ArticleCellular and molecular bioengineering2021
Towards an Insulin Resistant Adipose Model on a Chip.
Article in Cellular and molecular bioengineering, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 11 citations in OpenAlex.
- In Vitro Modeling of Interorgan Crosstalk: Multi-Organ-on-a-Chip for Studying Cardiovascular-Kidney-Metabolic Syndrome.Circulation research · 2025Review
- Optimization and validation of a fat-on-a-chip model for non-invasive therapeutic drug discovery.Frontiers in bioengineering and biotechnology · 2024Article
- Review
- Autologous Human Immunocompetent White Adipose Tissue-on-Chip.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Patient-derived pancreatic cancer-on-a-chip recapitulates the tumor microenvironment.Microsystems & nanoengineering · 2022Article
- Effects of Bergamot Polyphenols on Mitochondrial Dysfunction and Sarcoplasmic Reticulum Stress in Diabetic Cardiomyopathy.Nutrients · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
introductionAdipose tissue and adipocytes are primary regulators of insulin sensitivity and energy homeostasis. Defects in insulin sensitivity of the adipocytes predispose the body to insulin resistance (IR) that could lead to diabetes. However, the mechanisms mediating adipocyte IR remain elusive, which emphasizes the need to develop experimental models that can validate the insulin signaling pathways and discover new mechanisms in the search for novel therapeutics. Currently
methodsWe differentiated, maintained, and induced insulin resistance into primary adipocytes in a microfluidic organ-on-chip. We then characterized IR by looking at the insulin signaling pathway and lipid metabolism, and validated by studying a diabetic drug, rosiglitazone.
resultsWe confirmed the presence of insulin resistance through reduction of Akt phosphorylation, Glut4 expression, Glut4 translocation and glucose uptake. We also confirmed defects of disrupted insulin signaling through reduction of lipid accumulation from fatty acid uptake and elevation of glycerol secretion. Testing with rosiglitazone showed a significant improvement in insulin sensitivity and fatty acid metabolism as suggested by previous reports.
conclusionsThe adipose-chip exhibited key characteristics of IR and can serve as model to study diabetes and facilitate discovery of novel therapeutics.
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Registered trials
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