Ectopic lipid storage in Non-Alcoholic Fatty Liver Disease is not mediated by impaired mitochondrial oxidative capacity in skeletal muscle

Non-alcoholic fatty liver disease (NAFLD), characterized by lipid deposition within the liver (intrahepatocellular lipid, IHCL), is associated with insulin resistance and the metabolic syndrome. It has been suggested that impaired skeletal muscle mitochondrial function may contribute to ectopic lipid deposition, and the associated metabolic syndrome, by altering post-prandial energy storage. To test this hypothesis, we performed a cross-sectional study of 17 patients with NAFLD (mean ± SD; age 45±11 y; BMI 31.6±3.4 kg/m2) and 18 age- and BMI-matched healthy controls (age 44±11 y; BMI 30.5±5.2 kg/m2). We determined body composition by magnetic resonance imaging (MRI), IHCL and intramyocellular (soleus and tibialis anterior) lipids (IMCL) by proton magnetic resonance spectroscopy (1H-MRS) and skeletal muscle mitochondrial function by dynamic phosphorus magnetic resonance spectroscopy (31P-MRS) of quadriceps muscle. Although matched for BMI and total adiposity, after statistical adjustment for gender, patients with NAFLD (defined by IHCL ≥ 5.5%) had higher IHCL (25±16 vs. 2±2 %; p<0.0005), and a higher prevalence of the metabolic syndrome (76 vs. 28%) compared with healthy controls. Despite this, visceral: subcutaneous fat ratio, IMCL and muscle mitochondrial function were similar between the NAFLD and control groups, with no significant difference in the rate constants of post-exercise PCr recovery (1.55±0.4 vs. ...
Source: Clinical Science - Category: Biomedical Science Authors: Source Type: research