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The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Treatment with SRT1720, a SIRT1 activator, ameliorates fatty liver with reduced expression of lipogenic enzymes in MSG mice

Yamazaki, Yu, Usui, Isao, Kanatani, Yukiko, Matsuya, Yuji, Tsuneyama, Koichi, Fujisaka, Shiho, Bukhari, Agussalim, Suzuki, Hikari, Senda, Satoko, Imanishi, Shingo, Hirata, Kazuya, Ishiki, Manabu, Hayashi, Ryuji, Urakaze, Masaharu, Nemoto, Hideo, Kobayashi, Masashi, Tobe, Kazuyuki·2009·American Journal of Physiology-Endocrinology and Metabolism
DOI 10.1152/ajpendo.90997.2008
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Abstract

Nonalcoholic fatty liver disease (NAFLD) is an abnormal liver metabolism often observed with insulin resistance and metabolic syndrome. Calorie restriction is a useful treatment for NAFLD and reportedly prolongs the life spans of several species in which sirtuin plays an important role. In this study, we examined whether the activation of SIRT1, a mammalian ortholog of sirtuin, may ameliorate the development of NAFLD. Monosodium glutamate (MSG) mice, which exhibited obesity and insulin resistance, were treated with SRT1720, a specific SIRT1 activator from the age of 6–16 wk. Sixteen-week-old MSG mice exhibited increased liver triglyceride content and elevated levels of aminotransferase. SRT1720 treatment significantly reduced these levels without affecting body weight or food intake. These results suggested that the administration of SRT1720 ameliorated the development of NAFLD in MSG mice. The expressions of lipogenic genes, such as sterol regulatory element-binding protein-1c, acetyl-CoA carboxylase, and fatty acid synthase, and the serum lipid profiles, including free fatty acids, were elevated in MSG mice and were reduced by SRT1720 treatment. SRT1720 treatment also reduced the expressions of lipogenic genes in cultured HepG2 cells. Furthermore, SRT1720 treatment decreased the expressions of marker genes for oxidative stress and inflammatory cytokines in the liver of MSG mice. Taken together, SRT1720 treatment may reduce liver lipid accumulation, at least in part, by directly reducing the expressions of lipogenic genes. The reduction of oxidative stress and inflammation may also be involved in the amelioration of NAFLD.

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Crossref · 10.1152/ajpendo.90997.2008

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Research works printed but not linked: 25

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Metadata

Authors
Yamazaki, Y., Usui, I., Kanatani, Y., Matsuya, Y., Tsuneyama, K., Fujisaka, S., Bukhari, A., Suzuki, H., Senda, S., Imanishi, S., Hirata, K., Ishiki, M., Hayashi, R., Urakaze, M., Nemoto, H., Kobayashi, M., & Tobe, K.
Affiliations
  • First Department of Internal Medicine,
  • Graduate School of Medicine and Pharmaceutical Sciences,
  • The Department of Diagnostic Pathology,
  • University Hospital, University of Toyama, Toyama, Japan
Venue
American Journal of Physiology-Endocrinology and Metabolism
Publisher
American Physiological Society
Published
2009-11
Volume
297
Issue
5
Pages
E1179-E1186
ISSN
  • 0193-1849
  • 1522-1555
DOI
10.1152/ajpendo.90997.2008
Cited by
137
References
5
Language
en

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