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| Description | Latanoprost is a prostaglandin F2alpha analogue and a prostanoid selective FP receptor agonist with an ocular hypertensive effect. Latanoprost increases uveoscleral outflow and thereby reduces intraocular pressure. | ||
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| In vitro | Latanoprost functioned as both an indirect activator of AMP-activated protein kinase and a selective retinoid X receptor α (RXRα) antagonist able to selectively antagonise the transcription of a RXRα/peroxisome proliferator-activated receptor γ heterodimer[2]. Latanoprost induced morphological abnormality and viability decline of HCS cells in vitro. It induces cell cycle arrest of HCS cells. Latanoprost induces abnormal changes of plasma membrane, DNA fragmentation and ultrastructural abnormality of HCS cells. Caspase activation in HCS cells is also activated by Latanoprost treatment. Latanoprost induces MTP disruption and quantitative changes of mitochondrion-associated pro-apoptotic regulators in HCS cells[1]. Latanoprost is effective in inhibiting adipogenesis, reducing lipogenesis, promoting fatty acid oxidation and enhancing GLUT4 translocation and glucose uptake both in adipocytes and myotubes[2]. | ||
| In vivo | Latanoprost, a clinical drug for treating primary open-angle glaucoma and intraocular hypertension, effectively ameliorates glucose and lipid disorders in two mouse models of type 2 diabetes. Its treatment improves glucose tolerance. Chronic administration of latanoprost decreases serum lipids and enhances insulin signalling in white adipose tissue and skeletal muscle. It effectually activates AMPK and regulates glucose and lipid metabolism-relevant genes in diabetic mice[2]. |
| Quantity | 500 milligram |
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