title: In vitro study of antiadipogenic profile of latanoprost, travoprost, bimatoprost, and tafluprost in human orbital preadiopocytes.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  Human orbital adipose precursors were treated in vitro for 24 h (day 1) with PGF2α, latanoprost, travoprost, bimatoprost, and tafluprost in their commercial formulations (1:100 dilution). Expressions of adipogenic transcription factor, peroxisome proliferator-activated receptor-gamma (PPARγ), and CCAAT-enhancer-binding protein α (C/EBPα) were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR) at day 7. At 14 days, cells were stained with oil red O, intracellular lipid accumulation was evaluated by lipid absorbance, and adipocyte expression marker [Lipoprotein lipase (LPL)] was determined by real-time RT-PCR.
  
  
  RESULTS
  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 4 drugs showed that latanoprost had the weakest antiadipogenic effect, and bimatoprost induced the most significant reduction of adipogenesis.
  
  
  CONCLUSIONS
  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 patients with glaucoma.
authors: Department of Ophthalmology, Pusan National University Hospital, Busan, Korea.
authors: Hee Young
authors: HY
authors: Choi
authors: Ji Eun
authors: JE
authors: Lee
authors: Ji Woong
authors: JW
authors: Lee
authors: Hyun Jun
authors: HJ
authors: Park
authors: Ji Eun
authors: JE
authors: Lee
authors: Jae Ho
authors: JH
authors: Jung
mesh_terms: D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D050156:Adipogenesis / Q000187:drug effects*; D000328:Adult; D000577:Amides / Q000009:adverse effects; D000959:Antihypertensive Agents / Q000009:adverse effects*; D000069580:Bimatoprost; D022763:CCAAT-Enhancer-Binding Protein-alpha / Q000096:biosynthesis; D003008:Cloprostenol / Q000009:adverse effects / Q000031:analogs & derivatives; D015237:Dinoprost / Q000009:adverse effects* / Q000031:analogs & derivatives*; D006801:Humans; D066298:In Vitro Techniques; D000077338:Latanoprost; D008071:Lipoprotein Lipase / Q000096:biosynthesis; D009915:Orbit / Q000166:cytology / Q000187:drug effects*; D047495:PPAR gamma / Q000096:biosynthesis; D011460:Prostaglandins F / Q000009:adverse effects; D011461:Prostaglandins F, Synthetic / Q000009:adverse effects; D000069557:Travoprost; D055815:Young Adult
chemical_list: D000577:Amides; D000959:Antihypertensive Agents; D022763:CCAAT-Enhancer-Binding Protein-alpha; D047495:PPAR gamma; D011460:Prostaglandins F; D011461:Prostaglandins F, Synthetic; C485333:tafluprost; D003008:Cloprostenol; D000077338:Latanoprost; D015237:Dinoprost; D008071:Lipoprotein Lipase; D000069580:Bimatoprost; D000069557:Travoprost