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It is thought that prostamides act via a specific receptor (or several receptors) which is distinct from the prostaglandin receptors. No such receptor has been identified .
Importantly, prostaglandin F2α ethanolamide inhibits preadipocyte differentiation and increases their proliferation. This mechanism maintains a reserve of adipocyte progenitor cells. This might allow for healthier development of fat tissue, which is through hyperplasia that outbalances morbid hypertrophy and ectopic fat deposition. Hyperplasia allows for storing excess energy triglycerides in more and smaller fat cells, instead of continually increasing the size of fat cells that leads to inflammation, ectopic fat deposits and fat tissue hypoxia. These findings have been behind the foundation of the Fat Four Ps Hypothesis, namely, Preadipocyte Pool Preservation by prostaglandin F2α ethanolamide. This mechanism could be tightly balanced as it can be controlled through the feedback control loop that involves this anti-adipogenic metabolite and its pro-adipogenic precursor anandamide (AEA). This has further suggested prostaglandin F2α ethanolamide synthetic pharmaceutical analog Bimatoprost as a promising therapy for obesity.
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