ArticleInternational journal of molecular sciences2021
The Ketogenic Diet Reduces the Harmful Effects of Stress on Gut Mitochondrial Biogenesis in a Rat Model of Irritable Bowel Syndrome.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Mapping research landscapes: a bibliometric and visual analysis of ketogenic diet interventions in liver health (2013-2024).Frontiers in nutrition · 2025Pooled it
- Deciphering the mitochondria-gut microbiota axis in irritable bowel syndrome: pathogenic insights and therapeutic frontiers.Journal of translational medicine · 2026Review
- Canonical pathways and selective mechanisms of autophagy in inflammatory bowel disease.Advanced biotechnology · 2026Review
- Review
- The Interplay between the Gut and Ketogenic Diets in Health and Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- The Dual Role of Exogenous Hydrogen Sulfide (HAntioxidants (Basel, Switzerland) · 2025Article
- Potential inflammatory mechanisms of the ketogenic diet against febrile infection-related epilepsy syndrome.Acta epileptologica · 2025Review
- BECLIN-1/BECN1 at the barrier: a gatekeeper of epithelial and endothelial homeostasis.Autophagy reports · 2025Review
- Effect of a 12-Week Walking Program Monitored by Global Physical Capacity Score (GPCS) on Circulating Cell-Free mtDNA and DNase Activity in Patients with Irritable Bowel Syndrome.International journal of molecular sciences · 2024Article
- Toll-like receptor 4 plays a vital role in irritable bowel syndrome: a scoping review.Frontiers in immunology · 2024Article
- Benefits of Chronic Administration of a Carbohydrate-Free Diet on Biochemical and Morphometric Parameters in a Rat Model of Diet-Induced Metabolic Syndrome.Metabolites · 2023Article
- Systematic review and meta-analysis of calculating degree of comorbidity of irritable bowel syndrome with migraine.BioPsychoSocial medicine · 2023Article
- Plasma-Derived Exosomes from NAFLD Patients Modulate the Cannabinoid Receptors' Expression in Cultured HepaRG Cells.International journal of molecular sciences · 2023Article
- A Comparison of the Impact of Restrictive Diets on the Gastrointestinal Tract of Mice.Nutrients · 2022Article
- The Ketogenic Diet Improves Gut-Brain Axis in a Rat Model of Irritable Bowel Syndrome: Impact on 5-HT and BDNF Systems.International journal of molecular sciences · 2022Article
- Ketogenic diet for human diseases: the underlying mechanisms and potential for clinical implementations.Signal transduction and targeted therapy · 2022Review
- Article
- Intestinal Macrophage Autophagy and its Pharmacological Application in Inflammatory Bowel Disease.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Functional alterations in irritable bowel syndrome have been associated with defects in bioenergetics and the mitochondrial network. Effects of high fat, adequate-protein, low carbohydrate ketogenic diet (KD) involve oxidative stress, inflammation, mitochondrial function, and biogenesis. The aim was to evaluate the KD efficacy in reducing the effects of stress on gut mitochondria. Newborn Wistar rats were exposed to maternal deprivation to induce IBS in adulthood. Intestinal inflammation (COX-2 and TRL-4); cellular redox status (SOD 1, SOD 2, PrxIII, mtDNA oxidatively modified purines); mitochondrial biogenesis (PPAR-γ, PGC-1α, COX-4, mtDNA content); and autophagy (Beclin-1, LC3 II) were evaluated in the colon of exposed rats fed with KD (IBD-KD) or standard diet (IBS-Std), and in unexposed controls (Ctrl). IBS-Std rats showed dysfunctional mitochondrial biogenesis (PPAR-γ, PGC-1α, COX-4, and mtDNA contents lower than in Ctrl) associated with inflammation and increased oxidative stress (higher levels of COX-2 and TLR-4, SOD 1, SOD 2, PrxIII, and oxidatively modified purines than in Ctrl). Loss of autophagy efficacy appeared from reduced levels of Beclin-1 and LC3 II. Feeding of animals with KD elicited compensatory mechanisms able to reduce inflammation, oxidative stress, restore mitochondrial function, and baseline autophagy, possibly via the upregulation of the PPAR-γ/PGC-1α axis.
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Registered trials
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