onr:"swepub:oai:DiVA.org:umu-23321"
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03225naa a2200289 4500 | |
| 001 | oai:DiVA.org:umu-23321 | |
| 003 | SwePub | |
| 008 | 090610s2008 | |||||||||||000 ||eng| | |
| 024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-233212 URI |
| 024 | 7 | a https://doi.org/10.2337/db08-03072 DOI |
| 040 | a (SwePub)umu | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Edfalk, Sarau Umeå universitet,Umeå centrum för molekylär medicin (UCMM),Edlund Helena4 aut0 (Swepub:umu)saaedk98 |
| 245 | 1 0 | a Gpr40 is expressed in enteroendocrine cells and mediates free fatty acid stimulation of incretin secretion. |
| 264 | 1 | b American Diabetes Association,c 2008 |
| 338 | a print2 rdacarrier | |
| 520 | a OBJECTIVE: The G-protein-coupled receptor Gpr40 is expressed in beta-cells where it contributes to free fatty acid (FFA) enhancement of glucose-stimulated insulin secretion. However, other sites of Gpr40 expression, including the intestine, have been suggested. The transcription factor IPF1/PDX1 was recently shown to bind to an enhancer element within the 5'-flanking region of Gpr40, implying that IPF1/PDX1 might regulate Gpr40 expression. Here, we addressed whether 1) Gpr40 is expressed in the intestine and 2) Ipf1/Pdx1 function is required for Gpr40 expression. RESEARCH DESIGN AND METHODS: In the present study, Gpr40 expression was monitored by X-gal staining using Gpr40 reporter mice and by in situ hybridization. Ipf1/Pdx1-null and beta-cell specific mutants were used to investigate whether Ipf1/Pdx1 controls Gpr40 expression. Plasma insulin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and glucose levels in response to acute oral fat diet were determined in Gpr40 mutant and control mice. RESULTS: Here, we show that Gpr40 is expressed in endocrine cells of the gastrointestinal tract, including cells expressing the incretin hormones GLP-1 and GIP, and that Gpr40 mediates FFA-stimulated incretin secretion. We also show that Ipf1/Pdx1 is required for expression of Gpr40 in beta-cells and endocrine cells of the anterior gastrointestinal tract. CONCLUSIONS: Together, our data provide evidence that Gpr40 modulates FFA-stimulated insulin secretion from beta-cells not only directly but also indirectly via regulation of incretin secretion. Moreover, our data suggest a conserved role for Ipf1/Pdx1 and Gpr40 in FFA-mediated secretion of hormones that regulate glucose and overall energy homeostasis. | |
| 700 | 1 | a Steneberg, Päru Umeå universitet,Umeå centrum för molekylär medicin (UCMM),Edlund Helena4 aut0 (Swepub:umu)past0002 |
| 700 | 1 | a Edlund, Helena,d 1960-u Umeå universitet,Umeå centrum för molekylär medicin (UCMM),Edlund Helena4 aut0 (Swepub:umu)heed0001 |
| 710 | 2 | a Umeå universitetb Umeå centrum för molekylär medicin (UCMM)4 org |
| 773 | 0 | t Diabetesd : American Diabetes Associationg 57:9, s. 2280-7q 57:9<2280-7x 1939-327Xx 0012-1797 |
| 856 | 4 | u http://diabetes.diabetesjournals.org/content/57/9/2280.full.pdf |
| 856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-23321 |
| 856 | 4 8 | u https://doi.org/10.2337/db08-0307 |
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