ArticleMolecular and cellular biology2009
Glucose effects on beta-cell growth and survival require activation of insulin receptors and insulin receptor substrate 2.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
90 citing papers in PubMed, 147 citations in OpenAlex.
- Insulin enhances glucose-stimulated insulin secretion in healthy humans.Proceedings of the National Academy of Sciences of the United States of America · 2010Trial
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- Interactions between islet-resident macrophages and β cells in diabetes.Frontiers in immunology · 2025Review
- A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing Langerhans Islets with a Specific Emphasis on The Secretome.Biomedicines · 2023Review
- Noncanonical CDK4 signaling rescues diabetes in a mouse model by promoting β cell differentiation.The Journal of clinical investigation · 2023Article
- The hippo kinases MST1/2 in cardiovascular and metabolic diseases: A promising therapeutic target option for pharmacotherapy.Acta pharmaceutica Sinica. B · 2023Review
- The liver-derived exosomes stimulate insulin gene expression in pancreatic beta cells under condition of insulin resistance.Frontiers in endocrinology · 2023Article
- GPR92 activation in islet macrophages controls β cell function in a diet-induced obesity model.The Journal of clinical investigation · 2022Article
- E2F1 transcription factor mediates a link between fat and islets to promote β cell proliferation in response to acute insulin resistance.Cell reports · 2022Article
- Uncoupling protein 2 and aldolase B impact insulin release by modulating mitochondrial function and CaiScience · 2022Article
- Insulin regulates arginine-stimulated insulin secretion in humans.Metabolism: clinical and experimental · 2022Article
- Dysregulation of β-Cell Proliferation in Diabetes: Possibilities of Combination Therapy in the Development of a Comprehensive Treatment.Biomedicines · 2022Review
- Insulin action at a molecular level - 100 years of progress.Molecular metabolism · 2021Review
- Article
- Inhibition of PHLPP1/2 phosphatases rescues pancreatic β-cells in diabetes.Cell reports · 2021Article
- Immune regulation of islet homeostasis and adaptation.Journal of molecular cell biology · 2020Review
- Obesity Is Associated With Increased Basal and Postprandial β-Cell Insulin Secretion Even in the Absence of Insulin Resistance.Diabetes · 2020Article
- Luseogliflozin increases beta cell proliferation through humoral factors that activate an insulin receptor- and IGF-1 receptor-independent pathway.Diabetologia · 2020Article
- The role of macrophages in obesity-associated islet inflammation and β-cell abnormalities.Nature reviews. Endocrinology · 2020Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Insulin and insulin-like growth factor I (IGF-I) are ubiquitous hormones that regulate growth and metabolism of most mammalian cells, including pancreatic beta-cells. In addition to being an insulin secretagogue, glucose regulates proliferation and survival of beta-cells. However, it is unclear whether the latter effects of glucose occur secondary to autocrine activation of insulin signaling proteins by secreted insulin. To examine this possibility we studied the effects of exogenous glucose or insulin in beta-cell lines completely lacking either insulin receptors (betaIRKO) or insulin receptor substrate 2 (betaIRS2KO). Exogenous addition of either insulin or glucose activated proteins in the insulin signaling pathway in control beta-cell lines with the effects of insulin peaking earlier than glucose. Insulin stimulation of betaIRKO and betaIRS2KO cells led to blunted activation of phosphatidylinositol 3-kinase and Akt kinase, while surprisingly, glucose failed to activate either kinase but phosphorylated extracellular signal-regulated kinase. Control beta-cells exhibited low expression of IGF-1 receptors compared to compensatory upregulation in betaIRKO cells. The signaling data support the slow growth and reduced DNA and protein synthesis in betaIRKO and betaIRS2KO cells in response to glucose stimulation. Together, these studies provide compelling evidence that the growth and survival effects of glucose on beta-cells require activation of proteins in the insulin signaling pathway.
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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.