ArticleInternational journal of molecular sciences2019
Hypoxia Modulates Effects of Fatty Acids on NES2Y Human Pancreatic β-cells.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Lactobacillus johnsonii-derived leucic acid promotes fatty acid absorption and deposition by targeting CD36.Science China. Life sciences · 2025Article
- Effects of oleic acid and/or exercise on diet-induced thermogenesis and obesity in rats: involvement of beige adipocyte differentiation and macrophage M1 inhibition.Research in pharmaceutical sciences · 2023Article
- The development of endoplasmic reticulum-related gene signatures and the immune infiltration analysis of sepsis.Frontiers in immunology · 2023Article
- Carotenoid transporter CD36 expression depends on hypoxia-inducible factor-1α in mouse soleus muscles.Journal of clinical biochemistry and nutrition · 2022Article
- Editorial to Special Issue "Sleep Apnea and Intermittent Hypoxia 2.0".International journal of molecular sciences · 2022Article
- Molecular Mechanisms of Apoptosis Induction and Its Regulation by Fatty Acids in Pancreatic β-Cells.International journal of molecular sciences · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Saturated fatty acids (FAs) induce apoptosis in the human pancreatic NES2Y β-cell line while unsaturated FAs have nearly no detrimental effect. Moreover, unsaturated FAs are capable of inhibiting the pro-apoptotic effect of saturated FAs. Hypoxia is also known to have deleterious effects on β-cells function and viability. In the present study, we have tested the modulatory effect of hypoxia on the effect of FAs on the growth and viability of the human pancreatic NES2Y β-cells. This study represents the first study testing hypoxia effect on effects of FAs in pancreatic β-cells as well as in other cell types. We showed that hypoxia increased the pro-apoptotic effect of saturated stearic acid (SA). Endoplasmic reticulum stress signaling seemed to be involved while redistribution of FA transporters fatty acid translocase/cluster of differentiation 36 (FAT/CD36) and fatty acid-binding protein (FABP) do not seem to be involved in this effect. Hypoxia also strongly decreased the protective effect of unsaturated oleic acid (OA) against the pro-apoptotic effect of SA. Thus, in the presence of hypoxia, OA was unable to save SA-treated β-cells from apoptosis induction. Hypoxia itself had only a weak detrimental effect on NES2Y cells. Our data suggest that hypoxia could represent an important factor in pancreatic β-cell death induced and regulated by FAs and thus in the development of type 2 diabetes mellitus.
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Registered trials
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