ArticleInternational journal of endocrinology2014
Augmented β-Cell Function and Mass in Glucocorticoid-Treated Rodents Are Associated with Increased Islet Ir-β /AKT/mTOR and Decreased AMPK/ACC and AS160 Signaling.
Article in International journal of endocrinology, 2014. 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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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Mitigation of metabolic dyshomeostasis by glucocorticoid-receptor antagonism: Insights from animal and human studies.EXCLI journal · 2020Article
- Glucocorticoids: novel agents to stimulate beta-cell neogenesis?Annals of translational medicine · 2019Article
- 17β-Estradiol Regulates Glucose Metabolism and Insulin Secretion in Rat Islet β Cells Through GPER and Akt/mTOR/GLUT2 Pathway.Frontiers in endocrinology · 2019Article
- Article
- Glucose Homeostasis Is Not Affected in a Murine Model of Parkinson's Disease Induced by 6-OHDA.Frontiers in neuroscience · 2018Article
- Glucose homeostasis in two degrees of sepsis lethality induced by caecum ligation and puncture in mice.International journal of experimental pathology · 2017Article
- Impact of Glucocorticoid Excess on Glucose Tolerance: Clinical and Preclinical Evidence.Metabolites · 2016Review
- Glucocorticoids Inhibit Basal and Hormone-Induced Serotonin Synthesis in Pancreatic Beta Cells.PloS one · 2016Article
- Role of β and α1-adrenoceptors in pancreatic regulation of glucose homeostasis, apoptosis, and fibrosis in dexamethasone-treated rats: A new insight into β-arrestin2 crosstalk with cAMP, PKA-ERK1/2-CREB, and PKB-FOXO1 signaling pathways.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoid (GC) therapies may adversely cause insulin resistance (IR) that lead to a compensatory hyperinsulinemia due to insulin hypersecretion. The increased β-cell function is associated with increased insulin signaling that has the protein kinase B (AKT) substrate with 160 kDa (AS160) as an important downstream AKT effector. In muscle, both insulin and AMP-activated protein kinase (AMPK) signaling phosphorylate and inactivate AS160, which favors the glucose transporter (GLUT)-4 translocation to plasma membrane. Whether AS160 phosphorylation is modulated in islets from GC-treated subjects is unknown. For this, two animal models, Swiss mice and Wistar rats, were treated with dexamethasone (DEX) (1 mg/kg body weight) for 5 consecutive days. DEX treatment induced IR, hyperinsulinemia, and dyslipidemia in both species, but glucose intolerance and hyperglycemia only in rats. DEX treatment caused increased insulin secretion in response to glucose and augmented β-cell mass in both species that were associated with increased islet content and increased phosphorylation of the AS160 protein. Protein AKT phosphorylation, but not AMPK phosphorylation, was found significantly enhanced in islets from DEX-treated animals. We conclude that the augmented β-cell function developed in response to the GC-induced IR involves inhibition of the islet AS160 protein activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.