Differentiation of preadipose cells: paracrine role of prostacyclin upon stimulation of adipose cells by angiotensin-II.
Darimont C., Vassaux G., Ailhaud G., Negrel R.
Animal Study, published in Endocrinology (1994) — 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
- Animal Study
- Journal
- Endocrinology (1994)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 7956925
- DOI
- 10.1210/endo.135.5.7956925
Abstract (original English)
Prostacyclin (PGI2), the major metabolite of arachidonic acid in adipose tissue, has been shown to play a key role in the process of preadipose cell differentiation in vitro. Moreover, angiotensin-II (Ang II) is able to induce the production of PGI2 in suspensions of isolated adipocytes as well as in the interstitial fluid of rat adipose tissue. A possible role of Ang II in the control of the autocrine-paracrine adipogenic effect of PGI2 has been investigated, using cells of the Ob1771 preadipocyte clonal line cultured in serum-free chemically defined medium. Whereas both preadipose and adipose cells were able to produce PGI2 upon exposure to arachidonic acid, only adipose cells were able to do so when challenged with Ang II. In agreement with this observation, the ability of Ang II to induce preadipose cells to differentiate required the simultaneous presence of differentiated cells. Such coculture experiments show that the promoting effect of Ang II on preadipose cell differentiation was strongly reduced by aspirin, antibodies able to neutralize PGI2, and the AT2 receptor antagonist PD123177, but not by the AT1 receptor antagonist losartan. Together, these results support Ang II as being able, by means of binding to a receptor of the AT2 subtype present in adipose cells, to control the adipogenic effect of PGI2 through a paracrine mode of action.
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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