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Int. J. Mol. Sci. 2017, 18(8), 1710; doi:10.3390/ijms18081710

Endoplasmic Reticulum Stress Inducer Tunicamycin Alters Hepatic Energy Homeostasis in Mice

1,2,†,* , 1,2,†
,
1
,
1
,
1
and
1,2,*
1
Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China
2
Key Laboratory of Animal Disease-Resistant Nutrition of Ministry of Education, Sichuan Agricultural University, Chengdu 611130, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 22 July 2017 / Revised: 3 August 2017 / Accepted: 3 August 2017 / Published: 4 August 2017
(This article belongs to the Section Molecular Toxicology)
View Full-Text   |   Download PDF [6698 KB, uploaded 4 August 2017]   |  

Abstract

Disorders of hepatic energy metabolism, which can be regulated by endoplasmic reticulum (ER) stress, lead to metabolic diseases such as hepatic steatosis and hypoglycemia. Tunicamycin, a pharmacological ER stress inducer, is used to develop an anti-cancer drug. However, the effects of tunicamycin on hepatic energy metabolism have not been well elucidated. Mice were intraperitoneally injected with tunicamycin or vehicle. Twenty-four hours later, hepatic triglyceride and glycogen content and serum lipids profiles were analyzed, as well as the expression of lipogenic and gluconeogenic genes. Tunicamycin significantly induced hepatic a yellowish color and ER stress, as well as increasing serum levels of aspartate transaminase and alanine transaminase. Besides, tunicamycin remarkably increased hepatic triglyceride content and suppressed the expression of apolipoprotein B100. In addition, tunicamycin-treated mice had lower serum levels of triglyceride, apolipoprotein B, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol. Gene expression of peroxisome proliferator-activated receptor α was decreased by tunicamycin, but the protein level was increased. Furthermore, blood glucose level and hepatic glycogen content were decreased in tunicamycin-treated mice. Protein kinase B signaling was attenuated in the tunicamycin-treated liver, but the expression and activities of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase were unchanged. Tunicamycin alters hepatic energy homeostasis by increasing triglyceride accumulation and decreasing glycogen content. View Full-Text
Keywords: tunicamycin; liver; triglyceride; lipoprotein; glycogen; blood glucose; ER stress; Akt tunicamycin; liver; triglyceride; lipoprotein; glycogen; blood glucose; ER stress; Akt
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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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Feng, B.; Huang, X.; Jiang, D.; Hua, L.; Zhuo, Y.; Wu, D. Endoplasmic Reticulum Stress Inducer Tunicamycin Alters Hepatic Energy Homeostasis in Mice. Int. J. Mol. Sci. 2017, 18, 1710.

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