Tags

Type your tag names separated by a space and hit enter

Ghrelin stimulates, whereas des-octanoyl ghrelin inhibits, glucose output by primary hepatocytes.
J Clin Endocrinol Metab. 2005 Feb; 90(2):1055-60.JC

Abstract

Ghrelin exerts various metabolic activities, including regulation of glucose levels in humans. To verify whether the glucose response to ghrelin reflects a modulation of an insulin-independent hepatic phenomenon, we studied glucose output by primary porcine hepatocytes in suspension culture, after incubation with acylated ghrelin (AG), unacylated ghrelin (UAG), and hexarelin (HEX). AG induced glucose output dose dependently after 20 min of incubation (P < 0.001), whereas HEX, a GH secretagogue receptor type 1a (GHS-R1a) agonist, had no effect. UAG inhibited glucose release also dose dependently and after 20 min (P < 0.001). Moreover, UAG completely reversed AG-induced glucose output (P < 0.01). Using real-time PCR, GHS-R1a gene expression was undetectable in all the hepatocyte preparations studied. The lack of efficacy of HEX, the efficacy of UAG, and the absence of GHS-R1a expression indicate the involvement of a yet uncharacterized ghrelin receptor type. In conclusion, glucose output by primary hepatocytes is time- and dose-dependently stimulated by AG and inhibited by UAG. Moreover, UAG counteracts the stimulatory effect of AG on glucose release. These actions might be mediated by a different receptor than GHS-R1a, and apparently, we must consider AG and UAG as separate hormones that can modify each other's actions on glucose handling, at least in the liver.

Authors+Show Affiliations

Department of Internal Medicine, Section of Endocrinology, Erasmus MC, 3015 GE Rotterdam, The Netherlands. c.gauna@erasmusmc.nlNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15536157

Citation

Gauna, Carlotta, et al. "Ghrelin Stimulates, Whereas Des-octanoyl Ghrelin Inhibits, Glucose Output By Primary Hepatocytes." The Journal of Clinical Endocrinology and Metabolism, vol. 90, no. 2, 2005, pp. 1055-60.
Gauna C, Delhanty PJ, Hofland LJ, et al. Ghrelin stimulates, whereas des-octanoyl ghrelin inhibits, glucose output by primary hepatocytes. J Clin Endocrinol Metab. 2005;90(2):1055-60.
Gauna, C., Delhanty, P. J., Hofland, L. J., Janssen, J. A., Broglio, F., Ross, R. J., Ghigo, E., & van der Lely, A. J. (2005). Ghrelin stimulates, whereas des-octanoyl ghrelin inhibits, glucose output by primary hepatocytes. The Journal of Clinical Endocrinology and Metabolism, 90(2), 1055-60.
Gauna C, et al. Ghrelin Stimulates, Whereas Des-octanoyl Ghrelin Inhibits, Glucose Output By Primary Hepatocytes. J Clin Endocrinol Metab. 2005;90(2):1055-60. PubMed PMID: 15536157.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ghrelin stimulates, whereas des-octanoyl ghrelin inhibits, glucose output by primary hepatocytes. AU - Gauna,Carlotta, AU - Delhanty,Patric J D, AU - Hofland,Leo J, AU - Janssen,Joop A M J L, AU - Broglio,Fabio, AU - Ross,Richard J M, AU - Ghigo,Ezio, AU - van der Lely,Aart Jan, Y1 - 2004/11/09/ PY - 2004/11/13/pubmed PY - 2005/3/25/medline PY - 2004/11/13/entrez SP - 1055 EP - 60 JF - The Journal of clinical endocrinology and metabolism JO - J Clin Endocrinol Metab VL - 90 IS - 2 N2 - Ghrelin exerts various metabolic activities, including regulation of glucose levels in humans. To verify whether the glucose response to ghrelin reflects a modulation of an insulin-independent hepatic phenomenon, we studied glucose output by primary porcine hepatocytes in suspension culture, after incubation with acylated ghrelin (AG), unacylated ghrelin (UAG), and hexarelin (HEX). AG induced glucose output dose dependently after 20 min of incubation (P < 0.001), whereas HEX, a GH secretagogue receptor type 1a (GHS-R1a) agonist, had no effect. UAG inhibited glucose release also dose dependently and after 20 min (P < 0.001). Moreover, UAG completely reversed AG-induced glucose output (P < 0.01). Using real-time PCR, GHS-R1a gene expression was undetectable in all the hepatocyte preparations studied. The lack of efficacy of HEX, the efficacy of UAG, and the absence of GHS-R1a expression indicate the involvement of a yet uncharacterized ghrelin receptor type. In conclusion, glucose output by primary hepatocytes is time- and dose-dependently stimulated by AG and inhibited by UAG. Moreover, UAG counteracts the stimulatory effect of AG on glucose release. These actions might be mediated by a different receptor than GHS-R1a, and apparently, we must consider AG and UAG as separate hormones that can modify each other's actions on glucose handling, at least in the liver. SN - 0021-972X UR - https://www.unboundmedicine.com/medline/citation/15536157/Ghrelin_stimulates_whereas_des_octanoyl_ghrelin_inhibits_glucose_output_by_primary_hepatocytes_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2004-1069 DB - PRIME DP - Unbound Medicine ER -