The role of increased gastrointestinal alcohol production in patients with the metabolic syndrome: Implications for the pathogenesis of non-alcoholic fatty liver disease

Abstract

Aim. Explore the possibility that increased gastrointestinal alcohol production may play a role in the pathogenesis of non-alcoholic fatty liver disease in patients with the metabolic syndrome. Methods. Blood, urine and breath levels of alcohol measured in 20 patients with the metabolic syndrome were compared with those of 20 matched healthy controls. Results. Eighty per cent of the patients had dyslipidaemia, 60% systemic ypertension and 70% type 2 diabetes mellitus. Seventy five per cent had ultrasonographic features of fatty liver disease, with mean serum aminotransferase activities being significantly higher in the patients than in the controls, alanine aminotransferase (ALT) 57.4±44.79 U/l versus 17.4±4.60 U/l (95% CI 18.02 - 61.42, p<0.001), and aspartate
aminotransferase (AST) 52.5±36.21 U/l versus 23.4±4.86 U/l (95% CI 11.99 - 46.20, p<0.01). Adiponectin levels were lower (6 875 versus 15 475 ng/l; median value, p<0.01) in the patients with the metabolic syndrome and leptin levels significantly higher (13.56 versus 3.05 ng/l; median value, p<0.05). Alcohols were detected in body fluids of 60% of the patients, of which 35% tested positive for ethanol, 55% tested positive for methanol, and
30% tested positive for both. None of the controls tested positive for any alcohols.
Conclusions. Endogenous alcohol production may be involved in the pathogenesis of non-alcoholic fatty liver disease in patients with the metabolic syndrome.

JEMDSA Vol. 13 (2) 2008: pp. 48-56