONES;

EID: 78649694041     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2010.10.105     Document Type: Article

References (24)

1. Nagasumi K., Esaki R., Iwachidow K., Yasuhara Y., Ogi K., Tanaka H., Nakata M., Yano T., Shimakawa K., Taketomi S., Takeuchi K., Odaka H., Kaisho Y. Overexpression of GPR40 in pancreatic beta-cells augments glucose-stimulated insulin secretion and improves glucose tolerance in normal and diabetic mice. Diabetes 2009, 58:1067-1076.
2. Briscoe C.P., Tadayyon M., Andrews J.L., Benson W.G., Chambers J.K., Eilert M.M., Ellis C., Elshourbagy N.A., Goetz A.S., Minnick D.T., et al. The orphan G protein coupled receptor GPR40 is activated by medium and long chain fatty acids. J. Biol. Chem. 2003, 278:11303-11311.
3. Itoh Y., Kawamata Y., Harada M., Kobayashi M., Fujii R., Fukusumi S., Ogi K., Hosoya M., Tanaka Y., Uejima H., et al. Free fatty acids regulate insulin secretion from pancreatic β cells through GPR40. Nature 2003, 422:173-176.
4. Kotarsky K., Nilsson N.E., Flodgren E., Owman C., Olde B. A human cell surface receptor activated by free fatty acids and thiazolidinedione drugs. Biochem. Biophys. Res. Commun. 2003, 301:406-410.
5. Steneberg P., Rubins N., Bartoov-Shifman R., Walker M.D., Edlund H. The FFA receptor GPR40 links hyperinsulinemia, hepatic steatosis, and impaired glucose homeostasis in mouse. Cell Metab. 2005, 1:245-258.
6. Latour M.G., Alquier T., Oseid E., Tremblay C., Jetton T.L., Luo J., Lin D.C., Poitout V. GPR40 is necessary but not sufficient for fatty acid stimulation of insulin secretion in vivo. Diabetes 2007, 56:1087-1094.
7. Tan C.P., Feng Y., Zhou Y.P., Eiermann G.J., Petrov A., Zhou C., Lin S., Salituro G., Meinke P., Mosley R., et al. Selective small-molecule agonists of G protein-coupled receptor 40 promote glucose-dependent insulin secretion and reduce blood glucose in mice. Diabetes 2008, 57:2211-2219.
8. Lan H., Hoos L.M., Liu L., Tetzloff G., Hu W., Abbondanzo S.J., Vassileva G., Gustafson E.L., Hedrick J.A., Davis H.R. Lack of FFAR1/GPR40 does not protect mice from high-fat diet-induced metabolic disease. Diabetes 2008, 57:2999-3006.
9. Kebede M., Alquier T., Latour M.G., Semache M., Tremblay C., Poitout V. The fatty acid receptor GPR40 plays a role in insulin secretion in vivo after high-fat feeding. Diabetes 2008, 57:2432-2437.
10. Poitout V., Stout L.E., Armstrong M.B., Walseth T.F., Sorensen R.L., Robertson R.P. Morphological and functional characterization of βTC-6 cells-an insulin-secreting cell line derived from transgonic mice. Diabetes 1995, 44:306-313.
11. Zraika S., Dunlop M., Proietto J., Anrikopoulos S. Effects of free fatty acids on insulin secretion in obesity. Obesity Rev. 2002, 3:103-112.
12. Haber E.P., Ximenes H.M., Procopio J., Carvalho C.R., Curi R., Carpinelli A.R. Pleiotropic effects of fatty acids on pancreatic beta-cells. J. Cell. Physiol. 2003, 194:1-12.
13. Yaney G.C., Corkey B.E. Fatty acid metabolism and insulin secretion in pancreatic beta cells. Diabetologia 2003, 46:1297-1312.
14. Lee Y., Hirose H., Ohneda M., Johnson J.H., Mcgarry J.D., Unger R.H. β-Cell lipotoxicity in the pathogenesis of non-insulin dependent diabetes mellitus of obese rats: impairment in adipocyteb-cell relationships. PNAS 1994, 91:10878-10882.
15. Zhou Y.P., Grill V. Long-term exposure to fatty acids and ketones inhibits β-cell functions in human pancreatic islets of Langerhans. J. Clin. Endocrinol. Metab. 1995, 80:1584-1590.
16. Lupi R., Del Guerra S., Fierabracci V., Marselli L., Novelli M., Patane G., Boggi U., Mosca F., Piro S., Del Prato S., et al. Lipotoxicity in human pancreatic islets and the protective effect of metformin. Diabetes 2002, 51(Suppl. 1):S134-S137.
17. Shimabukuro M., Zhou Y.T., Levi M., Unger R.H. Fatty acid induced β cell apoptosis: a link between obesity and diabetes. Proc. Natl. Acad. Sci. USA 1998, 95:2498-2502.
18. Prentki M., Joly E., El-Assaad W., Roduit R. Malonyl-CoA signaling, lipid partitioning, and glucolipotoxicity: role in β-cell adaptation and failure in the etiology of diabetes. Diabetes 2002, 51(Suppl. 3):S405-S413.
19. Schnell S., Schaefer M., Schöfl C. Free fatty acids increase cytosolic free calcium and stimulate insulin secretion from β-cells through activation of GPR40. Mol. Cell. Endocrinol. 2007, 263:173-180.
20. Ahlgren U., Jonsson J., Jonsson L., Simu K., Edlund H. Beta-cell-specific inactivation of the mouse Ipf1/Pdx1 gene results in loss of the beta-cell phenotype and maturity onset diabetes. Genes 1998, 12:1763-1768.
21. Hart A.W., Baeza N., Apelqvist A., Edlund H. Attenuation of FGF signalling in mouse beta-cells leads to diabetes. Nature 2000, 408:864-868.
22. Li Y., Cao X., Li L.X., Brubaker P.L., Edlund H., Drucker D.J. β-Cell Pdx1 expression is essential for the glucoregulatory, proliferative, and cytoprotective actions of glucagon-like peptide-1. Diabetes 2005, 54:482-491.
23. Edfalk S., Steneberg P., Edlund H. Gpr40 is expressed in enteroendocrine cells and mediates free fatty acid stimulation of incretin secretion. Diabetes 2008, 57:2280-2287.
24. Stoddart L.A., Brown A.J., Milligan G. Uncovering the pharmacology of the G protein-coupled receptor GPR40: high apparent constitutive activity in guanosine 5′-O-(3-[35S]thio) triphosphate binding studies reflects binding of an endogenous agonist. Mol. Pharmacol. 2007, 71:994-1005.