ArticleThe Journal of biological chemistry2009
Noncanonical activation of Akt/protein kinase B in {beta}-cells by the incretin hormone glucose-dependent insulinotropic polypeptide.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Metabolic Adaptions/Reprogramming in Islet Beta-Cells in Response to Physiological Stimulators-What Are the Consequences.Antioxidants (Basel, Switzerland) · 2022Review
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- Possible vasculoprotective role of linagliptin against sodium arsenite-induced vascular endothelial dysfunction.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Glucose-dependent insulinotropic polypeptide signaling in pancreatic β-cells and adipocytes.Journal of diabetes investigation · 2012Review
- Reduction of both beta cell death and alpha cell proliferation by dipeptidyl peptidase-4 inhibition in a streptozotocin-induced model of diabetes in mice.Diabetologia · 2012Article
- Evidence for PTEN-independent Akt activation and Akt-independent p27(Kip1) expression in advanced bladder cancer.Oncology letters · 2011Article
- Akt as a victim, villain and potential hero in Parkinson's disease pathophysiology and treatment.Cellular and molecular neurobiology · 2011Article
- Glucose-dependent insulinotropic polypeptide stimulates the proliferation of colorectal cancer cells.Regulatory peptides · 2010Article
- GIP and GLP-1, the two incretin hormones: Similarities and differences.Journal of diabetes investigation · 2010Review
- Article
- Epac2-dependent rap1 activation and the control of islet insulin secretion by glucagon-like peptide-1.Vitamins and hormones · 2010Review
- Akt inhibitor Akt-IV blocks virus replication through an Akt-independent mechanism.Journal of virology · 2009Article
- Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide.The Journal of biological chemistry · 2009Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Therapeutics based on the actions of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), have recently been introduced for the treatment of type 2 diabetes mellitus. The serine/threonine kinase Akt is a major mediator of incretin action on the pancreatic islet, increasing beta-cell mass and function and promoting beta-cell survival. The mechanisms underlying incretin activation of Akt are thought to involve an essential phosphoinositide 3-kinase-mediated phosphorylation of threonine 308, similar to the prototypical Akt activator, insulin-like growth factor-I (IGF-I). In this study, using activity assays on immunoprecipitated Akt, we discovered that GIP and GLP-1 were capable of stimulating Akt in the INS-1 beta-cell line and isolated mouse islets via a mechanism that did not require phosphoinositide 3-kinase or phosphorylation of Thr(308) and Ser(473), and this pathway involved the production of cAMP. Furthermore, we found that GIP stimulated anti-apoptotic signaling via this alternate mode of Akt activation. We conclude that incretins can activate Akt via a novel noncanonical mechanism that may provide an alternative therapeutic target for the treatment of type 2 diabetes mellitus and have broader implications for Akt physiology in human health and disease.
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