Exploring the impacts of ketogenic diet on reversible hepatic steatosis: initial analysis in male mice.

Autor:	Ravaut G; CERMO-FC Research Center, Molecular Metabolism of Lipids Laboratory, Biological Sciences Department, University of Quebec in Montreal (UQAM), Montreal, QC, Canada., Carneiro A; CERMO-FC Research Center, Molecular Metabolism of Lipids Laboratory, Biological Sciences Department, University of Quebec in Montreal (UQAM), Montreal, QC, Canada., Mounier C; CERMO-FC Research Center, Molecular Metabolism of Lipids Laboratory, Biological Sciences Department, University of Quebec in Montreal (UQAM), Montreal, QC, Canada.
Jazyk:	angličtina
Zdroj:	Frontiers in nutrition [Front Nutr] 2024 Mar 21; Vol. 11, pp. 1290540. Date of Electronic Publication: 2024 Mar 21 (Print Publication: 2024).
DOI:	10.3389/fnut.2024.1290540
Abstrakt:	Metabolic dysfunction-associated fatty liver disease (MAFLD) is the most common chronic liver disease. Ketogenic diet (KD), a diet with very low intake in carbohydrates, gained popularity as a weight-loss approach. However, in mice models, it has been reported that an excess exposition of dietary fat induces hepatic insulin resistance and steatosis. However, data published is inconsistent. Herein, we investigated in a mouse model, the metabolic effects of KD and its contribution to the pathogenesis of NALFD. Mice were exposed to KD or CHOW diet for 12 weeks while a third group was exposed to KD for also 12 weeks and then switched to CHOW diet for 4 weeks to determine if we can rescue the phenotype. We evaluated the effects of diet treatments on fat distribution, glucose, and insulin homeostasis as well as hepatic steatosis. Mice fed with KD developed glucose intolerance but not insulin resistance accompanied by an increase of inflammation. KD-fed mice showed an increase of fat accumulation in white adipose tissue and liver. This effect could be explained by an increase in fat uptake by the liver with no changes of catabolism leading to MAFLD. Interestingly, we were able to rescue the phenotype by switching KD-fed mice for 4 weeks on a CHOW diet. Our studies demonstrate that even if mice develop hepatic steatosis and glucose intolerance after 12 weeks of KD, they do not develop insulin resistance and more importantly, the phenotype can be reversed by switching the mice from a KD to a CHOW. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2024 Ravaut, Carneiro and Mounier.)
Databáze:	MEDLINE
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