ArticleThe Journal of biological chemistry2011
Gastric inhibitory peptide controls adipose insulin sensitivity via activation of cAMP-response element-binding protein and p110β isoform of phosphatidylinositol 3-kinase.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 57 citations in OpenAlex.
- Adipose Tissue Remodeling Beyond Weight Loss: New Insights Into Incretin-Based Therapies and Bariatric Surgery.Current obesity reports · 2026Review
- Do Fasting GLP-1 and GIP Levels Predict the Initial Pharmacological Response to Semaglutide and Tirzepatide?Diagnostics (Basel, Switzerland) · 2026Article
- Review
- Adipose Tissue, at the Core of the Action of Incretin and Glucagon-Based Anti-Obesity Drugs.Current obesity reports · 2025Review
- A Contemporary Rationale for Agonism of the GIP Receptor in the Treatment of Obesity.Diabetes · 2025Review
- The Art and Science of Antidiabetic Medications and Obesity Management.Mini reviews in medicinal chemistry · 2025Review
- Glucose-Dependent Insulinotropic Polypeptide Inhibits AGE-Induced NADPH Oxidase-Derived Oxidative Stress Generation and Foam Cell Formation in Macrophages Partly via AMPK Activation.International journal of molecular sciences · 2024Article
- Review
- Obesity and Type 2 Diabetes: Adiposopathy as a Triggering Factor and Therapeutic Options.Molecules (Basel, Switzerland) · 2023Review
- Article
- Tirzepatide for the treatment of adults with type 2 diabetes: An endocrine perspective.Diabetes, obesity & metabolism · 2023Review
- GIPR Is Predominantly Localized to Nonadipocyte Cell Types Within White Adipose Tissue.Diabetes · 2022Article
- Potential Therapeutic Targeting Neurotransmitter Receptors in Diabetes.Frontiers in endocrinology · 2022Review
- GIPR agonism mediates weight-independent insulin sensitization by tirzepatide in obese mice.The Journal of clinical investigation · 2021Article
- A compendium of G-protein-coupled receptors and cyclic nucleotide regulation of adipose tissue metabolism and energy expenditure.Clinical science (London, England : 1979) · 2020Review
- Pharmacological antagonism of the incretin system protects against diet-induced obesity.Molecular metabolism · 2020Article
- PI3Kβ-A Versatile Transducer for GPCR, RTK, and Small GTPase Signaling.Endocrinology · 2019Review
- Gastric inhibitory polypeptide/glucose-dependent insulinotropic polypeptide signaling in adipose tissue.Journal of diabetes investigation · 2019Article
- Homogeneous Assays of Second Messenger Signaling and Hormone Secretion Using Thermofluorimetric Methods That Minimize Calibration Burden.Analytical chemistry · 2017Article
- TXNIP in Metabolic Regulation: Physiological Role and Therapeutic Outlook.Current drug targets · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Gastric inhibitory peptide (GIP) is an incretin hormone secreted in response to food intake. The best known function of GIP is to enhance glucose-dependent insulin secretion from pancreatic β-cells. Extra-pancreatic effects of GIP primarily occur in adipose tissues. Here, we demonstrate that GIP increases insulin-dependent translocation of the Glut4 glucose transporter to the plasma membrane and exclusion of FoxO1 transcription factor from the nucleus in adipocytes, establishing that GIP has a general effect on insulin action in adipocytes. Stimulation of adipocytes with GIP alone has no effect on these processes. Using pharmacologic and molecular genetic approaches, we show that the effect of GIP on adipocyte insulin sensitivity requires activation of both the cAMP/protein kinase A/CREB signaling module and p110β phosphoinositol-3' kinase, establishing a novel signal transduction pathway modulating insulin action in adipocytes. This insulin-sensitizing effect is specific for GIP because isoproterenol, which elevates adipocyte cAMP and activates PKA/CREB signaling, does not affect adipocyte insulin sensitivity. The insulin-sensitizing activity points to a more central role for GIP in intestinal regulation of peripheral tissue metabolism, an emerging feature of inter-organ communication in the control of metabolism.
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What OpenQuestion holds
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.