Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 129, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2020.110347
Keywords
Ginsenoside; HCBP6; HFD; Metabolism; NAFLD
Funding
- National Key Research and Development Program of China [2017YFC0908104]
- Natural Science Foundation of Beijing [7161006]
- Beijing Municipal Administration of Hospitals' Ascent Plan [DFL20151701]
- Program of Beijing Advanced Innovation Center for Big Data-Based Precision Medicine
- Beijing Municipal Administration of Hospitals [XMLX201711]
- National Natural Science Foundation of China [81700508]
- Beijing Hospitals Authority Youth Programme [QML20181801]
- Beijing Outstanding Talents Training and Support for Youth Individual Projects [2017000021469G250]
- National Science and Technology Major Project [2015ZX10004801-001-002]
- Collaborative Innovation Centre of Infectious Diseases
- Beijing Key Laboratory of Emerging Infectious Diseases, Beijing, China
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Background: Non-alcoholic fatty liver disease (NAFLD), which often accompanied by metabolic syndrome, such as obesity, diabetes and dyslipidemia, has become a global health problem. Our previous results show that HCV core protein binding protein 6 (HCBP6) could maintain the triglyceride homeostasis in liver cells. However, the role of HCBP6 in NAFLD and its associated metabolic disorders remains incompletely understood. Methods: Hepatic HCBP6 expression was determined by qRT-PCR, Western blot and immunohistochemistry analysis. HCBP6 knockout (HCBP6-KO) mice were constructed and fed a high-fat diet (HFD) to induce NAFLD. The effects of HCBP6 on glucose and lipid metabolism were measured by HE staining, qRT-PCR, Western blot and GTT. Wild-type and HCBP6-KO mice kept on a HFD were treated with ginsenosides Rh2, and HE staining and GTT were used to study the function of Rh2 in metabolism disorders. Results: HCBP6 is reduced in HFD-fed mice. HCBP6 deficiency increased the body weight, aggravated fatty liver and deteriorated lipid homeostasis as well as glucose homeostasis in HFD-induced mouse model of NAFLD. Moreover, HCBP6-KO mice failed to maintain body temperature upon cold challenge. Mechanistically, HCBP6 could regulate lipolysis and fatty acid oxidation via activation of AMKP in vivo. In addition, HCBP6 expression was upregulated by ginsenosides Rh2. Accordingly, ginsenosides Rh2 administrations improved HFD-induced fatty liver and glucose tolerance. Conclusions: These findings indicated that HCBP6 is essential in maintaining lipid and glucose homeostasis and body temperature. HCBP6 augmented by ginsenosides Rh2 may be a promising therapeutic strategy for the treatment of metabolic disorders in NAFLD mice.
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