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• W4319461908 abstract "Despite the existence of numerous studies supporting a pathological link between fructose consumption and the development of the metabolic syndrome and its sequelae, such as non-alcoholic fatty liver disease (NAFLD), this link remains a contentious issue. With this article, we shed a light on the impact of sugar/fructose intake on hepatic de novo lipogenesis (DNL), an outcome parameter known to be dysregulated in subjects with type 2 diabetes and/or NAFLD. In this review, we present findings from human intervention studies using physiological doses of sugar as well as mechanistic animal studies. There is evidence from both human and animal studies that fructose is a more potent inducer of hepatic lipogenesis than glucose. This is most likely due to the liver’s prominent physiological role in fructose metabolism, which may be disrupted under pathological conditions by increased hepatic expression of fructolytic and lipogenic enzymes. Increased DNL may not only contribute to ectopic fat deposition (i.e. in the liver), but it may also impair several metabolic processes through DNL-related fatty acids (e.g. beta-cell function, insulin secretion, or insulin sensitivity)." @default.
• W4319461908 created "2023-02-09" @default.
• W4319461908 creator A5009265471 @default.
• W4319461908 creator A5090394764 @default.
• W4319461908 date "2023-02-08" @default.
• W4319461908 modified "2023-10-18" @default.
• W4319461908 title "Fructose drives de novo lipogenesis affecting metabolic health" @default.
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• W4319461908 doi "https://doi.org/10.1530/joe-22-0270" @default.
• W4319461908 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36753292" @default.
• W4319461908 hasPublicationYear "2023" @default.
• W4319461908 type Work @default.

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