Peroxisomes and the fatty liver of malnutrition: an hypothesis

Abstract

Peroxisomes play a role in hepatic beta-oxidation of fat, a process that results in the production of hydrogen peroxide. The fatty infiltration of the liver that occurs in severely malnourished children remains unexplained. We observed an almost total absence of peroxisomes in the hepatocytes of these children. We suggest that lack of available peroxisomes could contribute to the development of fatty liver.

Biochemical and anthropometric correlates of bio-electrical impedance parameters in severely malnourished children: A cross-sectional study

“…In this study, the mean values of albumin and alkaline phosphatase were abnormal and also differed by oedema. Though fatty liver is frequently reported in SAM patients (24), there are mixed result regarding its markers. In malnourished pig models, serum alanine aminotransferase and bilirubin were increased, and liver showed evidence of increased triglyceride content (25).…”

Nonobese population in a developing country has a high prevalence of nonalcoholic fatty liver and significant liver disease

“…33 Molecular pathogenesis of obesity-associated liver disease and undernutrition-related liver damage are quite similar. 34,35 To answer this question, we conducted a case-control study of subjects with and without NAFL with a BMI <18.5 kg/m 2 and looked for markers of adiposity and MS. Interestingly, even in this subgroup, subjects with NAFL had higher indices of adiposity and higher prevalence of markers of MS versus those without NAFL. This highlights for the first time a ''third-world NAFL'' phenotype in which, instead of overt obesity, subtle measures of increased adiposity predispose to NAFL.…”

Recurrence of nonalcoholic steatohepatitis after liver transplantation

“…Endotoxin can in turn produce peroxisomal dysfunction, stimulate super oxide and hydrogen peroxide production, and release tumor necrosis factor from monocytes. 9,10 These consequences can overwhelm the protective mechanisms of the host against free radical production, and they can result in hepatic steatosis and liver cell necrosis. 9,10 Indeed, depletions of glutathione, vitamin E, and superoxide dismutase occur commonly in systemic illness, 9,10 and similar deficiencies of intrinsic antioxidants may be present before and after liver transplantation.…”