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

Lokman EF, Gu HF, Wan Mohamud WN, Östenson CG - Evid Based Complement Alternat Med (2015)

Bottom Line: Opening of ATP-sensitive potassium (K-ATP) channels by diazoxide and inhibition of calcium channels by nifedipine significantly decreased insulin response to GP.Conclusion.The antidiabetic effect of GP is associated with the stimulation of insulin release from the islets.

View Article: PubMed Central - PubMed

Affiliation: 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.

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.

No MeSH data available.


Related in: MedlinePlus

Effect of Gynostemma pentaphyllum (GP) with or without H89 and calphostin C (C) on glucose stimulated insulin secretion from isolated GK rat islets. ∗∗P < 0.01 (when compared with control group with no addition); #P < 0.05 (when compared with group with only GP). Results of insulin release (μU/islet/hour) are the means ± SEM of three independent experiments with three replicates for each experiment.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4493304&req=5

fig5: Effect of Gynostemma pentaphyllum (GP) with or without H89 and calphostin C (C) on glucose stimulated insulin secretion from isolated GK rat islets. ∗∗P < 0.01 (when compared with control group with no addition); #P < 0.05 (when compared with group with only GP). Results of insulin release (μU/islet/hour) are the means ± SEM of three independent experiments with three replicates for each experiment.

Mentions: PKA or PKC pathways potentiate the insulin response to a metabolic stimulus [26]. To understand if GP exerts its effect via the PKA and PKC pathways, H89 (PKA inhibitor) and calphostin C (PKC inhibitor) were used. Incubation of islets with GP at 16.7 mM glucose stimulated insulin release by 2.2-fold (P < 0.01) (Figure 5). H89 (10 μM) and calphostin C (10 μM) decreased insulin release from 22.1 ± 2.8 to 7.7 ± 3.9 and to 5.4 ± 0.2 μU/islet/hour, respectively, at 16.7 mM glucose compared to the control group. H89 decreased the insulin response to GP from 48.8 ± 0.9 to 26.07 ± 3.2 μU/islet/hour (P < 0.05). Calphostin C inhibitor did not affect the insulin response to GP at 16.7 mM glucose.


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

Lokman EF, Gu HF, Wan Mohamud WN, Östenson CG - Evid Based Complement Alternat Med (2015)

Effect of Gynostemma pentaphyllum (GP) with or without H89 and calphostin C (C) on glucose stimulated insulin secretion from isolated GK rat islets. ∗∗P < 0.01 (when compared with control group with no addition); #P < 0.05 (when compared with group with only GP). Results of insulin release (μU/islet/hour) are the means ± SEM of three independent experiments with three replicates for each experiment.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4493304&req=5

fig5: Effect of Gynostemma pentaphyllum (GP) with or without H89 and calphostin C (C) on glucose stimulated insulin secretion from isolated GK rat islets. ∗∗P < 0.01 (when compared with control group with no addition); #P < 0.05 (when compared with group with only GP). Results of insulin release (μU/islet/hour) are the means ± SEM of three independent experiments with three replicates for each experiment.
Mentions: PKA or PKC pathways potentiate the insulin response to a metabolic stimulus [26]. To understand if GP exerts its effect via the PKA and PKC pathways, H89 (PKA inhibitor) and calphostin C (PKC inhibitor) were used. Incubation of islets with GP at 16.7 mM glucose stimulated insulin release by 2.2-fold (P < 0.01) (Figure 5). H89 (10 μM) and calphostin C (10 μM) decreased insulin release from 22.1 ± 2.8 to 7.7 ± 3.9 and to 5.4 ± 0.2 μU/islet/hour, respectively, at 16.7 mM glucose compared to the control group. H89 decreased the insulin response to GP from 48.8 ± 0.9 to 26.07 ± 3.2 μU/islet/hour (P < 0.05). Calphostin C inhibitor did not affect the insulin response to GP at 16.7 mM glucose.

Bottom Line: Opening of ATP-sensitive potassium (K-ATP) channels by diazoxide and inhibition of calcium channels by nifedipine significantly decreased insulin response to GP.Conclusion.The antidiabetic effect of GP is associated with the stimulation of insulin release from the islets.

View Article: PubMed Central - PubMed

Affiliation: 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.

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.

No MeSH data available.


Related in: MedlinePlus