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Exp Clin Endocrinol Diabetes. 2004 Oct;112(9):520-5.

Insulin secretion is stimulated by ethanol extract of Anemarrhena asphodeloides in isolated islet of healthy Wistar and diabetic Goto-Kakizaki Rats.

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  • 1Department of Pharmacology, Hanoi Medical University, Hanoi, Vietnam.



The hypoglycemic effect of extract of Anemarrhena asphodeloides has been accounted for by the substance mangiferin which increases insulin sensitivity. The present study aimed to investigate whether an ethanol extract of Anemarrhena asphodeloides would stimulate insulin secretion and if so, further elucidate the mechanism behind this effect.


Isolated pancreatic islets of normal Wistar rats and spontaneously diabetic Goto-Kakizaki (GK) rats were batch incubated or perifused to study effect of Anemarrhena asphodeloides extract (TH2) on insulin release.


At 3.3 mM glucose, 2, 4, and 8 mg/ml TH2 increased the insulin release of Wistar rat islets 2.5-, 4.1-, and 5.7-fold, respectively (p < 0.05) and of GK rat islets 1.7-, 3.0-, and 6.3-fold, respectively (p < 0.01). Similarly at 16.7 mM glucose, 2, 4 and 8 mg/ml TH2 increased insulin release of Wistar rat islets 1.5-, 2.2-, and 3.8-fold, respectively (p < 0.05) and of GK rat 2.5-, 4.2-, and 11.9-fold, respectively (p < 0.01). In perifusions of islets, TH2 also increased insulin secretion that returned to basal levels when TH2 was omitted from the perifusate. Mangiferin had no effect on insulin secretion of islets. In islets depolarized by 30 mM KCl and B-cell K-ATP channels kept open by 0.25 mM diazoxide, TH2 (8 mg/ml) further enhanced insulin secretion at 3.3 but not at 16.7 mM glucose. Pertussis toxin suppressed the insulin stimulating effect of 2 and 8 mg/ml TH2 by 35 % and 47 % (p < 0.05 and p < 0.001, respectively).


Ethanol extract of the roots of Anemarrhena asphodeloides contains a substance, TH2, that stimulates insulin secretion both at 3.3 and 16.7 mM glucose in islets of normal Wistar and diabetic GK rats. The mechanism behind TH2-stimulated insulin secretion involves an effect on the exocytotic machinery of the B-cell, mediated via pertussis toxin-sensitive Gi- (or Ge-) proteins.

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