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Jae Ho Jung, Hee Young Choi, Ji Eun Lee, Hyun Jun Park, Ji Eun Lee; In Vitro study of Anti-adipogenic Profile of Latanoprost, Travoprost, Bimatoprost and Tafluprost in Human Orbital Preadiopocytes. Invest. Ophthalmol. Vis. Sci. 2012;53(14):1258.
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To investigate the effect of prostaglandin F2α (PGF2α), latanoprost, travoprost, bimatoprost, and tafluprost on human orbital preadipocyte differentiation and intracellular lipid storage, and to reveal the potential mechanisms by which topical prostaglandin analogs induce orbital fat volume reduction and cause deep superior sulcus syndrome.
Human orbital adipose precursors were treated in vitro for 24 hours (day 1) with PGF2α, latanoprost, travoprost, bimatoprost, and tafluprost in their commercial formulations (1:100 dilution). Expressions of adipogenic transcription factor, peroxisome proliferator activator gamma (PPARγ) and CCAAT-enhancer-binding proteins (C/EBP α) were determined by real time RT-PCR at day 7. At 14 days, cells were stained with oil red O and intracellular lipid accumulation was evaluated by lipid absorbance, and adipocyte expression gene (Lipoprotein lipase (LPL)) was determined by real time RT-PCR.
Our results showed that PGF2α and topical prostaglandin analogs down-regulated the expression of PPARγ and C/EBPα, and inhibited accumulation of intra-cytoplasmic lipid droplets and expression of LPL compared with the untreated control. Comparison between the four drugs showed that latanoprost had the weakest anti-adipogenic effect and bimatoprost induced the most significant reduction of adipogenesis.
Latanoprost, travoprost, bimatoprost, and tafluprost inhibited human preadipocyte differentiation and intracellular lipid accumulation. Morphologic and metabolic changes in orbital adipocytes caused by PGF2α analogs are a possible pathophysiologic explanation of superior eyelid deepening in glaucoma patients.
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