ArticleDiabetes2013
C-reactive protein causes insulin resistance in mice through Fcγ receptor IIB-mediated inhibition of skeletal muscle glucose delivery.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
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- The Association Between Pregnancy Complications and Long-term Maternal Cardiometabolic Health in the MIREC Cohort Study.The Journal of clinical endocrinology and metabolism · 2025Article
- The effect of hsCRP on TyG index-associated cardiovascular risk in patients with acute coronary syndrome undergoing PCI.Scientific reports · 2024Article
- CRP and soluble CTLA4 are determinants of anti-PD1 resistance in gastrointestinal cancer.American journal of cancer research · 2024Article
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- Endothelial ERα promotes glucose tolerance by enhancing endothelial insulin transport to skeletal muscle.Nature communications · 2023Article
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- Doxepin Exacerbates Renal Damage, Glucose Intolerance, Nonalcoholic Fatty Liver Disease, and Urinary Chromium Loss in Obese Mice.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Novel myostatin-specific antibody enhances muscle strength in muscle disease models.Scientific reports · 2021Article
- Correlation of glycemic regulation and endotrophin in patients with type 2 Diabetes; pilot study.Diabetology & metabolic syndrome · 2021Article
- Supplementation With the Sialic Acid Precursor N-Acetyl-D-Mannosamine Breaks the Link Between Obesity and Hypertension.Circulation · 2019Article
- Abdominal Fat Is Directly Associated With Inflammation In Persons With Type-2 Diabetes Regardless Of Glycemic Control - A Jordanian Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
- Fc Gamma Receptor IIb Expressed in Hepatocytes Promotes Lipid Accumulation and Gluconeogenesis.International journal of molecular sciences · 2018Article
- Hyposialylated IgG activates endothelial IgG receptor FcγRIIB to promote obesity-induced insulin resistance.The Journal of clinical investigation · 2018Article
- Article
- Effects of C-reactive protein on the expression of matrix metalloproteinases and their inhibitors via Fcγ receptors on 3T3-L1 adipocytes.International journal of medical sciences · 2017Article
- Nonnuclear Estrogen Receptor Activation Improves Hepatic Steatosis in Female Mice.Endocrinology · 2016Article
- Endothelial Fcγ Receptor IIB Activation Blunts Insulin Delivery to Skeletal Muscle to Cause Insulin Resistance in Mice.Diabetes · 2016Article
- Energy balance and macronutrient distribution in relation to C-reactive protein and HbA1c levels among patients with type 2 diabetes.Food & nutrition research · 2016Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Elevations in C-reactive protein (CRP) are associated with an increased risk of insulin resistance. Whether CRP plays a causal role is unknown. Here we show that CRP transgenic mice and wild-type mice administered recombinant CRP are insulin resistant. Mice lacking the inhibitory Fcγ receptor IIB (FcγRIIB) are protected from CRP-induced insulin resistance, and immunohistochemistry reveals that FcγRIIB is expressed in skeletal muscle microvascular endothelium and is absent in skeletal muscle myocytes, adipocytes, and hepatocytes. The primary mechanism in glucose homeostasis disrupted by CRP is skeletal muscle glucose delivery, and CRP attenuates insulin-induced skeletal muscle blood flow. CRP does not impair skeletal muscle glucose delivery in FcγRIIB(-/-) mice or in endothelial nitric oxide synthase knock-in mice with phosphomimetic modification of Ser1176, which is normally phosphorylated by insulin signaling to stimulate nitric oxide-mediated skeletal muscle blood flow and glucose delivery and is dephosphorylated by CRP/FcγRIIB. Thus, CRP causes insulin resistance in mice through FcγRIIB-mediated inhibition of skeletal muscle glucose delivery.
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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.