Arachidonic acid inhibits the production of angiotensin-converting enzyme in human primary adipocytes via a NF-κB-dependent pathway.
Xu L., Schüler R., Xu C., Seebeck N., Markova M., Murahovschi V.
Prospective Study, published in Ann Transl Med (2020) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- 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
- Prospective Study
- Journal
- Ann Transl Med (2020)
- Country
- China
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 33490164
- PMCID
- PMC7812212
- DOI
- 10.21037/atm-20-7514
- Citations
- 7
Abstract (original English)
Background The modulating mechanism of fatty acids on angiotensin-converting enzyme production (ACE) in human adipocytes is still elusive. Diet-induced regulation of the renin angiotensin system is thought to be involved in obesity and hypertension, and several previous studies have used mouse cell lines such as 3T3-L1 to investigate this. This study was carried out in human subcutaneous adipocytes for better understanding of the mechanism. Methods Human adipose stem cells were isolated from subcutaneous adipose tissue biopsies collected from four patients during bariatric surgery and differentiated into mature adipocytes. The mRNA expression and the activity of ACE were measured under different stimuli in cell cultures. Results Arachidonic acid (AA) decreased ACE mRNA expression and ACE activity in a dose-dependent manner while palmitic acid had no effect. The decrease of ACE by 100 µM AA was reversed by the addition of 5 µM nuclear factor-κB (NF-κB) inhibitor. Furthermore, when the production of 20-hydroxyeicosatetraenoic acid, a metabolite of AA, was stopped by the specific inhibitor HET0016 (10 µM) in the culture media, the effect of AA was blocked. Conclusions This study indicated that AA can decrease the expression and activity of ACE in cultured human adipocytes, via an inflammatory NF-κB-dependent pathway. Blocking 20-hydroxyeicosatetraenoic acid attenuated the ACE-decr
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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