ArticleJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry2011
Vanadyl bisacetylacetonate protects β cells from palmitate-induced cell death through the unfolded protein response pathway.
Article in Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 27 citations in OpenAlex.
- Metabolic disturbances in acute pancreatitis: mechanisms and therapeutic implications.Frontiers in endocrinology · 2025Review
- An Adequate Supply of Bis(ethylmaltolato)oxidovanadium(IV) Remarkably Reversed the Pathological Hallmarks of Alzheimer's Disease in Triple-Transgenic Middle-Aged Mice.Biological trace element research · 2022Article
- Alzheimer's Disease and Diabetes Mellitus in Comparison: The Therapeutic Efficacy of the Vanadium Compound.International journal of molecular sciences · 2021Review
- Bis(ethylmaltolato)oxidovanadium (IV) alleviates neuronal apoptosis through regulating peroxisome proliferator-activated receptor γ in a triple transgenic animal model of Alzheimer's disease.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2021Article
- Vanadium in Biological Action: Chemical, Pharmacological Aspects, and Metabolic Implications in Diabetes Mellitus.Biological trace element research · 2019Review
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5 authors at 1 institution in 1 country.
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Abstract
Endoplasmic reticulum (ER) stress induced by free fatty acids (FFA) is important to β-cell loss during the development of type 2 diabetes. To test whether vanadium compounds could influence ER stress and the responses in their mechanism of antidiabetic effects, we investigated the effects and the mechanism of vanadyl bisacetylacetonate [VO(acac)(2)] on β cells upon treatment with palmitate, a typical saturated FFA. The experimental results showed that VO(acac)(2) could enhance FFA-induced signaling pathways of unfolded protein responses by upregulating the prosurvival chaperone immunoglobulin heavy-chain binding protein/78-kDa glucose-regulated protein and downregulating the expression of apoptotic C/EBP homologous protein, and consequently the reduction of insulin synthesis. VO(acac)(2) also ameliorated FFA-disturbed Ca(2+) homeostasis in β cells. Overall, VO(acac)(2) enhanced stress adaption, thus protecting β cells from palmitate-induced apoptosis. This study provides some new insights into the mechanisms of antidiabetic vanadium compounds.
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