Abstract
We studied the effects of exercise on muscle mitochondria, and lipid and glycogen content in non-alcoholic steatohepatitis (NASH) model rats. Male Sprague-Dawley rats were randomly separated into 3 groups: the control group was fed standard chow; the NASH group was fed a methionine-choline-deficient high-fat diet (MCD); the NASH-exercise group was fed the MCD and exercised three times a week. Exercise training consisted of continuous running for thirty minutes at a 13 m/min, 6° slope on a motor-driven rodent treadmill for 6 weeks. Mitochondria content in NASH group decreased in the both fiber types compared with those of the control group. As compared between the NASH and NASH-exercise groups, however, exercise not only promoted significant improvements in liver fibrosis and cirrhosis and triglyceride (TG) content but also increased mitochondria content in type I muscle fiber in particular. These data suggest that exercise improved hepatic steatosis in NASH model rats and can prevent the progression of NASH.
Highlights
Nonalcoholic fatty liver disease (NAFLD) was characterized as a cause of potentially progressive liver damage, and was associated with metabolic disease
It has been reported that a difference of intramuscular lipid (IMCL) content among physiological status accounted for differences in lipid droplet density and the IMCL content varies according to the muscle fiber type [6]
non-alcoholic steatohepatitis (NASH) is defined histologically when a combination of macrovesicular steatosis, hepatocyte injury, inflammation, and fibrosis are observed in the absence of a chronic abuse of alcohol [1] [21]
Summary
Nonalcoholic fatty liver disease (NAFLD) was characterized as a cause of potentially progressive liver damage, and was associated with metabolic disease. NASH has been recognized recently to increase metabolic disease and is affected by multifactorial factors, insulin resistance, excess intracellular fatty acids, and mitochondrial dysfunction [1]. Many other physiological factors can modulate hepatic triglyceride storage, including exercise and dietary composition [2]. Skeletal muscle insulin resistance increased net hepatic TG synthesis in NAFLD [4], and the severity of NASH is associated with substitution of intramuscular lipid (IMCL) content [5]. It has been reported that a difference of IMCL content among physiological status accounted for differences in lipid droplet density and the IMCL content varies according to the muscle fiber type [6]. The muscle fiber type-specific IMCL in NASH has not been reported so far
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