Antidiabetic mechanism of Bakumondo-inshi.

To determine the antidiabetic mechanism of Bakumondo-inshi (BI), we examined its effects on glucose absorption, alpha-glucosidase activity, sodium-dependent glucose transporter and facilitative glucose transporter isoform 5 (GLUT5) in small intestine. The oral administration of BI into KK-Ay mice caused a significant decrease in the glucose absorption in small intestine. The small intestine content of active glucose transporter isoform (SGLUT) protein content from KK-Ay mouse significantly decreased in the BI-treated KK-Ay mice compared to that in the controls. However, the small intestine content of facilitative glucose transporter isoform, GLUT5 protein content did not change. The alpha-glucosidase activity in small intestine significantly decreased in the BI-treated KK-Ay mice. These results suggest that the antidiabetic effect of BI is derived, at least in part, from a decrease of glucose absorption in small intestine , due to the reduction of SGLUT protein content in total membrane of the small intestine and the reduction of alpha-glucosidase activity. Because of its therapeutic mechanism, BI could be a new category of therapeutic agent for non-insulin dependent diabetic mellitus.

Antidiabetic effect of seishin-kanro-to in KK-Ay mice.

The hypoglycemic effect of Seishin-kanro-to (SK) was investigated in KK-Ay mice, one of the non-insulin dependent diabetic mellitus types. SK (1700 mg/kg) reduced the blood glucose of KK-Ay mice from 557 +/- 17 to 383 +/- 36 mg/100 ml 7 hours after single oral administration (P < 0.001). SK also decreased the blood glucose and improved glucose tolerance 5 weeks after repeated administration in KK-Ay mice. These results support, therefore, the use of SK in patients with diabetes and confirm its role as a traditional medicine. In addition, the active plants of SK were identified as the rhizome of Anemarrhena asphodeloides Bunge and the radix of Rehmannia glutinosa Liboschitz.

Hypoglycemic activity of some triterpenoid glycosides.

Four triterpenoid glycosides isolated from the rhizomes of Polygala senega var. latifolia, senegins II-IV (1-3) and desmethoxysenegin II (4), were tested for hypoglycemic activity in normal and KK-Ay mice. Compounds 1 and 2 reduced the blood glucose of normal mice 4 h after intraperitoneal administration and also significantly lowered the glucose level of KK-Ay mice under similar conditions. Compounds 3 and 4, as well as senegose A (5), an oligosaccharide ester, were inactive when tested against normal mice.

Hypoglycemic effect of the rhizomes of Polygala senega in normal and diabetic mice and its main component, the triterpenoid glycoside senegin-II.

The hypoglycemic effect of the rhizomes of Polygala senega L. var. latifolia Torrey et Gray (Polygalaceae) was investigated in normal and KK-Ay mice, one of the model animals of non-insulin dependent diabetes mellitus (NIDDM). The n-butanol extract of senega rhizomes (SN) (5 mg/kg) reduced the blood glucose of normal mice from 191 +/- 3 to 120 +/- 3 mg/dl 4 hours after intraperitoneal administration (P < 0.001), and also showed a significant decrease in the glucose level of KK-Ay mice from 469 +/- 38 to 244 +/- 14 mg/dl under similar conditions (P < 0.001). But streptozotocin-induced diabetic mice did not experience a change in the blood glucose after administration of SN. We propose that the hypoglycemic effect of SN occurs without altering the insulin concentration. Moreover, SN needs the presence of insulin in order to act. In addition, one of the active components of the hypoglycemic effect was identified as a triterpenoid glycoside, senegin-II.

Effect of ginseng radix on GLUT2 protein content in mouse liver in normal and epinephrine-induced hyperglycemic mice.

The oral administration of the water extract of Ginseng Radix (GR) to normal and epinephrine-induced hyperglycemic mice caused a significant decrease in the blood glucose level 4 h after its administration. The hepatic content of facilitative glucose transporter isoform 2, liver type glucose transporter (GLUT2) protein content from mouse liver significantly increased in the orally GR-treated normal and epinephrine-induced hyperglycemic mice compared to that in the controls. These results suggest that the hypoglycemic activity of GR is presumably due, at least in part, to the increment of GLUT2 protein content.

Intraperitoneal administration of Senegae Radix extract and its main component, senegin-II, affects lipid metabolism in normal and hyperlipidemic mice.

The hypolipidemic effect of Senegae Radix, i.e. "Senega," was investigated in normal and hyperlipidemic mice. The n-butanol fraction of the methanol extract of Senegae Radix (SN) (5 mg/kg) significantly reduced the blood triglyceride level of normal mice 7 h after intraperitoneal administration (p < 0.05) and also significantly reduced the blood triglyceride level of cholesterol-fed mice under similar conditions (p < 0.05). SN (5 mg/kg) also reduced the blood triglyceride and cholesterol levels after repeated administration to cholesterol-fed mice. SN also decreased the blood triglyceride level in Triton-induced hyperlipidemia. It is suggested that this fraction contains one or more hypolipidemic components including the main triterpenoid glycoside, senegin-II, which significantly reduces the levels of blood triglycerides in normal mice.

Hypoglycemic effect of the rhizomes of ophiopogonis tuber in normal and diabetic mice.

The hypoglycemic effect of the rhizomes of Ophiopogonis Tuber (Liliaceae) was investigated in normal and streptozotocin-induced diabetic mice. The n-butanol extract of rhizomes of Ophiopogonis Tuber (BM) (100 mg/kg) reduced the blood glucose of normal mice from 201 +/- 13 to 151 +/- 7 mg/100 ml 4h after intraperitoneal administration (p < 0.054), and also significantly lowered the blood glucose of streptozotocin-induced diabetic mice from 590 +/- 28 to 470 +/- 37 mg/100 ml under similar conditions (p < 0.05). BM also tended to suppress epinephrine-induced hyperglycemia in mice. We concluded that the hypoglycemic effect of BM does not alter the insulin concentration.