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Evid Based Complement Alternat Med. 2015;2015:120572. doi: 10.1155/2015/120572. Epub 2015 Jun 23.

Evaluation of Antidiabetic Effects of the Traditional Medicinal Plant Gynostemma pentaphyllum and the Possible Mechanisms of Insulin Release.

Author information

1
Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, SE-171 76 Stockholm, Sweden ; Diabetes and Endocrine Unit, Cardiovascular, Diabetes and Nutrition Research Centre (CDNRC), Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia.
2
Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, SE-171 76 Stockholm, Sweden.
3
Diabetes and Endocrine Unit, Cardiovascular, Diabetes and Nutrition Research Centre (CDNRC), Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia.

Abstract

AIMS:

To evaluate the antidiabetic effects of Gynostemma pentaphyllum (GP) in Goto-Kakizaki (GK) rat, an animal model of type 2 diabetes, and to investigate the mechanisms of insulin release.

METHODS:

Oral glucose tolerance test was performed and plasma insulin levels were measured.

RESULTS:

An oral treatment with GP (0.3 g/kg of body weight daily) for two weeks in GK rats improved glucose tolerance versus placebo group (P < 0.01). Plasma insulin levels were significantly increased in the GP-treated group. The insulin release from GP-treated GK rats was 1.9-fold higher as compared to the control group (P < 0.001). GP stimulated insulin release in isolated GK rat islets at high glucose. Opening of ATP-sensitive potassium (K-ATP) channels by diazoxide and inhibition of calcium channels by nifedipine significantly decreased insulin response to GP. Furthermore, the protein kinase A (PKA) inhibitor H89 decreased the insulin response to GP (P < 0.05). In addition, GP-induced insulin secretion was decreased after preincubation of GK islets with pertussis toxin to inhibit exocytotic Ge proteins (P < 0.05).

CONCLUSION:

The antidiabetic effect of GP is associated with the stimulation of insulin release from the islets. GP-induced insulin release is partly mediated via K-ATP and L-type Ca(2+) channels, the PKA system and also dependent on pertussis toxin sensitive Ge-protein.

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