ArticleJournal of diabetes investigation2016
Src regulates insulin secretion and glucose metabolism by influencing subcellular localization of glucokinase in pancreatic β-cells.
Article in Journal of diabetes investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 34 citations in OpenAlex.
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- Prediction of traditional Chinese medicine for diabetes based on the multi-source ensemble method.Frontiers in pharmacology · 2025Article
- Mechanistic Exploration ofBioMed research international · 2025Article
- Shared genetic architecture between periodontal disease and type 2 diabetes: a large scale genome-wide cross-trait analysis.Endocrine · 2024Article
- NGF effects promote the maturation of rat pancreatic beta cells by regulating GLUT2 levels and distribution, and glucokinase activity.PloS one · 2024Article
- Integrated investigation and discovery of therapeutic targets for 3-hydroxybakuchiol against diabetes based on molecular docking studies and cell experiments.BMC complementary medicine and therapies · 2023Article
- Exploring the underlying mechanisms of fisetin in the treatment of hepatic insulin resistance via network pharmacology and in vitro validation.Nutrition & metabolism · 2023Article
- Non-Synonymous Variants in Fat QTL Genes among High- and Low-Milk-Yielding Indigenous Breeds.Animals : an open access journal from MDPI · 2023Article
- Src: coordinating metabolism in cancer.Oncogene · 2022Review
- Integrin and autocrine IGF2 pathways control fasting insulin secretion in β-cells.The Journal of biological chemistry · 2020Article
- Integrated Network Pharmacology Analysis and Experimental Validation to Reveal the Mechanism of Anti-Insulin Resistance Effects ofDrug design, development and therapy · 2020Article
- Src regulates insulin secretion and glucose metabolism by influencing subcellular localization of glucokinase in pancreatic β-cells.Journal of diabetes investigation · 2016Article
- A Di-Rhamnolipid (RhaBioFactors (Oxford, England)Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AIMS/
introductionSrc, a non-receptor tyrosine kinase, regulates a wide range of cellular functions, and hyperactivity of Src is involved in impaired glucose metabolism in pancreatic β-cells. However, the physiological role of Src in glucose metabolism in normal, unstressed β-cells remains unclear. In the present study, we investigated the role of Src in insulin secretion and glucose metabolism. MATERIALS AND
methodsSrc was downregulated using small interfering ribonucleic acid in INS-1 cells, and glucose-induced insulin secretion, adenosine triphosphate content, intracellular calcium concentration, glucose utilization and glucokinase activity were measured. Expression levels of messenger ribonucleic acid and protein of glucokinase were examined by semiquantitative real-time polymerase chain reaction and immunoblotting, respectively. Cells were fractionated by digitonin treatment, and subcellular localization of glucokinase was examined by immunoblotting. Interaction between glucokinase and neuronal nitric oxide synthase was estimated by immunoprecipitation.
resultsIn Src downregulated INS-1 cells, glucose-induced insulin secretion was impaired, whereas insulin secretion induced by high K(+) was not affected. Intracellular adenosine triphosphate content and elevation of intracellular calcium concentration by glucose stimulation were suppressed by Src downregulation. Src downregulation reduced glucose utilization in the presence of high glucose, which was accompanied by a reduction in glucokinase activity without affecting its expression. However, Src downregulation reduced glucokinase in soluble, cytoplasmic fraction, and increased it in pellet containing intaracellular organelles. In addition, interaction between glucokinase and neuronal nitric oxide synthase was facilitated by Src downregulation.
conclusionsSrc plays an important role in glucose-induced insulin secretion in pancreatic β-cells through maintaining subcellular localization and activity of glucokinase.
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