ArticleEMBO molecular medicine2014
Fas (CD95) expression in myeloid cells promotes obesity‐induced muscle insulin resistance.
Article in EMBO molecular medicine, 2014. 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, 29 citations in OpenAlex.
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- The Response of Antioxidant Enzymes and Antiapoptotic Markers to an Oral Glucose Tolerance Test (OGTT) in Children and Adolescents with Excess Body Weight.International journal of molecular sciences · 2023Observational
- Adipose tissue macrophages as potential targets for obesity and metabolic diseases.Frontiers in immunology · 2023Review
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- Fas-Associated Factor 1 Promotes Hepatic Insulin Resistance via JNK Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
- Adipocyte-specific gp130 signalling mediates exercise-induced weight reduction.International journal of obesity (2005) · 2020Article
- A Novel Subset of CD95Frontiers in immunology · 2020Article
- Roles of follicle stimulating hormone and its receptor in human metabolic diseases and cancer.American journal of translational research · 2020Review
- Beyond adiponectin and leptin: adipose tissue-derived mediators of inter-organ communication.Journal of lipid research · 2019Review
- LncRNA GACAT3 predicts poor prognosis and promotes cell proliferation in breast cancer through regulation of miR-497/CCND2.Cancer biomarkers : section A of Disease markers · 2018Article
- Article
- Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation.Nature immunology · 2017Article
- Altered Methylation Profile of Lymphocytes Is Concordant with Perturbation of Lipids Metabolism and Inflammatory Response in Obesity.Journal of diabetes research · 2016Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low-grade inflammation in adipose tissue and liver has been implicated in obesity-associated insulin resistance and type 2 diabetes. Yet, the contribution of inflammatory cells to the pathogenesis of skeletal muscle insulin resistance remains elusive. In a large cohort of obese human individuals, blood monocyte Fas (CD95) expression correlated with systemic and skeletal muscle insulin resistance. To test a causal role for myeloid cell Fas expression in the development of skeletal muscle insulin resistance, we generated myeloid/haematopoietic cell-specific Fas-depleted mice. Myeloid/haematopoietic Fas deficiency prevented the development of glucose intolerance in high fat-fed mice, in ob/ob mice, and in mice acutely challenged by LPS. In vivo, ex vivo and in vitro studies demonstrated preservation of muscle insulin responsiveness with no effect on adipose tissue or liver. Studies using neutralizing antibodies demonstrated a role for TNFα as mediator between myeloid Fas and skeletal muscle insulin resistance, supported by significant correlations between monocyte Fas expression and circulating TNFα in humans. In conclusion, our results demonstrate an unanticipated crosstalk between myeloid cells and skeletal muscle in the development of obesity-associated insulin resistance.
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