ArticlePloS one2015
OXPHOS-Mediated Induction of NAD+ Promotes Complete Oxidation of Fatty Acids and Interdicts Non-Alcoholic Fatty Liver Disease.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- LRPPRC: A Multifunctional Protein Involved in Energy Metabolism and Human Disease.Frontiers in physiology · 2019Pooled it
- Targeting LRPPRC lactylation disrupts metabolic-immune crosstalk and restores antitumor immunity in hepatocellular carcinoma.Translational cancer research · 2026Article
- Characterizing the tuberculosis and type 2 diabetes mellitus comorbidity in a South African cohort using untargeted GCxGC-TOFMS metabolomics.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- NAD + in fatty liver disease: mechanistic insights and associated targets.Cell biology and toxicology · 2025Review
- LRPPRC confers enhanced oxidative phosphorylation metabolism in triple-negative breast cancer and represents a therapeutic target.Journal of translational medicine · 2025Article
- Correlation of organelle interactions in the development of non-alcoholic fatty liver disease.Frontiers in immunology · 2025Review
- Pleozymes: Pleiotropic Oxidized Carbon Nanozymes Enhance Cellular Metabolic Flexibility.Nanomaterials (Basel, Switzerland) · 2024Article
- Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction.Diabetes, obesity & metabolism · 2024Article
- Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury.Cell death discovery · 2024Review
- Mitochondrial defects triggered by amg-1 mutation elicit UPRmt and phagocytic clearance during spermatogenesis in C. elegans.Development (Cambridge, England) · 2024Article
- Nonalcoholic Fatty Liver Disease and Staging of Hepatic Fibrosis.Advances in experimental medicine and biology · 2024Review
- Rotundic acid improves nonalcoholic steatohepatitis in mice by regulating glycolysis and the TLR4/AP1 signaling pathway.Lipids in health and disease · 2023Article
- Macrophage-derived Osteopontin (SPP1) Protects From Nonalcoholic Steatohepatitis.Gastroenterology · 2023Article
- Progress in Nonalcoholic Fatty Liver Disease: SIRT Family Regulates Mitochondrial Biogenesis.Biomolecules · 2022Review
- Expression signature of the Leigh syndrome French-Canadian type.Molecular genetics and metabolism reports · 2022Article
- Metabolomic profiling of triple negative breast cancer cells suggests that valproic acid can enhance the anticancer effect of cisplatin.Frontiers in cell and developmental biology · 2022Article
- Avocado oil alleviates non-alcoholic fatty liver disease by improving mitochondrial function, oxidative stress and inflammation in rats fed a high fat-High fructose diet.Frontiers in pharmacology · 2022Article
- Mitochondria in Diabetic Kidney Disease.Cells · 2021Review
- Neuroprotection in Glaucoma: NADCells · 2021Review
- Diabetic Retinopathy: The Role of Mitochondria in the Neural Retina and Microvascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
OXPHOS is believed to play an important role in non-alcoholic fatty liver disease (NAFLD), however, precise mechanisms whereby OXPHOS influences lipid homeostasis are incompletely understood. We previously reported that ectopic expression of LRPPRC, a protein that increases cristae density and OXPHOS, promoted fatty acid oxidation in cultured primary hepatocytes. To determine the biological significance of that observation and define underlying mechanisms, we have ectopically expressed LRPPRC in mouse liver in the setting of NAFLD. Interestingly, ectopic expression of LRPPRC in mouse liver completely interdicted NAFLD, including inflammation. Consistent with mitigation of NAFLD, two markers of hepatic insulin resistance--ROS and PKCε activity--were both modestly reduced. As reported by others, improvement of NAFLD was associated with improved whole-body insulin sensitivity. Regarding hepatic lipid homeostasis, the ratio of NAD+ to NADH was dramatically increased in mouse liver replete with LRPPRC. Pharmacological activators and inhibitors of the cellular respiration respectively increased and decreased the [NAD+]/[NADH] ratio, indicating respiration-mediated control of the [NAD+]/[NADH] ratio. Supporting a prominent role for NAD+, increasing the concentration of NAD+ stimulated complete oxidation of fatty acids. Importantly, NAD+ rescued impaired fatty acid oxidation in hepatocytes deficient for either OXPHOS or SIRT3. These data are consistent with a model whereby augmented hepatic OXPHOS increases NAD+, which in turn promotes complete oxidation of fatty acids and protects against NAFLD.
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