Dihydrocapsiate, as a compound of capsinoid family, is an orally active TRPV1 agonist. Dihydrocapsiate can be used for the research of metabolism disease
In Vitro
Dihydrocapsiate (10, 25 and 50 μM; 48 hours; human preadipocytes) does not affect cell viability. Dihydrocapsiate (10 and 20 μM; 8 days; mature adipocytes) markedly decreases the expression levels of other adipogenic markers (such as SREBP1, FABP4, PLIN1, ADIPOQ and LEPTIN) and inflammatory markers (MCP1 and TNFα), whereas it enhances the expression levels of PGC1α (master regulator of mitochondrial biogenesis) and TBX1 (marker of “brite” cell). Dihydrocapsiate (25~200 μM; RAW 264.7 cells) prevents NO release and intracellular ROS generation. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability AssayCell Line: Human preadipocytes Concentration: 10, 25 and 50 μM Incubation Time: 48 hours Result: Did not affect cell viability. RT-PCRCell Line: Mature adipocytes Concentration: 10 and 20 μM Incubation Time: 8 days Result: Markedly decreased the expression levels of other adipogenic markers (such as SREBP1, FABP4, PLIN1, ADIPOQ and LEPTIN) and inflammatory markers (MCP1 and TNFα), whereas it enhanced the expression levels of PGC1α (master regulator of mitochondrial biogenesis) and TBX1 (marker of “brite” cell).
In Vivo
Dihydrocapsiate (2 and 10 mg/kg; p.o.) improves morphometric parameters and insulin levels, prevents high fat diet (HFD)-induced adipocyte size and enhances energy expenditure-related genes in WAT, alleviates HFD-induced hepatic steatosis, prevents HFD-induced fat deposition and enhances mitochondrial biogenesis genes in BAT and improves intestinal morphology and modulates SCFA availability. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: HFD-fed mice Dosage: 2 and 10 mg/kg Administration: P.o. Result: Improved morphometric parameters and insulin levels, prevented HFD-induced adipocyte size and enhanced energy expenditure-related genes in WAT, alleviated HFD-induced hepatic steatosis, prevented HFD-induced fat deposition and enhanced mitochondrial biogenesis genes in BAT and improved intestinal morphology and modulates SCFA availability.
