Authors: Yoshida, T.¹; Yamagishi, S.¹; Matsui, T.¹; Nakamura, K.¹; Ueno, T.¹; Takeuchi, M.²; Sata, M.¹

Source: The Journal of International Medical Research, Volume 36, Number 2, March 2008 , pp. 237-243(7)

Publisher: Field House Publishing

Abstract:

This study examined whether telmisartan, a unique angiotensin II type 1 receptor blocker (ARB) with peroxisome proliferator-activated receptor-γ (PPAR-γ)-modulating activity, improved insulin resistance in advanced glycation end-product (AGE)-exposed human hepatoma (Hep3B) cells. AGE increased phosphorylation of insulin receptor substrate-1 (IRS-1) at serine-307 residues in Hep3B cells. It also decreased tyrosine phosphorylation of IRS-1 and, subsequently, reduced the association of the p85 subunit of phosphatidylinositol 3-kinase with IRS-1 and glycogen synthesis in insulin-exposed Hep3B cells, all of which were inhibited by telmisartan. The insulin-sensitizing properties of telmisartan in AGE-exposed Hep3B cells were significantly blocked by GW9662, an inhibitor of PPAR-γ. Candesartan, another ARB, did not affect AGEs-induced serine phosphorylation of IRS-1 at serine-307 residues in Hep3B cells. Our study suggests that telmisartan could improve AGE-elicited insulin resistance in Hep3B cells by inhibiting serine phosphorylation of IRS-1, at least in part, via activation of PPAR-γ. Telmisartan may play a protective role against hepatic insulin resistance in diabetes.

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Keywords: ADVANCED GLYCATION END-PRODUCTS (AGES); TELMISARTAN; PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-GAMMA(P; INSULIN RECEPTOR SUBSTRATE-1 (IRS-1); HEPATIC INSULIN RESISTANCE; HUMAN HEPATOMA CELLS

Document Type: Research article

Affiliations: 1: Department of Medicine, Kurume University School of Medicine, Kurume, Japan 2: Department of Pathophysiological Science, Faculty of Pharmaceutical Science, Hokuriku University, Kanazawa, Japan

Publication date: 2008-03-01

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