ArticleMolecular and cellular endocrinology2018
Adrenergic receptor stimulation suppresses oxidative metabolism in isolated rat islets and Min6 cells.
Article in Molecular and cellular endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Chronic Epinephrine-Induced Endoplasmic Reticulum and Oxidative Stress Impairs Pancreatic β-Cells Function and Fate.International journal of molecular sciences · 2024Article
- Phenylacetylglutamine as a novel biomarker of type 2 diabetes with distal symmetric polyneuropathy by metabolomics.Journal of endocrinological investigation · 2023Article
- Tissue-specific responses that constrain glucose oxidation and increase lactate production with the severity of hypoxemia in fetal sheep.American journal of physiology. Endocrinology and metabolism · 2022Article
- Circulating GLP-1 Levels in Patients with Pheochromocytoma/Paraganglioma.International journal of endocrinology · 2022Article
- Insulinoma-derived pseudo-islets for diabetes research.American journal of physiology. Cell physiology · 2021Article
- Pancreatic Islets Exhibit Dysregulated Adaptation of Insulin Secretion after Chronic Epinephrine Exposure.Current issues in molecular biology · 2021Article
- Augmented glucose production is not contingent on high catecholamines in fetal sheep with IUGR.The Journal of endocrinology · 2021Article
- Chronically elevated norepinephrine concentrations lower glucose uptake in fetal sheep.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Chronic Adrenergic Signaling Causes Abnormal RNA Expression of Proliferative Genes in Fetal Sheep Islets.Endocrinology · 2018Article
- Impact of thermal stress on placental function and fetal physiology.Animal reproductionArticle
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Insulin secretion is stimulated by glucose metabolism and inhibited by catecholamines through adrenergic receptor stimulation. We determined whether catecholamines suppress oxidative metabolism in β-cells through adrenergic receptors. In Min6 cells and isolated rat islets, epinephrine decreased oxygen consumption rates compared to vehicle control or co-administration of epinephrine with α2-adrenergic receptor antagonist yohimbine. Epinephrine also decreased forskolin-stimulated oxygen consumption rates, indicating cAMP dependent and independent actions. Furthermore, glucose oxidation rates were decreased with epinephrine, independent of the exocytosis of insulin, which was blocked with yohimbine. We evaluated metabolic targets through proteomic analysis after 4 h epinephrine exposure that revealed 466 differentially expressed proteins that were significantly enriched for processes including oxidative metabolism, protein turnover, exocytosis, and cell proliferation. These results demonstrate that acute α2-adrenergic stimulation suppresses glucose oxidation in β-cells independent of nutrient availability and insulin exocytosis, while cAMP concentrations are elevated. Proteomics and immunoblots revealed changes in electron transport chain proteins that were correlated with lower metabolic reducing equivalents, intracellular ATP concentrations, and altered mitochondrial membrane potential implicating a new role for adrenergic control of mitochondrial function and ultimately insulin secretion.
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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 Socratic graph.