ReviewInternational journal of molecular sciences2022
Metabolic Syndrome and β-Oxidation of Long-Chain Fatty Acids in the Brain, Heart, and Kidney Mitochondria.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Virgin Coconut Oil Attenuates Diabetic Kidney Disease via Gut Microbiota-Metabolism-Inflammation Axis Modulation in Type 2 Diabetic Mice.Food science & nutrition · 2026Article
- Mitochondrial Resilience: Unraveling the Triadic Interplay of Phosphocreatine, Cyclophilin D, and STAT3 in Heart Failure.Journal of cardiovascular translational research · 2026Review
- Current Appraisal and Gaps in Knowledge in Cardio-Kidney Metabolic Syndrome Definition.International journal of molecular sciences · 2026Review
- Rethinking Human Energy Metabolism.Current issues in molecular biology · 2026Review
- Distinct CSF lipidomic profiles are associated with five proteomic subtypes in patients with Alzheimer's disease.Molecular neurodegeneration advances · 2026Article
- Imbalance in MICOS Proteins in Rat Liver Mitochondria in an Induced Hyperthyroidism Model.Cells · 2025Article
- MASLD: Lipotoxicity and Imaging Parallels from Liver Steatosis to Kidney Injury.Life (Basel, Switzerland) · 2025Review
- Biomolecular Basis of Life.Metabolites · 2025Review
- Protection Strategies Against Palmitic Acid-Induced Lipotoxicity in Metabolic Syndrome and Related Diseases.International journal of molecular sciences · 2025Review
- In silico dietary interventions using whole-body metabolic models reveal sex-specific and differential dietary risk profiles for metabolic syndrome.Frontiers in physiology · 2025Article
- Resting energy expenditure and kidney disease: a narrative review.Frontiers in nutrition · 2025Review
- From Adipose to Ailing Kidneys: The Role of Lipid Metabolism in Obesity-Related Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Unlocking lung regeneration: insights into progenitor cell dynamics and metabolic control.Cell regeneration (London, England) · 2024Review
- Identifying the key role of mitochondrial respiration and lipid metabolism in regulating axillary osmidrosis through proteomics analysis.Archives of dermatological research · 2024Article
- An extra honey polyphenols-rich diet ameliorates the high-fat diet induced chronic kidney disease via modulating gut microbiota in C57BL/6 mice.Renal failure · 2024Article
- Role of Fatty Acids β-Oxidation in the Metabolic Interactions Between Organs.International journal of molecular sciences · 2024Review
- Association between serum unsaturated fatty acids levels and infertility among American women from the National Health and Nutrition Examination Survey 2013-2014.Lipids in health and disease · 2024Article
- Proteo-metabolomics and patient tumor slice experiments point to amino acid centrality for rewired mitochondria in fibrolamellar carcinoma.Cell reports. Medicine · 2024Article
- The Uncoupling Effect of 17β-Estradiol Underlies the Resilience of Female-Derived Mitochondria to Damage after Experimental TBI.Life (Basel, Switzerland) · 2024Article
- Critical Role of Mitochondrial Fatty Acid Metabolism in Normal Cell Function and Pathological Conditions.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We present evidence that metabolic syndrome (MetS) represents the postreproductive stage of the human postembryonic ontogenesis. Accordingly, the genes governing this stage experience relatively weak evolutionary selection pressure, thus representing the metabolic phenotype of distant ancestors with β-oxidation of long-chain fatty acids (FAs) as the primary energy source. Mitochondria oxidize at high-rate FAs only when succinate, glutamate, or pyruvate are present. The heart and brain mitochondria work at a wide range of functional loads and possess an intrinsic inhibition of complex II to prevent oxidative stress at periods of low functional activity. Kidney mitochondria constantly work at a high rate and lack inhibition of complex II. We suggest that in people with MetS, oxidative stress is the central mechanism of the heart and brain pathologies. Oxidative stress is a secondary pathogenetic mechanism in the kidney, while the primary mechanisms are kidney hypoxia caused by persistent hyperglycemia and hypertension. Current evidence suggests that most of the nongenetic pathologies associated with MetS originate from the inconsistencies between the metabolic phenotype acquired after the transition to the postreproductive stage and excessive consumption of food rich in carbohydrates and a sedentary lifestyle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.