Gender dimorphism in adipose tissue response to stress conditions: A plausible mechanism to explain the conflicting data regarding trauma and obesity.
Diebel ME., Diebel LN., Liberati DM.
Laboratory Study on Chronic Inflammation, published in J Trauma Acute Care Surg (2016) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- J Trauma Acute Care Surg (2016)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 27389130
- DOI
- 10.1097/TA.0000000000001170
- Citations
- 5
Abstract (original English)
Introduction Obesity is a chronic low-grade inflammatory condition associated with the elaboration of proinflammatory cytokines and adipokines from adipose tissue. Gender dimorphism (in part due to sex hormones) has been identified after injury and hemorrhagic shock. We hypothesized that the sex hormones estrogen (E2) and testosterone (DHT) have disparate effects on inflammatory mediator production from adipose tissue under stress conditions. This was studied in an in vitro model. Methods Mature adipocytes differentiated from adipose-derived stem cells were cocultured (2:1) with macrophages (RAW 264.7) and subjected to hypoxia/reoxygenation (H/R) and/or incubation with physiologic (10 μM) or stress (10 μM) concentrations of epinephrine (epi). Estrogen or DHT was added in a range of physiologic concentrations, and culture supernatants were obtained 12 hours after incubation, and tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and adiponectin levels were measured by enzyme-linked immunosorbent assay. Results Basal TNF-α and IL-6 release from cocultures was significantly increased in response to epi and/or H/R conditions. Estrogen decreased cytokine release to basal levels, whereas DHT had no effect. Of note, varying the concentration of epi had no effect on cytokine release. Basal levels of adiponectin release were significantly decreased in response to epi and/or H/R cond
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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