Telmisartan increases lipoprotein lipase expression via peroxisome proliferator-activated receptor-alpha in HepG2 cells. (May 2014)

• Record Type: Journal Article
• Authors: Yin, Shi Nan; Liu, Min; Jing, Dan Qing; Mu, Yi Ming; Lu, Ju Ming; Pan, Chang Yu
• Is Part Of: Endocrine research. Volume 39:Number 2(2014:May)
• Page Start: 67
• Page End: 73
• Publication Date: 2014-05
• Subjects: Endocrinology, Experimental -- Periodicals; Endocrinology -- Periodicals; Endocrinology -- Periodicals; Research -- Periodicals; 616.4
• DOI: 10.3109/07435800.2013.828741
• Languages: English
• ISSNs: 0743-5800

Abstract

<abstract> <title>Abstract</title> <p>In addition to their hypotensive properties, angiotensin receptor blockers (ARBs) have been shown to exert clinical antidyslipidemic effects. The mechanism underlying these ARB lipid metabolic effects remains unclear. Some ARBs, for example, telmisartan, activate peroxisome proliferator-activated activated receptor-gamma (PPAR-gamma). We hypothesized that PPAR-gamma–activating ARBs might exert antidyslipidemic effects via PPAR-alpha. In this study, we assessed the effect of telmisartan on the expression of PPAR-alpha and lipoprotein lipase (LPL). PPAR-alpha expression was detected by reverse-transcription polymerase chain reaction and Western blot in HepG2 hepatocytes as well as differentiated C2C12 myocytes treated with increasing concentrations of telmisartan (0.1–10 μmol/L) for 48 h. Results showed that 1 μmol/L and 10 μmol/L telmisartan significantly increased the expression of PPAR-alpha mRNA and protein in HepG2 cells (<italic>p</italic> < 0.01). No effect was shown in differentiated C2C12 cells. Similarly, 1 µmol/L and 10 μmol/L telmisartan significantly increased the expression of LPL mRNA and protein in HepG2 cells (<italic>p</italic> < 0.01), and this increase was significantly (<italic>p</italic> < 0.01) inhibited by the PPAR-alpha–specific antagonist MK886. These results indicate that certain of the antidyslipidemic effects of telmisartan might be mediated via increased PPAR-alpha–dependent induction of LPL expression.</p> </abstract>