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Gynura procumbens extract improves insulin sensitivity and suppresses hepatic gluconeogenesis in C57BL/KsJ- db/db mice

View Article: PubMed Central - PubMed

ABSTRACT

Background/objectives: This study was designed to investigate whether Gynura procumbens extract (GPE) can improve insulin sensitivity and suppress hepatic glucose production in an animal model of type 2 diabetes.

Materials/methods: C57BL/Ksj-db/db mice were divided into 3 groups, a regular diet (control), GPE, and rosiglitazone groups (0.005 g/100 g diet) and fed for 6 weeks.

Results: Mice supplemented with GPE showed significantly lower blood levels of glucose and glycosylated hemoglobin than diabetic control mice. Glucose and insulin tolerance test also showed the positive effect of GPE on increasing insulin sensitivity. The homeostatic index of insulin resistance was significantly lower in mice supplemented with GPE than in the diabetic control mice. In the skeletal muscle, the expression of phosphorylated AMP-activated protein kinase, pAkt substrate of 160 kDa, and PM-glucose transporter type 4 increased in mice supplemented with GPE when compared to that of the diabetic control mice. GPE also decreased the expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase in the liver.

Conclusions: These findings demonstrate that GPE might improve insulin sensitivity and inhibit gluconeogenesis in the liver.

No MeSH data available.


Related in: MedlinePlus

Effect of G. procumbens extract (GPE) supplementation on PM-GLUT4, pAMPK, and pAS160 expression in the skeletal muscle.Western blotting and signal intensities were determined by densitometric analysis using Multi Gauge V3.1 software. Representative blots of PM-GLUT4, pAMPK, and pAS160 protein expression are shown with protein expression levels quantified relative to the expression level observed in samples from db/db-control mice. Each value is expressed as mean ± SD of experiments performed in triplicate. a-c Values denoted by different letters are significantly different (P < 0.05), as analyzed by Duncan's multiple range test. PM-GLUT4: plasma membrane-glucose transporter type 4, pAMPK: phosphorylated AMP-activated protein kinase, pAS160: phosphorylated Akt substrate of 160 kDa.
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Figure 3: Effect of G. procumbens extract (GPE) supplementation on PM-GLUT4, pAMPK, and pAS160 expression in the skeletal muscle.Western blotting and signal intensities were determined by densitometric analysis using Multi Gauge V3.1 software. Representative blots of PM-GLUT4, pAMPK, and pAS160 protein expression are shown with protein expression levels quantified relative to the expression level observed in samples from db/db-control mice. Each value is expressed as mean ± SD of experiments performed in triplicate. a-c Values denoted by different letters are significantly different (P < 0.05), as analyzed by Duncan's multiple range test. PM-GLUT4: plasma membrane-glucose transporter type 4, pAMPK: phosphorylated AMP-activated protein kinase, pAS160: phosphorylated Akt substrate of 160 kDa.

Mentions: In this study, we studied the expression of PM-GLUT4, GLUT4, pAMPK, AMPK, pAS160, and AS160 in the skeletal muscle. RG supplementation, positive control, showed the highest PM-GLUT4, pAMPK, and pAS160 levels in the skeletal muscle. GPE supplementation also increased PM-GLUT4, pAMPK, and pAS160 levels in the skeletal muscle. As shown in Fig. 3, the expression of GLUT4 in the plasma membrane of the skeletal muscle significantly increased, reaching levels that were 2.2 and 3.3-fold higher in db/db-GPE and db/db-RG mice than those measured in db/db-control mice, respectively. No significant difference was observed in AMPK expression among db/db-RG, db/db-GPE and db/db-control mice. However, the phosphorylation levels of AMPK and AS160, two upstream regulators of GLUT4 translocation to the plasma membrane, were significantly increased by GPE supplementation. This means that GPE has the ability to stimulate glucose uptake through activation of the AMPK-AS160-GLUT4 pathway in the skeletal muscle.


Gynura procumbens extract improves insulin sensitivity and suppresses hepatic gluconeogenesis in C57BL/KsJ- db/db mice
Effect of G. procumbens extract (GPE) supplementation on PM-GLUT4, pAMPK, and pAS160 expression in the skeletal muscle.Western blotting and signal intensities were determined by densitometric analysis using Multi Gauge V3.1 software. Representative blots of PM-GLUT4, pAMPK, and pAS160 protein expression are shown with protein expression levels quantified relative to the expression level observed in samples from db/db-control mice. Each value is expressed as mean ± SD of experiments performed in triplicate. a-c Values denoted by different letters are significantly different (P < 0.05), as analyzed by Duncan's multiple range test. PM-GLUT4: plasma membrane-glucose transporter type 4, pAMPK: phosphorylated AMP-activated protein kinase, pAS160: phosphorylated Akt substrate of 160 kDa.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037068&req=5

Figure 3: Effect of G. procumbens extract (GPE) supplementation on PM-GLUT4, pAMPK, and pAS160 expression in the skeletal muscle.Western blotting and signal intensities were determined by densitometric analysis using Multi Gauge V3.1 software. Representative blots of PM-GLUT4, pAMPK, and pAS160 protein expression are shown with protein expression levels quantified relative to the expression level observed in samples from db/db-control mice. Each value is expressed as mean ± SD of experiments performed in triplicate. a-c Values denoted by different letters are significantly different (P < 0.05), as analyzed by Duncan's multiple range test. PM-GLUT4: plasma membrane-glucose transporter type 4, pAMPK: phosphorylated AMP-activated protein kinase, pAS160: phosphorylated Akt substrate of 160 kDa.
Mentions: In this study, we studied the expression of PM-GLUT4, GLUT4, pAMPK, AMPK, pAS160, and AS160 in the skeletal muscle. RG supplementation, positive control, showed the highest PM-GLUT4, pAMPK, and pAS160 levels in the skeletal muscle. GPE supplementation also increased PM-GLUT4, pAMPK, and pAS160 levels in the skeletal muscle. As shown in Fig. 3, the expression of GLUT4 in the plasma membrane of the skeletal muscle significantly increased, reaching levels that were 2.2 and 3.3-fold higher in db/db-GPE and db/db-RG mice than those measured in db/db-control mice, respectively. No significant difference was observed in AMPK expression among db/db-RG, db/db-GPE and db/db-control mice. However, the phosphorylation levels of AMPK and AS160, two upstream regulators of GLUT4 translocation to the plasma membrane, were significantly increased by GPE supplementation. This means that GPE has the ability to stimulate glucose uptake through activation of the AMPK-AS160-GLUT4 pathway in the skeletal muscle.

View Article: PubMed Central - PubMed

ABSTRACT

Background/objectives: This study was designed to investigate whether Gynura procumbens extract (GPE) can improve insulin sensitivity and suppress hepatic glucose production in an animal model of type 2 diabetes.

Materials/methods: C57BL/Ksj-db/db mice were divided into 3 groups, a regular diet (control), GPE, and rosiglitazone groups (0.005 g/100 g diet) and fed for 6 weeks.

Results: Mice supplemented with GPE showed significantly lower blood levels of glucose and glycosylated hemoglobin than diabetic control mice. Glucose and insulin tolerance test also showed the positive effect of GPE on increasing insulin sensitivity. The homeostatic index of insulin resistance was significantly lower in mice supplemented with GPE than in the diabetic control mice. In the skeletal muscle, the expression of phosphorylated AMP-activated protein kinase, pAkt substrate of 160 kDa, and PM-glucose transporter type 4 increased in mice supplemented with GPE when compared to that of the diabetic control mice. GPE also decreased the expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase in the liver.

Conclusions: These findings demonstrate that GPE might improve insulin sensitivity and inhibit gluconeogenesis in the liver.

No MeSH data available.


Related in: MedlinePlus