edoc

Glucose-dependent insulinotropic polypeptide induces cytokine expression, lipolysis, and insulin resistance in human adipocytes

Timper, Katharina and Grisouard, Jean and Sauter, Nadine S. and Herzog-Radimerski, Tanja and Dembinski, Kaethi and Peterli, Ralph and Frey, Daniel M. and Zulewski, Henryk and Keller, Ulrich and Muller, Beat and Christ-Crain, Mirjam. (2013) Glucose-dependent insulinotropic polypeptide induces cytokine expression, lipolysis, and insulin resistance in human adipocytes. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 304 (1). pp. 1-8.

Full text not available from this repository.

Official URL: http://edoc.unibas.ch/dok/A6419825

Downloads: Statistics Overview

Abstract

Obesity-related insulin resistance is linked to a chronic state of systemic and adipose tissue-derived inflammation. Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone also acting on adipocytes. We investigated whether GIP affects inflammation, lipolysis, and insulin resistance in human adipocytes. Human subcutaneous preadipocyte-derived adipocytes, differentiated in vitro, were treated with human GIP to analyze mRNA expression and protein secretion of cytokines, glycerol, and free fatty acid release and insulin-induced glucose uptake. GIP induced mRNA expression of IL-6, IL-1beta, and the IL-1 receptor antagonist IL-1Ra, whereas TNFalpha, IL-8, and monocyte chemotactic protein (MCP)-1 remained unchanged. Cytokine induction involved PKA and the NF-kappaB pathway as well as an autocrine IL-1 effect. Furthermore, GIP potentiated IL-6 and IL-1Ra secretion in the presence of LPS, IL-1beta, and TNFalpha. GIP induced lipolysis via activation of hormone-sensitive lipase and was linked to NF-kappaB activation. Finally, chronic GIP treatment impaired insulin-induced glucose uptake possibly due to the observed impaired translocation of glucose transporter GLUT4. In conclusion, GIP induces an inflammatory and prolipolytic response via the PKA -NF-kappaB-IL-1 pathway and impairs insulin sensitivity of glucose uptake in human adipocytes.
Faculties and Departments:03 Faculty of Medicine > Bereich Medizinische Fächer (Klinik) > Ehemalige Einheiten Medizinische Fächer (Klinik) > Klinische Endokrinologie (Keller)
03 Faculty of Medicine > Departement Klinische Forschung > Bereich Medizinische Fächer (Klinik) > Ehemalige Einheiten Medizinische Fächer (Klinik) > Klinische Endokrinologie (Keller)
03 Faculty of Medicine > Departement Biomedizin > Former Units at DBM > Metabolism (Keller/Müller)
UniBasel Contributors:Keller, Ulrich O. and Müller, Beat
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:American Physiological Society
ISSN:0002-9513
e-ISSN:1522-1490
Note:Publication type according to Uni Basel Research Database: Journal article
Identification Number:
Last Modified:30 Nov 2017 12:48
Deposited On:02 Oct 2015 10:00

Repository Staff Only: item control page