Fatostatin (125256-00-0) blocks adipogenesis by inhibiting the activation of SREBP. Inhibits the ER-Golgi translocation of SREBPs via binding to their escort protein (SCAP). Fatostatin prevents increases in body weight, blood glucose, and hepatic fat accumulation in obese ob/ob mice.1?Inhibits high glucose-induced TGF-β in mesangial cells.2?Cell permeable.
Fatostatin A is Cell permeable inhibitor of SREBP activation.
ChEBI: 4-(4-methylphenyl)-2-(2-propyl-4-pyridinyl)thiazole is a member of thiazoles.
Fatostatin (125B11) (30 mg/kg; 150 μL; i.p. injection; daily for 28 days) reduces adiposity, ameliorated fatty liver by reducing triglyceride (TG) storage, and lowered hyperglycemia in ob/ob mice[2].
| Animal Model: | Four-to-five-week-old homozygous male obese (ob/ob) mice (C57BL/6J)[2] |
| Dosage: | 30 mg/kg; 150 μL |
| Administration: | i.p. injection; daily for 28 days |
| Result: | Blocked increases in body weight, blood glucose, and hepatic fat accumulation in obese ob/ob mice, even under uncontrolled food intake. |
1) Kamisuki et al. (2009), A small molecule that blocks fat synthesis by inhibiting the activation of SREBP; Chem. Biol., 16 882
2) Uttarwar et al. (2012), SREBP-1 activation by glucose mediates TGF-β upregulation in mesangial cells; Am. J. Physiol. Renal Physiol., 302 F329
