ArticlePloS one2014
The islet estrogen receptor-α is induced by hyperglycemia and protects against oxidative stress-induced insulin-deficient diabetes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
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- NRF2 deficiency leads to inadequate beta cell adaptation during pregnancy and gestational diabetes.Redox biology · 2025Article
- The role of estrogen in the sex difference for the risk factors of heart failure with preserved ejection fraction.Biology direct · 2025Review
- Therapeutic Potential of Quercetin in the Management of Type-2 Diabetes Mellitus.Life (Basel, Switzerland) · 2022Review
- Efficacy of glucagon-like peptide-1 and estrogen dual agonist in pancreatic islets protection and pre-clinical models of insulin-deficient diabetes.Cell reports. Medicine · 2022Article
- Differential Function and Maturation of Human Stem Cell-Derived Islets After Transplantation.Stem cells translational medicine · 2022Article
- Prolonged Islet Allograft Function is Associated With Female Sex in Patients After Islet Transplantation.The Journal of clinical endocrinology and metabolism · 2022Article
- Exposure to maternal obesity programs sex differences in pancreatic islets of the offspring in mice.Diabetologia · 2020Article
- Conjugated Estrogens and Bazedoxifene ImproveJournal of the Endocrine Society · 2019Article
- Repression of insulin gene transcription by indirect genomic signaling via the estrogen receptor in pancreatic beta cells.In vitro cellular & developmental biology. Animal · 2019Article
- Males Require Estrogen Signaling Too: Sexual Dimorphism in the Regulation of Glucose Homeostasis by Nuclear ERα.Diabetes · 2019Article
- Loss of Nuclear and Membrane Estrogen Receptor-α Differentially Impairs Insulin Secretion and Action in Male and Female Mice.Diabetes · 2019Article
- Catechol estrogens stimulate insulin secretion in pancreatic β-cells via activation of the transient receptor potential A1 (TRPA1) channel.The Journal of biological chemistry · 2019Article
- Estrogens Promote Misfolded Proinsulin Degradation to Protect Insulin Production and Delay Diabetes.Cell reports · 2018Article
- Androgen excess in pancreatic β cells and neurons predisposes female mice to type 2 diabetes.JCI insight · 2018Article
- Estrogen receptor α protects pancreatic β-cells from apoptosis by preserving mitochondrial function and suppressing endoplasmic reticulum stress.The Journal of biological chemistry · 2018Article
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Authors and funding
11 authors at 8 institutions in 3 countries.
Funding
Abstract
The female steroid, 17β-estradiol (E2), is important for pancreatic β-cell function and acts via at least three estrogen receptors (ER), ERα, ERβ, and the G-protein coupled ER (GPER). Using a pancreas-specific ERα knockout mouse generated using the Cre-lox-P system and a Pdx1-Cre transgenic line (PERαKO ⁻/⁻), we previously reported that islet ERα suppresses islet glucolipotoxicity and prevents β-cell dysfunction induced by high fat feeding. We also showed that E2 acts via ERα to prevent β-cell apoptosis in vivo. However, the contribution of the islet ERα to β-cell survival in vivo, without the contribution of ERα in other tissues is still unclear. Using the PERαKO ⁻/⁻ mouse, we show that ERα mRNA expression is only decreased by 20% in the arcuate nucleus of the hypothalamus, without a parallel decrease in the VMH, making it a reliable model of pancreas-specific ERα elimination. Following exposure to alloxan-induced oxidative stress in vivo, female and male PERαKO ⁻/⁻ mice exhibited a predisposition to β-cell destruction and insulin deficient diabetes. In male PERαKO ⁻/⁻ mice, exposure to E2 partially prevented alloxan-induced β-cell destruction and diabetes. ERα mRNA expression was induced by hyperglycemia in vivo in islets from young mice as well as in cultured rat islets. The induction of ERα mRNA by hyperglycemia was retained in insulin receptor-deficient β-cells, demonstrating independence from direct insulin regulation. These findings suggest that induction of ERα expression acts to naturally protect β-cells against oxidative injury.
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