Differential response of preadipocytes and adipocytes to prostacyclin and prostaglandin E2: physiological implications.
Vassaux G., Gaillard D., Darimont C., Ailhaud G., Negrel R.
Animal Study, published in Endocrinology (1992) — 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 (1992)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 1330499
- DOI
- 10.1210/endo.131.5.1330499
Abstract (original English)
The major prostaglandins (PGs) locally produced in adipose tissue both in rodent and man are PGE2 and prostacyclin (PGI2). We have recently described PGI2 as an autocrine promoter and/or amplifier of terminal differentiation of cultured preadipocytes in several species. The effectiveness and specificity of PGI2 as an adipogenic agent are related to its ability to induce in preadipocytes intracellular increases of both cAMP and free calcium. Moreover, PGs of the E series are well known to exert an antilipolytic effect in mature adipocytes. These observations have prompted us to address two questions of physiological interest: 1) Is PGI2 still able to increase cAMP in differentiated adipocytes, behaving thus as a lipolytic agent, and 2) Is PGE2 able to negatively modulate cAMP production in adipose precursor cells, behaving thus as a counteracting effector of PGI2 action? Our results, with respect to cAMP production and/or lipolysis and antilipolysis, demonstrate clearly that in adipose tissue of both rat and man, PGI2 exclusively affects adipose precursor cells whereas PGE2 exclusively affects adipocytes. We propose a model of concerted action for both PGs in the development of adipose tissue mass, PGI2 behaving as an adipogenic-hyperplastic effector and PGE2 as an antilipolytic-hypertrophic effector.
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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