ArticleAmerican journal of physiology. Endocrinology and metabolism2015
Increased GIP signaling induces adipose inflammation via a HIF-1α-dependent pathway and impairs insulin sensitivity in mice.
Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06606821 (The Effects of Tirzepatide on Coronary Plaque Lipid Content and Myocardial Microvascular Function in Overweight and Obese People With Coronary Disease - The IDEAL-COR Study), which is not on this map. Cited by 50 papers, 2 of them syntheses that pooled it.
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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.
The trial behind it
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.
The Effects of Tirzepatide on Coronary Plaque Lipid Content and Myocardial Microvascular Function in Overweight and Obese People With Coronary Disease - The IDEAL-COR Study
Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 citations in OpenAlex.
- Anti-inflammatory effects of tirzepatide: a systematic review and meta-analysis.Reviews in endocrine & metabolic disorders · 2026Pooled it
- GIP as a Potential Therapeutic Target for Atherosclerotic Cardiovascular Disease-A Systematic Review.International journal of molecular sciences · 2020Pooled it
- Trial
- Trial
- Review
- The role of GIP in carbohydrate metabolism: Implications in the development of therapies for T2DM, a narrative review.Histology and histopathology · 2026Review
- The role of the incretin GIP in inflammation.Journal of endocrinological investigation · 2026Review
- Revitalizing GIP: Therapeutic Potential in Metabolic and Neurodegenerative Disorders.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Association between plasma glucose-dependent insulinotropic polypeptide and active adiponectin in normoglycemic women.Endocrine connections · 2026Article
- Metaflammation's Role in Systemic Dysfunction in Obesity: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Curcumin alleviates visceral adiposity via inhibiting GIP release from hypoxic intestinal damage in MASH rats.NPJ science of food · 2025Article
- Impact of Dietary Fiber on Inflammation in Humans.International journal of molecular sciences · 2025Review
- GLP-1 receptor agonist-based therapies and cardiovascular risk: a review of mechanisms.The Journal of endocrinology · 2024Review
- Anti-Influenza A Potential ofInternational journal of molecular sciences · 2024Article
- (D-AlaInternational journal of molecular sciences · 2024Article
- Adipose Tissue Hypoxia in Obesity: Clinical Reappraisal of Hypoxia Hypothesis.Advances in experimental medicine and biology · 2024Review
- Article
- Relevance and consequence of chronic inflammation for obesity development.Molecular and cellular pediatrics · 2023Review
- The expanding incretin universe: from basic biology to clinical translation.Diabetologia · 2023Review
- GIPR/GLP-1R dual agonist therapies for diabetes and weight loss-chemistry, physiology, and clinical applications.Cell metabolism · 2023Review
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
Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone secreted in response to dietary fat and glucose. The blood GIP level is elevated in obesity and diabetes. GIP stimulates proinflammatory gene expression and impairs insulin sensitivity in cultured adipocytes. In obesity, hypoxia within adipose tissue can induce inflammation. The aims of this study were 1) to examine the proinflammatory effect of increased GIP signaling in adipose tissues in vivo and 2) to clarify the association between GIP and hypoxic signaling in adipose tissue inflammation. We administered GIP intraperitoneally to misty (lean) and db/db (obese) mice and examined adipose tissue inflammation and insulin sensitivity. We also examined the effects of GIP and hypoxia on expression of the GIP receptor (GIPR) gene and proinflammatory genes in 3T3-L1 adipocytes. GIP administration increased monocyte chemoattractant protein-1 (MCP-1) expression and macrophage infiltration into adipose tissue and increased blood glucose in db/db mice. GIPR and hypoxia-inducible factor-1α (HIF-1α) expressions were positively correlated in the adipose tissue in mice. GIPR expression increased dramatically in differentiated adipocytes. GIP treatment of adipocytes increased MCP-1 and interleukin-6 (IL-6) production. Adipocytes cultured either with RAW 264 macrophages or under hypoxia expressed more GIPR and HIF-1α, and GIP treatment increased gene expression of plasminogen activator inhibitor 1 and IL-6. HIF-1α gene silencing diminished both macrophage- and hypoxia-induced GIPR expression and GIP-induced IL-6 expression in adipocytes. Thus, increased GIP signaling plays a significant role in adipose tissue inflammation and thereby insulin resistance in obese mice, and HIF-1α may contribute to this process.
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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.