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Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease

Department of Endocrinology and Metabolism, Academic Medical Center, Meibergdreef 9, 1105AZ Amsterdam, The Netherlands
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Nutrients 2017, 9(9), 981; https://doi.org/10.3390/nu9090981
Received: 28 July 2017 / Revised: 25 August 2017 / Accepted: 4 September 2017 / Published: 6 September 2017
(This article belongs to the Special Issue Nutrition and Non-alcoholic Fatty Liver Disease)
Increased fructose consumption has been suggested to contribute to non-alcoholic fatty liver disease (NAFLD), dyslipidemia, and insulin resistance, but a causal role of fructose in these metabolic diseases remains debated. Mechanistically, hepatic fructose metabolism yields precursors that can be used for gluconeogenesis and de novo lipogenesis (DNL). Fructose-derived precursors also act as nutritional regulators of the transcription factors, including ChREBP and SREBP1c, that regulate the expression of hepatic gluconeogenesis and DNL genes. In support of these mechanisms, fructose intake increases hepatic gluconeogenesis and DNL and raises plasma glucose and triglyceride levels in humans. However, epidemiological and fructose-intervention studies have had inconclusive results with respect to liver fat, and there is currently no good human evidence that fructose, when consumed in isocaloric amounts, causes more liver fat accumulation than other energy-dense nutrients. In this review, we aim to provide an overview of the seemingly contradicting literature on fructose and NAFLD. We outline fructose physiology, the mechanisms that link fructose to NAFLD, and the available evidence from human studies. From this framework, we conclude that the cellular mechanisms underlying hepatic fructose metabolism will likely reveal novel targets for the treatment of NAFLD, dyslipidemia, and hepatic insulin resistance. Finally, fructose-containing sugars are a major source of excess calories, suggesting that a reduction of their intake has potential for the prevention of NAFLD and other obesity-related diseases. View Full-Text
Keywords: fructose; hepatic steatosis; NAFLD; de novo lipogenesis; lipid synthesis; ChREBP; insulin resistance; obesity; metabolic syndrome fructose; hepatic steatosis; NAFLD; de novo lipogenesis; lipid synthesis; ChREBP; insulin resistance; obesity; metabolic syndrome
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Ter Horst, K.W.; Serlie, M.J. Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease. Nutrients 2017, 9, 981.

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