Abstract
Non-alcoholic fatty liver disease (NAFLD) is a serious metabolic condition affecting millions of people worldwide. A “Western-style diet” has been shown to induce pediatric NAFLD with the potential disruption of skeletal muscle composition and metabolism. To determine the in vivo effect of a “Western-style diet” on pediatric skeletal muscle fiber type and fuel utilization, 28 juvenile Iberian pigs were fed either a control diet (CON) or a high-fructose, high-fat diet (HFF), with or without probiotic supplementation, for 10 weeks. The HFF diets increased the total triacylglycerol content of muscle tissue but decreased intramyocellular lipid (IMCL) content and the number of type I (slow oxidative) muscle fibers. HFF diets induced autophagy as assessed by LC3I and LC3II, and inflammation, as assessed by IL-1α. No differences in body composition were observed, and there was no change in insulin sensitivity, but HFF diets increased several plasma acylcarnitines and decreased expression of lipid oxidation regulators PGC1α and CPT1, suggesting disruption of skeletal muscle metabolism. Our results show that an HFF diet fed to juvenile Iberian pigs produces a less oxidative skeletal muscle phenotype, similar to a detraining effect, and reduces the capacity to use lipid as fuel, even in the absence of insulin resistance and obesity.
Highlights
Pediatric non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in children in developed countries, with a significant rise observed in countries undergoing epidemiological transition [1]
Significant (p ≤ 0.05) interaction between diet and probiotics is reported and discussed for the control diet (CON)-N, CON-P, HFF-N, or HFF-P groups; otherwise, results are discussed as a comparison between the diets (CON versus HFF) and/or effect of probiotic supplementation
HFF-fed pigs presented gut dysbiosis and hyperplasia that were positively correlated with the severity of the hepatic injury, as well as metabolic changes in liver, plasma, and colon digesta consistent with choline depletion and dysregulation of one-carbon metabolism [21,22]
Summary
Pediatric non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in children in developed countries, with a significant rise observed in countries undergoing epidemiological transition [1]. Untreated NAFLD can progress to non-alcoholic steatohepatitis (NASH) with hepatocellular degeneration and inflammation, fibrosis, and eventually cirrhosis and liver failure [4]. Several studies have reported an association between NAFLD and skeletal muscle loss and weakness in both aging and pediatric populations. A low skeletal muscle mass is associated with a greater risk of NAFLD, both independently and when combined with obesity [5,6,7,8,9,10]. Individuals with sarcopenia are 33% more likely to develop NAFLD, 56% more likely to experience significant fibrosis associated with NAFLD, and 142%
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