title: Does vitamin C deficiency promote fatty liver disease development?
abstract: Obesity and the subsequent reprogramming of the white adipose tissue are linked to human disease-complexes including metabolic syndrome and concurrent non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). The dietary imposed dyslipidemia promotes redox imbalance by the generation of excess levels of reactive oxygen species and induces adipocyte dysfunction and reprogramming, leading to a low grade systemic inflammation and ectopic lipid deposition, e.g., in the liver, hereby promoting a vicious circle in which dietary factors initiate a metabolic change that further exacerbates the negative consequences of an adverse life-style. Large epidemiological studies and findings from controlled in vivo animal studies have provided evidence supporting an association between poor vitamin C (VitC) status and propagation of life-style associated diseases. In addition, overweight per se has been shown to result in reduced plasma VitC, and the distribution of body fat in obesity has been shown to have an inverse relationship with VitC plasma levels. Recently, a number of epidemiological studies have indicated a VitC intake below the recommended daily allowance (RDA) in NAFLD-patients, suggesting an association between dietary habits, disease and VitC deficiency. In the general population, VitC deficiency (defined as a plasma concentration below 23 μM) affects around 10% of adults, however, this prevalence is increased by an adverse life-style, deficiency potentially playing a broader role in disease progression in specific subgroups. This review discusses the currently available data from human surveys and experimental models in search of a putative role of VitC deficiency in the development of NAFLD and NASH.
authors.affiliation: Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Ridebanevej 9, Frederiksberg C, 1870 Copenhagen, Denmark. dhi@sund.ku.dk.
authors.forename: David Højland
authors.initials: DH
authors.lastname: Ipsen
authors.affiliation: Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Ridebanevej 9, Frederiksberg C, 1870 Copenhagen, Denmark. ptn@sund.ku.dk.
authors.forename: Pernille
authors.initials: P
authors.lastname: Tveden-Nyborg
authors.affiliation: Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Ridebanevej 9, Frederiksberg C, 1870 Copenhagen, Denmark. jopl@sund.ku.dk.
authors.forename: Jens
authors.initials: J
authors.lastname: Lykkesfeldt
mesh_terms: D050154:Adiposity; D000818:Animals; D001205:Ascorbic Acid / Q000097:blood / Q000627:therapeutic use; D001206:Ascorbic Acid Deficiency / Q000175:diagnosis / Q000453:epidemiology* / Q000378:metabolism / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D015897:Comorbidity; D006801:Humans; D007249:Inflammation / Q000453:epidemiology; D008019:Life Style; D065626:Non-alcoholic Fatty Liver Disease / Q000175:diagnosis / Q000453:epidemiology* / Q000378:metabolism / Q000503:physiopathology; D009752:Nutritional Status; D009765:Obesity / Q000175:diagnosis / Q000453:epidemiology* / Q000378:metabolism / Q000503:physiopathology; D015995:Prevalence; D011379:Prognosis; D018570:Risk Assessment; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D001205:Ascorbic Acid