As our understanding of the many functions of vitamin D has grown

As our understanding of the many functions of vitamin D has grown, the presence

of vitamin D deficiency (VDD) has become more evident in Western populations. Concomitantly, nonalcoholic fatty liver disease (NAFLD) has become the most common find more cause of chronic liver disease. NAFLD and VDD are often found together, and while this is not unexpected, given their similar associations with obesity and sedentary lifestyle, a growing body of evidence points to a closely linked and potentially causative relationship between VDD and NAFLD. The epidemiologic association between VDD and NAFLD as well as the role of VDD in the pathogenesis of NAFLD and the available evidence on the clinical utility of vitamin D replacement in NAFLD populations are discussed. (Hepatology 2013;53:1166–1174) click here In the last decade, the importance of vitamin D beyond its effects on calcium homeostasis has become more evident and its functions in immune modulation, cell differentiation and proliferation, and the inflammatory response have all been well described. However, an interesting paradox has developed: while our understanding of the physiological functions of vitamin D have become better known, vitamin D deficiency (VDD) has silently become increasingly more common in Western populations. Concomitantly, the last decade has seen nonalcoholic fatty liver disease (NAFLD)

rise to become the most common cause of chronic liver disease in Western nations. Given that VDD and NAFLD have both indirect and direct associations with obesity and sedentary lifestyle, it is not unexpected that VDD would coexist with NAFLD. A growing body of evidence points to a linked and potentially causative relationship between VDD and NAFLD. This review will assess the role of VDD in the pathogenesis of NAFLD, identify trends in the epidemiology of VDD and NAFLD, and evaluate available evidence on the clinical utility

of vitamin D replacement in NAFLD populations. Vitamin medchemexpress D is a secosteroid that is obtained both exogenously (Vitamin D2) and endogenously (Vitamin D3). Since dietary vitamin D (D2) is naturally contained in very few foods, dietary supplementation and dermal synthesis (D3) are the primary sources of vitamin D. Previtamin D3 is synthesized in skin by UV sunlight from 7-dehydrocholesterol which is then converted to vitamin D3 or cholecalciferol[1] (Fig. 1). Dietary vitamin D2 is fat soluble and is absorbed by the small intestine and incorporated into chylomicrons where it is transported to the liver bound to vitamin D-binding protein (DBP). In the liver, vitamin D undergoes hydroxylation by 25-hydroxylase (CYP2R1) leading to formation of 25-hydroxyvitamin D [25(OH)D3] or calcidiol.[2] 25(OH)D3 is transported to the kidney where it undergoes hydroxylation by 1a-hydroxylase (CYP27B1) to its active form 1a,25-dihydroxyvitamin D [1,25(OH)2D3].

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