ArticleInternational journal of obesity (2005)2021
The nuclear retinoid-related orphan receptor RORα controls adipose tissue inflammation in patients with morbid obesity and diabetes.
Article in International journal of obesity (2005), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Marine n-3 polyunsaturated fatty acids slow sleep impairment progression by regulating central circadian rhythms in type 2 diabetes.Cell reports. Medicine · 2025Trial
- Article
- Multi-omics mediation pipeline reveals differential pathways of maternal SNPs affecting newborn adiposity outcomes.BMC genomic data · 2025Article
- Association Between RORA Polymorphisms and Obesity.Biochemical genetics · 2025Article
- Targeting RORα in macrophages to boost diabetic bone regeneration.Cell proliferation · 2023Article
- CCL17 and CCL22 chemokines are upregulated in human obesity and play a role in vascular dysfunction.Frontiers in endocrinology · 2023Article
- Identification of hub genes regulating the cell activity and function of adipose-derived stem cells under oxygen-glucose deprivation.Frontiers in molecular biosciences · 2022Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsInflammation governs adipose tissue (AT) dysfunction in obesity. Retinoic acid receptor-related orphan receptor alpha (RORα) is associated with inflammation and insulin resistance in animal studies, but its role in human obesity remains elusive. We investigated the expression and function of RORα on AT inflammation in patients with morbid obesity with/without diabetes. SUBJECTS/
methodsWe assessed RORα expression in paired biopsies of subcutaneous and omental AT from 41 patients (body mass index (BMI) 43.3 ± 0.8 kg/m
resultsRORα expression was significantly higher in omental AT than in subcutaneous AT (p = 0.03) and was positively associated with BMI (r = 0.344, p = 0.027) and homeostasis model assessment of insulin resistance (r = 0.319, p = 0.041). In ex vivo assays, IL-8/CXCL8 and MCP-1/CCL2 chemokine release was significantly higher in omental fat explants from diabetic patients than from non-diabetics and was significantly diminished by RORα blockade (p < 0.05). Inhibition of RORα improved protein kinase B signaling and decreased NF-κB activity in omental AT from patients with diabetes (p < 0.05). Under dynamic flow conditions, RORα blockade prevented mononuclear cell attachment to human dysfunctional endothelial cells.
conclusionsRORα blockade represents a potential therapy to prevent AT dysfunction and inflammation associated with insulin resistance in human obesity.
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