Abstract
Non-alcoholic fatty liver disease (NAFLD) represents the most common chronic liver disease and it is considered the hepatic manifestation of metabolic syndrome (MetS). Diet represents the key element in NAFLD and MetS treatment, but some nutrients could play a role in their pathophysiology. Among these, fructose added to foods via high fructose corn syrup (HFCS) and sucrose might participate in NAFLD and MetS onset and progression. Fructose induces de novo lipogenesis (DNL), endoplasmic reticulum stress and liver inflammation, promoting insulin resistance and dyslipidemia. Fructose also reduces fatty acids oxidation through the overproduction of malonyl CoA, favoring steatosis. Furthermore, recent studies suggest changes in intestinal permeability associated with fructose consumption that contribute to the risk of NAFLD and MetS. Finally, alterations in the hunger–satiety mechanism and in the synthesis of uric acid link the fructose intake to weight gain and hypertension, respectively. However, further studies are needed to better evaluate the causal relationship between fructose and metabolic diseases and to develop new therapeutic and preventive strategies against NAFLD and MetS.
Highlights
The relationship between non-alcoholic fatty liver disease (NAFLD) and metabolic disorders has been widely reported
Free sugars play a key role in the development of obesity, type 2 diabetes mellitus (DMT2), dental caries, metabolic syndrome (MetS), cardiovascular diseases and NAFLD
Fructose is passively absorbed in the enterocytes by facilitative glucose transporter 5 (GLUT5) and to a lesser extent by facilitative glucose transporter 2 (GLUT2), which plays a major role in the liver
Summary
The relationship between non-alcoholic fatty liver disease (NAFLD) and metabolic disorders has been widely reported. The global prevalence of NAFLD and MetS are 24% [2] and 25% [3], respectively Both conditions are strongly associated with obesity and the risk of developing cardiovascular diseases, diabetes, chronic kidney disease, and non-alcoholic steatohepatitis (NASH) related liver complications [4–8]. Free sugars play a key role in the development of obesity, type 2 diabetes mellitus (DMT2), dental caries, metabolic syndrome (MetS), cardiovascular diseases and NAFLD. Some studies highlight the association between fructose and cardiometabolic diseases, other studies deny this relationship which could be distorted by diet energy surplus. The aim of this narrative review is to evaluate epidemiological, pathophysiological and clinical evidence on the association between the consumption of added fructose and NAFLD and MetS
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