ArticleFrontiers in nutrition2024
Exploring the impacts of ketogenic diet on reversible hepatic steatosis: initial analysis in male mice.
Article in Frontiers in nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Sex-specific systemic and brain metabolic responses to a standardized ketogenic diet in mice.Lab animal · 2026Article
- Sex-Specific Metabolic Footprint of Ketogenic Diet in C57BL/6J Mice.Biomedicines · 2026Article
- Divergent Hepatic Outcomes of Chronic Ketone Supplementation: Ketone Salts Preserve Liver Health While Ketone Esters and Precursors Drive Inflammation and Steatosis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Butyrate improves testicular spermatogenic dysfunction induced by a high-fat diet.Translational andrology and urology · 2025Article
- Dietary Influences on Gut Microbiota and Their Role in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Nutrients · 2024Review
- Sex- and Age-Specific Differences in Mice Fed a Ketogenic Diet.Nutrients · 2024Article
- Metabolic Effects of Ketogenic Diets: Exploring Whole-Body Metabolism in Connection with Adipose Tissue and Other Metabolic Organs.International journal of molecular sciences · 2024Review
- Diagnostic indicators and lifestyle interventions of metabolic-associated fatty liver disease.Frontiers in nutrition · 2024Review
- Targeting ketone body metabolism to treat fatty liver disease.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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