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Unacylated ghrelin is active on the INS-1E rat insulinoma cell line independently of the growth hormone secretagogue receptor type 1a and the corticotropin releasing factor 2 receptor.

Authors: Gauna, Carlotta  Delhanty, Patric J D  van Aken, Maarten O  Janssen, Joop A M J L  Themmen, Axel P N  Hofland, Leo J  Culler, Michael  Broglio, Fabio  Ghigo, Ezio  van der Lely, Aart Jan 
Citation: Gauna C, etal., Mol Cell Endocrinol. 2006 Jun 7;251(1-2):103-11. Epub 2006 Apr 27.
Pubmed: (View Article at PubMed) PMID:16647196
DOI: Full-text: DOI:10.1016/j.mce.2006.03.040

Both unacylated ghrelin (UAG) and acylated ghrelin (AG) exert metabolic effects. To investigate the interactions between AG and UAG on ghrelin receptors we evaluated the effects of AG and UAG on INS-1E rat insulinoma cells, using insulin secretion after 30min static incubation as a read-out. A possible involvement of the growth hormone secretagogue receptor type 1a (GHS-R1a) or the corticotropin-releasing factor 2 (CRF2) receptor (CRF2R), as a putative receptor for UAG, was also studied determining their mRNA expression and the functional effects of receptor antagonists on insulin release. Both UAG and AG stimulated insulin release dose-dependently in the nanomolar range. The AG-induced insulin output was antagonized by two GHS-R1a antagonists ([d-Lys(3)]GHRP-6 and BIM28163), which did not block UAG actions. These effects occurred in the presence of low levels of GHS-R1a mRNA. Neither CRF2R expression nor effects of the CRF2R antagonist (astressin(2)B) on insulin output were observed. In conclusion, we provide a sensitive and reproducible assay for specific effects of UAG, which in this study is responsible for insulin release by INS-1E cells. Our data support the existence of a specific receptor for UAG, other than the CRF2R and GHS-R1a. The stimulatory effect on insulin secretion by AG in this cell line is mediated by the GHS-R1a.


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CRRD Object Information
CRRD ID: 12905046
Created: 2017-06-05
Species: All species
Last Modified: 2017-06-05
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.