Suppressive effects of polygonati rhizoma on hepatic glucose output, GLUT2 mRNA expression and its protein content in rat liver
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Abstract:
The intraperitoneal administration of the methanol extract of Polygonati Rhizoma (OM) into normal rats caused a significant decrease in the blood glucose level at 4 h after its administration of 800 mg/kg (P < 0.01), but not the serum insulin level. Using the perfused rat liver in vitro, a significant decrease of the hepatic glucose output was observed by the infusion of OM (P < 0.05 at 250 micrograms/ml OM). In addition, the hepatic content of facilitative glucose transporter isoform 2 (GLUT2) mRNA and its protein content in the total membrane fraction from rat liver significantly decreased in the intraperitoneally OM-treated rats when compared to that in the controls (mRNA P < 0.01, protein P < 0.001). On the other hand, OM (500 micrograms/ml) exhibited no apparent stimulatory effect on the insulin secretion from the isolated rat pancreatic islets. These results suggest that the hypoglycemic effect of OM is derived, at least in part, from the decrease in hepatic glucose output, due presumably to the reduction of GLUT2 mRNA expression and its protein content in total membrane of the liver, and that because of its unique therapeutic mechanism, OM could be a new category of therapeutic agent for non-insulin-dependent diabetes mellitus.
Insights
The methanol extract of Polygonati Rhizoma (OM) lowers blood glucose in rats by reducing liver glucose output, not by increasing insulin. This suggests OM may be a novel treatment for non-insulin-dependent diabetes mellitus.
Area of Science:
- Pharmacology
- Biochemistry
- Endocrinology
Background:
- Polygonati Rhizoma (OM) is a traditional herbal medicine.
- Non-insulin-dependent diabetes mellitus (NIDDM) is a growing health concern.
- Understanding the mechanisms of glucose-lowering agents is crucial for NIDDM treatment.
Purpose of the Study:
- To investigate the hypoglycemic effect of the methanol extract of Polygonati Rhizoma (OM).
- To elucidate the mechanism underlying OM's glucose-lowering action.
- To explore the potential of OM as a therapeutic agent for NIDDM.
Main Methods:
- Administration of OM to normal rats and measurement of blood glucose and serum insulin levels.
- In vitro perfusion of rat liver to assess hepatic glucose output.
- Quantification of facilitative glucose transporter isoform 2 (GLUT2) mRNA and protein expression in rat liver.
- Assessment of insulin secretion from isolated rat pancreatic islets upon OM exposure.
Main Results:
- OM administration significantly reduced blood glucose levels in rats without affecting serum insulin.
- OM significantly decreased hepatic glucose output in perfused rat liver.
- OM treatment led to a significant reduction in hepatic GLUT2 mRNA and protein expression.
- OM did not stimulate insulin secretion from isolated pancreatic islets.
Conclusions:
- The hypoglycemic effect of OM is attributed to reduced hepatic glucose output, likely via decreased GLUT2 expression.
- OM's unique mechanism suggests its potential as a novel therapeutic agent for NIDDM.
- Further research into OM's therapeutic potential for diabetes is warranted.