ArticleNutrients2018
IDH2 Deficiency Aggravates Fructose-Induced NAFLD by Modulating Hepatic Fatty Acid Metabolism and Activating Inflammatory Signaling in Female Mice.
Article in Nutrients, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Cuproptosis-Related Genes in Immune Infiltration and Diagnosis in Hepatitis B Virus-Related Acute Liver Failure.Exploration (Beijing, China) · 2026Article
- Exploring the correlation between ferroptosis-associated biomarkers and MRI-derived parameters in liver fibrosis associated with metabolic dysfunction-associated steatotic liver disease.Clinical and experimental medicine · 2026Article
- Gut microbes, diet, and genetics as drivers of metabolic liver disease: a narrative review outlining implications for precision medicine.The Journal of nutritional biochemistry · 2024Review
- Increased RTN3 phenocopies nonalcoholic fatty liver disease by inhibiting the AMPK-IDH2 pathway.MedComm · 2023Article
- IDH2: A novel biomarker for environmental exposure in blood circulatory system disorders.Oncology letters · 2022Review
- A modified standard American diet induces physiological parameters associated with metabolic syndrome in C57BL/6J mice.Frontiers in nutrition · 2022Article
- The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- The Contribution of Dietary Fructose to Non-alcoholic Fatty Liver Disease.Frontiers in pharmacology · 2021Review
- High Fructose Corn Syrup-Moderate Fat Diet Potentiates Anxio-Depressive Behavior and Alters Ventral Striatal Neuronal Signaling.Frontiers in neuroscience · 2021Article
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Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fructose is a strong risk factor for non-alcoholic fatty liver disease (NAFLD), resulting from the disruption of redox systems by excessive reactive oxygen species production in the liver cells. Of note, recent epidemiological studies indicated that women are more prone to developing metabolic syndrome in response to fructose-sweetened beverages. Hence, we examined whether disruption of the redox system through a deletion of NADPH supplying mitochondrial enzyme, NADP⁺-dependent isocitrate dehydrogenase (IDH2), exacerbates fructose-induced NAFLD conditions in C57BL/6 female mice. Wild-type (WT) and IDH2 knockout (KO) mice were treated with either water or 34% fructose water over six weeks. NAFLD phenotypes and key proteins and mRNAs involved in the inflammatory pathway (e.g., NF-κB p65 and IL-1β) were assessed. Hepatic lipid accumulation was significantly increased in IDH2 KO mice fed fructose compared to the WT counterpart. Neutrophil infiltration was observed only in IDH2 KO mice fed fructose. Furthermore, phosphorylation of NF-κB p65 and expression of IL-1β was remarkably upregulated in IDH2 KO mice fed fructose, and expression of IκBα was decreased by fructose treatment in both WT and IDH2 KO groups. For the first time, we report our novel findings that IDH2 KO female mice may be more susceptible to fructose-induced NAFLD and the associated inflammatory response, suggesting a mechanistic role of IDH2 in metabolic diseases.
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