Modern approaches to the treatment of combed non-alcoholic fatty liver disease and cardiovascular disease
Journal Title: Сучасна гастроентерологія - Year 2019, Vol 0, Issue 3
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a major cause of chronic liver disease and it progresses from simple steatosis to steatohepatitis, fibrosis and cirrhosis. It has been proven that NAFLD is a multisystem disease, affecting extra-hepatic organs, including heart and vessels. For example, NAFLD increases risk of cardiovascular (CVD) diseases. Although the primary liver pathology in NAFLD affects hepatic structure and function, the majority of deaths among NAFLD patients are attributable to CVD. Key physiological functions of the liver, including glucose and lipid metabolism, undergo significant alterations at NAFLD and may be associated with a systemic inflammatory «milieu», which is partially initiated by liver-secreted cytokines and molecules. Different molecules secreted from adipose tissue such as adiponectin, leptin and pro-inflammatory cytokines such as tumour necrosis factor-α, and interleukins, can be involved in the pathogenesis of NAFLD and NAFLD-induced CVD. S-adenosyl-L-methionine (SAMe) is an important, metabolically pleiotropic molecule that participates in multiple cellular reactions as the precursor for the synthesis of glutathione. SAMe is a principle methyl donor required for methylation of nucleic acids, phospholipids, biogenic amines and proteins. SAMe synthesis is depressed in chronic liver disease and so there has been considerable interest in the utility of SAMe to ameliorate severity of NAFLD and NAFLD-induced CVD. The review presents discussable data, published in the scientific literature, that demonstrate physiological and pathophysiological roles of SAMe and its therapeutic use in NAFLD and NAFLD-induced CVD.
Authors and Affiliations
N. B. Gubergrits, N. V. Byelyayeva
Keywords
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- EP ID EP615653
- DOI 10.30978/MG-2019-3-41
- Views 116
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