ArticleStem cell research & therapy2022
iPSCs derived from insulin resistant offspring of type 2 diabetic patients show increased oxidative stress and lactate secretion.
Article in Stem cell research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 10 citations in OpenAlex.
- Biphasic oxygen-regulating cyanobacterial hydrogel for synergistic ischemic stroke gas therapy and post-stroke depression prevention.Materials today. Bio · 2026Article
- Evaluating iPSC-based interventions for diabetes: a systematic review and meta-analysis.Diabetology & metabolic syndrome · 2026Article
- Insulin resistance: mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Recent advances in reprogramming lactate metabolism in polycystic ovary syndrome.Journal of ovarian research · 2025Review
- RFX3 is essential for the generation of functional human pancreatic islets from stem cells.Diabetologia · 2025Article
- Applications and prospects of biomaterials in diabetes management.Frontiers in bioengineering and biotechnology · 2025Review
- Deletion of RFX6 impairs iPSC-derived islet organoid development and survival, with no impact on PDX1Diabetologia · 2024Article
- Review
- Metabolite profiles of diabetes mellitus and response to intervention in anti-hyperglycemic drugs.Frontiers in endocrinology · 2023Review
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Authors and funding
8 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe genetic factors associated with insulin resistance (IR) are not well understood. Clinical studies on first-degree relatives of type 2 diabetic (T2D) patients, which have the highest genetic predisposition to T2D, have given insights into the role of IR in T2D pathogenesis. Induced pluripotent stem cells (iPSCs) are excellent tools for disease modeling as they can retain the genetic imprint of the disease. Therefore, in this study, we aimed to investigate the genetic perturbations associated with insulin resistance (IR) in the offspring of T2D parents using patient-specific iPSCs.
methodsWe generated iPSCs from IR individuals (IR-iPSCs) that were offspring of T2D parents as well as from insulin-sensitive (IS-iPSCs) individuals. We then performed transcriptomics to identify key dysregulated gene networks in the IR-iPSCs in comparison to IS-iPSCs and functionally validated them.
resultsTranscriptomics on IR-iPSCs revealed dysregulated gene networks and biological processes indicating that they carry the genetic defects associated with IR that may lead to T2D. The IR-iPSCs had increased lactate secretion and a higher phosphorylation of AKT upon stimulation with insulin. IR-iPSCs have increased cellular oxidative stress indicated by a high production of reactive oxygen species and higher susceptibility to H
conclusionsIR-iPSCs generated from offspring of diabetic patients confirm that oxidative stress and increased lactate secretion, associated with IR, are inherited in this population, and may place them at a high risk of T2D. Overall, our IR-iPSC model can be employed for T2D modeling and drug screening studies that target genetic perturbations associated with IR in individuals with a high risk for T2D.
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