Abstract
Non-alcoholic fatty liver disease (NAFLD) is a consequence of sedentary life style and high fat diets with an estimated prevalence of about 30% in western countries. It is associated with insulin resistance, obesity, glucose intolerance and drug toxicity. Additionally, polymorphisms within, e.g., APOC3, PNPLA3, NCAN, TM6SF2 and PPP1R3B, correlate with NAFLD. Several studies have already investigated later stages of the disease. This study explores the early steatosis stage of NAFLD with the aim of identifying molecular mechanisms underlying the etiology of NAFLD. We analyzed liver biopsies and serum samples from patients with high- and low-grade steatosis (also pre-disease states) employing transcriptomics, ELISA-based serum protein analyses and metabolomics. Here, we provide a detailed description of the various related datasets produced in the course of this study. These datasets may help other researchers find new clues for the etiology of NAFLD and the mechanisms underlying its progression to more severe disease states.
Highlights
Background & SummaryWith an estimated prevalence of about 30% in western countries, Non-alcoholic fatty liver disease (NAFLD) is a major public health issue[1].Sedentary life-style and excessive food consumption correlate with rate at which NAFLD cases appear.Epidemiologic studies showing a prevalence of the disease that differs between countries as well as between groups in the same country, appear to reflect an interplay of environmental and genetic factors in its etiology[1]
This study explores the early steatosis stage of NAFLD with the aim of identifying molecular mechanisms underlying the etiology of NAFLD
We provide a detailed description of the various related datasets produced in the course of this study. These datasets may help other researchers find new clues for the etiology of NAFLD and the mechanisms underlying its progression to more severe disease states
Summary
With an estimated prevalence of about 30% in western countries, NAFLD is a major public health issue[1]. A two-step progression from simple steatosis to steatohepatitis and fibrosis has been proposed[13], and suggests that after fat accumulation in the liver due to insulin resistance, lipids are peroxidized with cytokines and Fas ligand induced by excessive ROS. This two-step progression has been questioned[5]. In the current study we analyzed patient liver biopsies and associated serum samples, from patients with the insulin resistance phenotype confirmed by the HOMA-IR model[24] We describe these valuable data sets deposited in public repositories, which might support other researchers in identifying new clues for the etiology of NAFLD and the mechanisms underlying its progression to more severe disease states.
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