ISSN: 2578-4641
Authors: Kulvinder KK*, Gautam A and Mandeep S
Nonalcoholic fatty liver disease (NAFLD) is a rapidly escalating disorder which impacts a large population worldwide. Nevertheless, cardiovascular disease (CVD) represents the biggest etiology for mortality with regards to patients of NAFLD. Atherogenic dyslipidemia, possessing the properties of plasma hypetriglyceridemia, enhancement of small dense (low density lipoproteins)LDL’s particles in addition to reduction of high density lipoproteins cholesterol HDL-C) concentrations are generally seen in patients with a presentation of NAFLD. Thus here we conducted a systematic review utilizing search engine PubMed, Google scholar ;web of science; embase; Cochrane review library utilizing the MeSH terms like NAFLD; CVD; atherosclerosis; insulin resistance(IR); NASH; chronic heart failure; dyslipidemia; hepatokines; endothelial impairment; pro inflammatory cytokines; FA’s oxidation; SREBP1c; ChREBP; Sirtuin; LKB1; lipogenesis; mitochondrial lipid β oxidation; genetic mutations from 2010 to 2022. We found a total of 500 articles out of which we selected 143 articles for this review. No meta-analysis was done. Thus here we have detailed the more recent genetic corroboration, with provision of distinctive type of metabolic pathways implicated in NAFLD pathogenesis. Assessment of the genetic results that are accessible pointed that the crucial process that correlated NAFLD modulated dyslipidemia, along with escalation of risk of CVD implied is the changes in the handling of fatty acids β oxidation in the liver mitochondria. NAFLD correlated genes possessing reported anti-atherosclerotic or cardio protective actions in addition to existent Pharmacologic approaches that are concentrated on tackling both treatment of NAFLD in addition to reducing the risk of CVD. Further research demonstrates that inhibitors of de novo’’ lipogenesis (DNL) might prove to be of benefit.
Keywords: NAFLD; CVD; Dyslipidemia; Mitochondrial - Fatty Acids Β Oxidation; Atherosclerosis
