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Int. J. Mol. Sci. 2015, 16(12), 29207-29218; doi:10.3390/ijms161226156

The Dipeptidyl Peptidase-4 Inhibitor Teneligliptin Attenuates Hepatic Lipogenesis via AMPK Activation in Non-Alcoholic Fatty Liver Disease Model Mice

1
Department of Gastroenterology, Internal Medicine, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu 501-1194, Japan
2
Informative Clinical Medicine, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu 501-1194, Japan
*
Author to whom correspondence should be addressed.
Academic Editor: Amedeo Lonardo
Received: 19 October 2015 / Revised: 24 November 2015 / Accepted: 30 November 2015 / Published: 8 December 2015
(This article belongs to the Special Issue Non-Alcoholic Fatty Liver Disease Research 2016)
View Full-Text   |   Download PDF [3031 KB, uploaded 8 December 2015]   |  

Abstract

Non-alcoholic fatty liver disease (NAFLD), which is strongly associated with metabolic syndrome, is increasingly a major cause of hepatic disorder. Dipeptidyl peptidase (DPP)-4 inhibitors, anti-diabetic agents, are expected to be effective for the treatment of NAFLD. In the present study, we established a novel NAFLD model mouse using monosodium glutamate (MSG) and a high-fat diet (HFD) and investigated the effects of a DPP-4 inhibitor, teneligliptin, on the progression of NAFLD. Male MSG/HFD-treated mice were divided into two groups, one of which received teneligliptin in drinking water. Administration of MSG and HFD caused mice to develop severe fatty changes in the liver, but teneligliptin treatment improved hepatic steatosis and inflammation, as evaluated by the NAFLD activity score. Serum alanine aminotransferase and intrahepatic triglyceride levels were significantly decreased in teneligliptin-treated mice (p < 0.05). Hepatic mRNA levels of the genes involved in de novo lipogenesis were significantly downregulated by teneligliptin (p < 0.05). Moreover, teneligliptin increased hepatic expression levels of phosphorylated AMP-activated protein kinase (AMPK) protein. These findings suggest that teneligliptin attenuates lipogenesis in the liver by activating AMPK and downregulating the expression of genes involved in lipogenesis. DPP-4 inhibitors may be effective for the treatment of NAFLD and may be able to prevent its progression to non-alcoholic steatohepatitis. View Full-Text
Keywords: AMPK; DPP-4 inhibitor; lipogenesis; non-alcoholic fatty liver disease; NAFLD; SREBP1c; teneligliptin AMPK; DPP-4 inhibitor; lipogenesis; non-alcoholic fatty liver disease; NAFLD; SREBP1c; teneligliptin
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Ideta, T.; Shirakami, Y.; Miyazaki, T.; Kochi, T.; Sakai, H.; Moriwaki, H.; Shimizu, M. The Dipeptidyl Peptidase-4 Inhibitor Teneligliptin Attenuates Hepatic Lipogenesis via AMPK Activation in Non-Alcoholic Fatty Liver Disease Model Mice. Int. J. Mol. Sci. 2015, 16, 29207-29218.

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