ArticleAnnals of translational medicine2020
Arachidonic acid inhibits the production of angiotensin-converting enzyme in human primary adipocytes via a NF-κB-dependent pathway.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Exploring the Potential of Calebin-A in Targeting Obesity-Related Genes and Pathways.Journal of cellular and molecular medicine · 2026Article
- Crosstalk between renin and arachidonic acid (and its metabolites).Lipids in health and disease · 2025Review
- Fecal 16S rRNA sequencing and metabolomics reveal abnormal metabolism activity in preterm infants with different gestational ages.Frontiers in cellular and infection microbiology · 2025Article
- Inflammation Resolution in the Cardiovascular System: Arterial Hypertension, Atherosclerosis, and Ischemic Heart Disease.Antioxidants & redox signaling · 2024Review
- DAPK2 activates NF-κB through autophagy-dependent degradation of I-κBα during thyroid cancer development and progression.Annals of translational medicine · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe 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.
methodsHuman 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.
resultsArachidonic 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.
conclusionsThis 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-decreasing effects of AA.
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