Ipsen David Højland, Tveden-Nyborg Pernille, Lykkesfeldt Jens
Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Ridebanevej 9, Frederiksberg C, 1870 Copenhagen, Denmark.
Nutrients. 2014 Dec 1;6(12):5473-99. doi: 10.3390/nu6125473.
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.
肥胖以及随之而来的白色脂肪组织重编程与包括代谢综合征、并发非酒精性脂肪性肝病（NAFLD）和非酒精性脂肪性肝炎（NASH）在内的人类疾病复合体相关。饮食导致的血脂异常通过产生过量的活性氧促进氧化还原失衡，并诱导脂肪细胞功能障碍和重编程，导致低度全身炎症和异位脂质沉积，例如在肝脏中，从而促进恶性循环，即饮食因素引发代谢变化，进一步加剧不良生活方式的负面后果。大型流行病学研究以及体内对照动物研究的结果提供了证据，支持维生素C（VitC）状态不佳与生活方式相关疾病的传播之间存在关联。此外，超重本身已被证明会导致血浆VitC降低，并且肥胖人群体内脂肪的分布与血浆VitC水平呈负相关。最近，一些流行病学研究表明，NAFLD患者的VitC摄入量低于推荐每日摄入量（RDA），这表明饮食习惯、疾病与VitC缺乏之间存在关联。在一般人群中，VitC缺乏（定义为血浆浓度低于23μM）影响约10%的成年人，然而，不良生活方式会增加这种患病率，缺乏可能在特定亚组的疾病进展中发挥更广泛的作用。本综述讨论了来自人类调查和实验模型的现有数据，以寻找VitC缺乏在NAFLD和NASH发展中的假定作用。
