Coronarin A (30 or 100 mg/kg; i.p. or p.o.; once daily for 22 days) ameliorates hyperglycemia in mice[1].
Coronarin A (100 mg/kg; p.o.; once daily for 22 days) inhibits the mTOR/S6K1 pathway to activate PI3K/Akt and ERK/β-catenin signaling in livers of ob/ob mice[1].
Pharmacokinetic properties of Coronarin A after single administrationa in ob/ob mice[1].
| Coronarin A | t1/2 (h) | tmax (h) | Cmax (ng/mL) | AUC0-t (ng·h/mL) | AUC0-∞ (ng·h/mL) | MRT (h) |
| i.p. | 14.8 | 1.0 | 1073 | 4571 | 11045 | 21.7 |
| p.o. | 3.01 | 1.0 | 388 | 1694 | 1856 | 4.88 |
Data are presented as the mean of three mice.
aCoronarin A was intraperitoneally or orally administered at 30 mg/kg to ob/ob mice.
| Animal Model: | Male ob/ob mice[1] |
| Dosage: | 30 mg/kg (IP) or 100 mg/kg (PO) |
| Administration: | Oral or intraperitoneal administration, once daily for 22 days |
| Result: | Significantly decreased the non-fasting and fasting blood glucose. Significantly reduced the serum insulin concentration at 15 min after glucose loading, reduced the average daily food intake while the body weight was unaffected. Increased hepatic glycogen content and the expression levels of gluconeogenic gene Pck1 and G6pc were significantly decreased. |
| Animal Model: | Female ob/ob mice[1] |
| Dosage: | 30 mg/kg |
| Administration: | Intraperitoneal or oral administration (Pharmacokinetic Analysis) |
| Result: | Intraperitoneal injection exhibited higher plasma exposure than oral gavage at the same dose of 30 mg/kg, with Cmax value of 1073 and 388 ng/mL, respectively. |
