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Biochem Biophys Res Commun. 2015 Mar 20;458(4):862-8. doi: 10.1016/j.bbrc.2015.02.046. Epub 2015 Feb 18.

Protective effects of aerobic swimming training on high-fat diet induced nonalcoholic fatty liver disease: regulation of lipid metabolism via PANDER-AKT pathway.

Author information

1
Department of Endocrinology, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning, China.
2
Department of Immunology, Liaoning Medical University, Jinzhou, Liaoning, China.
3
Department of Neurobiology, Liaoning Medical University, Jinzhou, Liaoning, China.
4
Department of Physiology, Liaoning Medical University, Jinzhou, Liaoning, China.
5
Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning, China.
6
Department of Physiology and Pathophysiology, Peking University Diabetes Center, Peking University Health Science Center, Beijing, China; Shenzhen University Diabetes Center, Shenzhen University Health Science Center, Shenzhen, China.
7
Department of Endocrinology, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning, China. Electronic address: cliuxmei@outlook.com.

Abstract

This study aimed to investigate the mechanism by which aerobic swimming training prevents high-fat-diet-induced nonalcoholic fatty liver disease (NAFLD). Forty-two male C57BL/6 mice were randomized into normal-diet sedentary (ND; n = 8), ND exercised (n = 8), high-fat diet sedentary (HFD; n = 13), and HFD exercised groups (n = 13). After 2 weeks of training adaptation, the mice were subjected to an aerobic swimming protocol (60 min/day) 5 days/week for 10 weeks. The HFD group exhibited significantly higher mRNA levels of fatty acid transport-, lipogenesis-, and β-oxidation-associated gene expressions than the ND group. PANDER and FOXO1 expressions increased, whereas AKT expression decreased in the HFD group. The aerobic swimming program with the HFD reversed the effects of the HFD on the expressions of thrombospondin-1 receptor, liver fatty acid-binding protein, long-chain fatty-acid elongase-6, Fas cell surface death receptor, and stearoyl-coenzyme A desaturase-1, as well as PANDER, FOXO1, and AKT. In the HFD exercised group, PPARα and AOX expressions were much higher. Our findings suggest that aerobic swimming training can prevent NAFLD via the regulation of fatty acid transport-, lipogenesis-, and β-oxidation-associated genes. In addition, the benefits from aerobic swimming training were achieved partly through the PANDER-AKT-FOXO1 pathway.

KEYWORDS:

Exercise; FOXO1; Fatty acid transport; Fatty acid β-oxidation; Lipogenesis; PPARα

PMID:
25701781
DOI:
10.1016/j.bbrc.2015.02.046
[Indexed for MEDLINE]

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