Abstract
Non-alcoholic fatty liver disease (NAFLD) is an increasingly common condition associated with type 2 diabetes (T2DM) and cardiovascular disease (CVD). Since systemic metabolic dysfunction underlies NAFLD, the current nomenclature has been revised, and the term metabolic-associated fatty liver disease (MAFLD) has been proposed. The new definition emphasizes the bidirectional relationships and increases awareness in looking for fatty liver disease among patients with T2DM and CVD or its risk factors, as well as looking for these diseases among patients with NAFLD. The most recommended treatment method of NAFLD is lifestyle changes, including dietary fructose limitation, although other treatment methods of NAFLD have recently emerged and are being studied. Given the focus on the liver–gut axis targeting, bacteria may also be a future aim of NAFLD treatment given the microbiome signatures discriminating healthy individuals from those with NAFLD. In this review article, we will provide an overview of the associations of fructose consumption, gut microbiota, diabetes, and CVD in patients with NAFLD.
Highlights
In 1986, the term nonalcoholic fatty liver disease (NAFLD) was proposed by Schaner and Thaler [1]
The definition of NAFLD combines the presence of steatosis in more than 5% of hepatocytes and metabolic risk factors, especially obesity and T2DM, and exclusion of excessive alcohol consumption defined as ≥30 g per day for men and ≥20 g per day for women, or other chronic liver diseases [9]
One meta-analysis found that the risk of T2DM is greater in patients with advanced NAFLD with fibrosis [84], and in another meta-analysis evaluating whether NAFLD predicted T2DM, NAFLD predicted the risk of T2DM independent of age and obesity, irrespective of the NAFLD diagnosis method [85]
Summary
In 1986, the term nonalcoholic fatty liver disease (NAFLD) was proposed by Schaner and Thaler [1]. Consumption fructose increased over the century mainly to theofuse of disease, obesity, and diabetes, where it promotes hepatic de novo lipogenesis, leading to high-fructose corn syrup [17]. This phenomenon has been studied in the context of liver lipid accumulation in the liver and insulin resistance [18,19,20]. A new perspective on disease, obesity, and diabetes, where it promotes hepatic de novo lipogenesis, leading to emerged during the last decade when scientists focused on the relationship of lipid accumulation in the liver and insulin resistance [18,19,20]. Review article, we have summarized the current state of knowledge regarding NAFLD and its association with fructose consumption, microbiota, diabetes, and CVD
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