Added Fructose in Non-Alcoholic Fatty Liver Disease and in Metabolic Syndrome: A Narrative Review

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 th...

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Bibliographic Details
Published in:Nutrients 2022-03, Vol.14 (6), p.1127
Main Authors: Coronati, Mattia, Baratta, Francesco, Pastori, Daniele, Ferro, Domenico, Angelico, Francesco, Del Ben, Maria
Format: Article
Language:English
Subjects:
Cereals
Diabetes
Diet
Dyslipidemia
Endoplasmic reticulum
Energy
Enzymes
Fatty acids
Fatty liver
Food
Fructose
Glucose
HFCS
Humans
Hunger
Hypertension
Inflammation
Insulin
Insulin resistance
Lifestyles
Lipogenesis
Liver
Liver diseases
Metabolic disorders
Metabolic syndrome
Metabolic Syndrome - metabolism
Metabolites
Microbiota
NAFLD
Non-alcoholic Fatty Liver Disease - metabolism
Nutrients
Obesity
Oxidation
Oxidation resistance
Pathophysiology
Permeability
Review
Satiety
Soft drinks
Steatosis
Sucrose
Tumor necrosis factor-TNF
Uric acid
Weight control
Young adults
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Summary: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.
ISSN:2072-6643
2072-6643
DOI:10.3390/nu14061127