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Ueno T, Nakamura A, Nakayama H, et al. Adiponectin suppresses endoplasmic reticulum stress in nonalcoholic steatohepatitis. Exp Ther Med. 2011;2(6):1035-1040doi: 10.3892/etm.2011.348.
Ueno, T., Nakamura, A., Nakayama, H., Otabe, S., Yuan, X., Fukutani, T., Iwamoto, H., Nakamura, T., Koga, H., Torimura, T., Sata, M., & Yamada, K. (2011). Adiponectin suppresses endoplasmic reticulum stress in nonalcoholic steatohepatitis. Experimental and therapeutic medicine, 2(6), 1035-1040. https://doi.org/10.3892/etm.2011.348
Ueno, Takato, et al. "Adiponectin suppresses endoplasmic reticulum stress in nonalcoholic steatohepatitis." Experimental and therapeutic medicine vol. 2,6 (2011): 1035-1040. doi: https://doi.org/10.3892/etm.2011.348
Ueno T, Nakamura A, Nakayama H, Otabe S, Yuan X, Fukutani T, Iwamoto H, Nakamura T, Koga H, Torimura T, Sata M, Yamada K. Adiponectin suppresses endoplasmic reticulum stress in nonalcoholic steatohepatitis. Exp Ther Med. 2011 Nov;2(6):1035-1040. doi: 10.3892/etm.2011.348. Epub 2011 Sep 02. PMID: 22977616; PMCID: PMC3440812.
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Exp Ther Med. 2011 Nov;2(6):1035-1040. doi: 10.3892/etm.2011.348. Epub 2011 Sep 02.

Adiponectin suppresses endoplasmic reticulum stress in nonalcoholic steatohepatitis.

Experimental and therapeutic medicine

Takato Ueno, Anna Nakamura, Hitomi Nakayama, Shuichi Otabe, Xiaohong Yuan, Tomoka Fukutani, Hideki Iwamoto, Toru Nakamura, Hironori Koga, Takuji Torimura, Michio Sata, Kentaro Yamada

Affiliations

  1. Research Center for Innovative Cancer Therapy, Kurume University;

PMID: 22977616 PMCID: PMC3440812 DOI: 10.3892/etm.2011.348

Abstract

In this study, we examined whether adiponectin suppresses endoplasmic reticulum (ER) stress in nonalcoholic steatohepatitis (NASH) using male transgenic mice expressing nSREBP-1c in adipose tissue, nSREBP-1c/adiponectin double-transgenic mice expressing human adiponectin in the liver, and wild-type male mice as the control. Histological findings similar to those observed in liver specimens from patients with NASH were observed in the livers from the nSREBP-1c transgenic mice at 30 weeks of age. By contrast, the NASH-like liver histology was markedly attenuated in age-matched nSREBP-1c/adiponectin double-transgenic mice. The nSREBP-1c/adiponectin double-transgenic mice showed human adiponectin production in the liver and a restored circulating human adiponectin level. Human adiponectin messenger ribonucleic acid (mRNA) expression in the liver was identified in the nSREBP-1c/adiponectin double-transgenic mice, but adiponectin receptor 1 and 2 mRNA expression in the liver was normal. TNFα mRNA was decreased in the liver of the nSREBP-1c/adiponectin double-transgenic mice compared with the nSREBP-1c transgenic mice. The protein expressions of X-box-binding protein-1, activating transcription factor 4, acetyl-CoA carboxylase, TNFα and NFκB were down-regulated in liver tissues from the nSREBP-1c/adiponectin double-transgenic mice. Mouse adiponectin and activating transcription factor 6 expressions were almost the same in the three groups. Post-load plasma glucose levels were significantly lower in the nSREBP-1c/adiponectin double-transgenic mice compared with the nSREBP-1c transgenic mice. These results indicate that adiponectin expressed in the liver suppresses ER stress and attenuates hepatic steatosis, inflammation and insulin resistance in NASH. Adiponectin may open the way to novel therapies for human NASH.

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