Tags

Type your tag names separated by a space and hit enter

Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease.
Nutrients 2017; 9(9)N

Abstract

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.

Authors+Show Affiliations

Department of Endocrinology and Metabolism, Academic Medical Center, Meibergdreef 9, 1105AZ Amsterdam, The Netherlands. k.w.terhorst@amc.nl.Department of Endocrinology and Metabolism, Academic Medical Center, Meibergdreef 9, 1105AZ Amsterdam, The Netherlands. m.j.serlie@amc.nl.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

28878197

Citation

Ter Horst, Kasper W., and Mireille J. Serlie. "Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease." Nutrients, vol. 9, no. 9, 2017.
Ter Horst KW, Serlie MJ. Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease. Nutrients. 2017;9(9).
Ter Horst, K. W., & Serlie, M. J. (2017). Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease. Nutrients, 9(9), doi:10.3390/nu9090981.
Ter Horst KW, Serlie MJ. Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease. Nutrients. 2017 Sep 6;9(9) PubMed PMID: 28878197.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease. AU - Ter Horst,Kasper W, AU - Serlie,Mireille J, Y1 - 2017/09/06/ PY - 2017/07/28/received PY - 2017/08/25/revised PY - 2017/09/04/accepted PY - 2017/9/8/entrez PY - 2017/9/8/pubmed PY - 2018/5/22/medline KW - ChREBP KW - NAFLD KW - de novo lipogenesis KW - fructose KW - hepatic steatosis KW - insulin resistance KW - lipid synthesis KW - metabolic syndrome KW - obesity JF - Nutrients JO - Nutrients VL - 9 IS - 9 N2 - 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. SN - 2072-6643 UR - https://www.unboundmedicine.com/medline/citation/28878197/Fructose_Consumption_Lipogenesis_and_Non_Alcoholic_Fatty_Liver_Disease_ L2 - http://www.mdpi.com/resolver?pii=nu9090981 DB - PRIME DP - Unbound Medicine ER -