In obese people having fatty liver disease, mitochondrial respiration is reduced in visceral but not subcutaneous adipose tissue.

A cross-sectional research was conducted to test the hypothesis that although deficit mitochondrial activity is a basic characteristic of both visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT), it may impact adipose tissue insulin resistance in distinct ways in obesity, non-alcoholic fatty liver (NAFL), and non-alcoholic steatohepatitis (NASH).

Using stable isotope dilution and hyperinsulinemic-normoglycemic clamp tests, an estimation of tissue-specific insulin sensitivity was conducted. Mitochondrial respiration, mRNA and protein expression, and morphology of tissue in SAT and VAT biopsies from obese people with NASH or NAFL, and without NAFL (n = 22 per group) were also assessed.

Contrasted to people without liver disease, subjects with NASH and NAFL displayed 33% and 30% reduced maximal mitochondrial respiration, respectively, in VAT. However, it was not evident in SAT. Across all groups, lower adipose tissue insulin sensitivity (β = 0.9851) and higher overall VAT protein expression of tumor necrosis factor-alpha (β = -0.085) were both related to VAT's lower maximum mitochondrial respiration.

When compared to VAT from adults without NAFL, those with NASH were distinguished by having reduced oxidative phosphorylation complex IV expression and greater macrophage marker CD68 mRNA expression.

NAFLD patients have specific anomalies of VAT energy metabolism, that are correlated with adipose tissue malfunction and may facilitate the development of NASH from NAFL.