ArticleScientific reports2020
Saturated fatty acids induce insulin resistance in podocytes through inhibition of IRS1 via activation of both IKKβ and mTORC1.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Insulin resistance and hyperinsulinaemia in kidney disease: mechanisms and metabolic effects.Nature reviews. Nephrology · 2026Review
- Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.Clinical kidney journal · 2026Review
- PRDM16 deficiency promotes podocyte injury by impairing insulin receptor signaling.Cell death and differentiation · 2025Article
- Skeletal muscle lncRNA profile associated with fatty acids in Nellore beef cattle.Scientific reports · 2025Article
- From fat to filter: the effect of adipose tissue-derived signals on kidney function.Nature reviews. Nephrology · 2025Review
- mTOR pathway: A key player in diabetic nephropathy progression and therapeutic targets.Genes & diseases · 2025Review
- PEX11B palmitoylation couples peroxisomal dysfunction with Schwann cells fail in diabetic neuropathy.Journal of biomedical science · 2025Article
- Autophagy-lysosome pathway in insulin & glucagon homeostasis.Frontiers in endocrinology · 2025Review
- The mineralocorticoid receptor in diabetic kidney disease.American journal of physiology. Renal physiology · 2024Review
- Dietary fatty acid pattern and its association with metabolic profile among overweight and obese adults.BMC endocrine disorders · 2024Article
- Ribonucleotide reductase M2 (RRM2): Regulation, function and targeting strategy in human cancer.Genes & diseases · 2024Review
- Anti-Inflammatory and Anti-Quorum Sensing Effect ofCurrent issues in molecular biology · 2023Article
- Role of ceramides in diabetic foot ulcers (Review).International journal of molecular medicine · 2023Review
- The Dark Side of Sphingolipids: Searching for Potential Cardiovascular Biomarkers.Biomolecules · 2023Review
- Triglyceride profiles are associated with subacute exposure to bisphenol A in healthy young adults.The Science of the total environment · 2022Article
- Circulating Free Fatty Acid and Phospholipid Signature Predicts Early Rapid Kidney Function Decline in Patients With Type 1 Diabetes.Diabetes care · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Diabetic nephropathy (DN), a microvascular complication of diabetes, is the leading cause of end-stage renal disease worldwide. Multiple studies have shown that podocyte dysfunction is a central event in the progression of the disease. Beside chronic hyperglycemia, dyslipidemia can induce insulin resistance and dysfunction in podocytes. However, the exact mechanisms of free fatty acid (FFA)-induced podocyte insulin unresponsiveness are poorly understood. We used a type 2 diabetic mouse model (db/db) and mouse podocytes exposed to palmitic acid for 24 h followed by an insulin stimulation. Renal function and pathology were evaluated at 25 weeks of age to confirm the DN development. Our results demonstrate that saturated FFA activated the serine/threonine kinases IκB kinase (IKK)β/IκBα and mTORC1/S6K1, but not protein kinase C and c-jun N-terminal kinase, in podocytes and glomeruli of db/db mice. Activation of both kinases promoted serine 307 phosphorylation of IRS1, a residue known to provoke IRS1 inhibition. Using IKK, mTORC1 and ceramide production inhibitors, we were able to blunt IRS1 serine 307 phosphorylation and restore insulin stimulation of Akt. In conclusion, our results indicate that FFA and diabetes contribute to insulin resistance through the activation of IKKβ and S6K1 leading to podocyte dysfunction and DN.
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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.