Isolated primary human visceral fat cells release more angiotensin II than subcutaneous adipocytes
(English)Manuscript (preprint) (Other academic)
Background. Visceral obesity relates strongly to the metabolic syndrome and hence to hypertension. Although a local renin-angiotensin-system (RAS) in fat tissue is known, very few studies have dealt with RAS in isolated primary human fat cells, in particular from the visceral compartment.
Methods. Measurement of angiotensin II (Ang II) in medium from isolated primary human fat cells from visceral and subcutaneous adipose tissues and analyses of RAS-components in human fat cells and fat tissues.
Results. Primary human fat cells from omental adipose tissue produced more Ang II than subcutaneous cells. Treatment with insulin did not affect Ang II production and body-massindex of the fat-donors was unrelated to Ang II production. The PPAR gamma agonist rosiglitazone inhibited Ang II production in both types of isolated fat cells while addition of the Ang II receptor antagonist eprosartan inhibited the production in only subcutaneous fat cells. Addition of 50 or 200 nM of Ang II inhibited the PPAR gamma response elementactivity (PPRE-activity) in visceral, but not in the subcutaneous adipocytes.
Conclusions. Since high PPRE-activity induced by rosiglitazone inhibited the Ang II production, it is possible that reduced PPRE-activity in the visceral human fat cells, demonstrated by us earlier, can explain the comparatively high Ang II production in these cells. This could form the basis for a local paracrine viscous circle in visceral fat where low PPRE-activity increases Ang II production that is further enhanced by Ang II-mediated inhibition of PPRE-activity which ultimately leads to high concentrations of Ang II in human adipose tissue.
Fat cells, angiotensin II, human, insulin, peroxisome proliferator activated receptor gamma
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-19167OAI: oai:DiVA.org:liu-19167DiVA: diva2:223498