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Central Administration of Galanin Receptor 1 Agonist Boosted Insulin Sensitivity in Adipose Cells of Diabetic Rats.

Zhang Z, Fang P, He B, Guo L, Runesson J, Langel Ü, Shi M, Zhu Y, Bo P - J Diabetes Res (2016)

Bottom Line: The aim of the study was further to investigate whether central M617, a galanin receptor 1 agonist, can benefit insulin sensitivity.The results showed that central injection of M617 significantly increased plasma adiponectin contents, glucose infusion rates in hyperinsulinemic-euglycemic clamp tests, GLUT4 mRNA expression levels, GLUT4 contents in plasma membranes, and total cell membranes of the adipose cells but reduced the plasma C-reactive protein concentration in nondiabetic and diabetic rats.The ratios of GLUT4 contents were higher in plasma membranes to total cell membranes in both nondiabetic and diabetic M617 groups than each control.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology, Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu 225001, China.

ABSTRACT
Our previous studies testified the beneficial effect of central galanin on insulin sensitivity of type 2 diabetic rats. The aim of the study was further to investigate whether central M617, a galanin receptor 1 agonist, can benefit insulin sensitivity. The effects of intracerebroventricular administration of M617 on insulin sensitivity and insulin signaling were evaluated in adipose tissues of type 2 diabetic rats. The results showed that central injection of M617 significantly increased plasma adiponectin contents, glucose infusion rates in hyperinsulinemic-euglycemic clamp tests, GLUT4 mRNA expression levels, GLUT4 contents in plasma membranes, and total cell membranes of the adipose cells but reduced the plasma C-reactive protein concentration in nondiabetic and diabetic rats. The ratios of GLUT4 contents were higher in plasma membranes to total cell membranes in both nondiabetic and diabetic M617 groups than each control. In addition, the central administration of M617 enhanced the ratios of pAkt/Akt and pAS160/AS160, but not phosphorylative cAMP response element-binding protein (pCREB)/CREB in the adipose cells of nondiabetic and diabetic rats. These results suggest that excitation of central galanin receptor 1 facilitates insulin sensitivity via activation of the Akt/AS160 signaling pathway in the fat cells of type 2 diabetic rats.

No MeSH data available.


Related in: MedlinePlus

The i.c.v. injection of M617 significantly elevated ratios of pAkt/Akt and pAS160/AS160, but not ratios of pCREB/CREB in fat cells (n = 8). The ratios of pAkt/Akt (a) and pAS160/AS160 (b) were higher but not pCREB/CREB (c) in diabetic M617 group (D-M617) and nondiabetic M617 group (N-M617) than diabetic controls (DC) and nondiabetic controls (NC), respectively. The ratios of pAkt/Akt and pAS160/AS160 were lower, but pCREB/CREB were higher in D-M617 and DC than N-M617 and NC groups, respectively. All data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●P < 0.05, ●●P < 0.01 versus N-M617; ○P < 0.05, ○○P < 0.01 versus DC.
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fig6: The i.c.v. injection of M617 significantly elevated ratios of pAkt/Akt and pAS160/AS160, but not ratios of pCREB/CREB in fat cells (n = 8). The ratios of pAkt/Akt (a) and pAS160/AS160 (b) were higher but not pCREB/CREB (c) in diabetic M617 group (D-M617) and nondiabetic M617 group (N-M617) than diabetic controls (DC) and nondiabetic controls (NC), respectively. The ratios of pAkt/Akt and pAS160/AS160 were lower, but pCREB/CREB were higher in D-M617 and DC than N-M617 and NC groups, respectively. All data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●P < 0.05, ●●P < 0.01 versus N-M617; ○P < 0.05, ○○P < 0.01 versus DC.

Mentions: As shown in Figure 6, the injection of M617 into the brain significantly elevated the ratios of pAkt/Akt (F[3, 32] = 10.8, P < 0.0001) and pAS160/AS160 (F[3, 32] = 18.9, P < 0.0001) but reduced the ratios of pCREB/CREB (F[3, 32] = 17.9, P < 0.0001) in adipose cells. The ratios of pAkt/Akt and pAS160/AS160 in the diabetic M617 group were enhanced by 70.9% (P < 0.01) and 31.8% (P < 0.05) compared with diabetic controls but decreased by 18.4% (P < 0.05) and 24.2% (P < 0.01) compared with the nondiabetic M617 group. The ratios of pCREB/CREB in the diabetic M617 group were increased by 36.1% (P < 0.01) compared with the nondiabetic M617 group, while they are not significantly altered (P > 0.05) compared with diabetic controls. As compared with nondiabetic controls, the ratios of pAkt/Akt and pAS160/AS160 in the diabetic control group were reduced by 43.1% (P < 0.01) and 33.9% (P < 0.01), but the ratios of pCREB/CREB were elevated by 34.6% (P < 0.01). Compared with nondiabetic controls, the ratios of pAkt/Akt and pAS160/AS160 in the nondiabetic M617 group were increased by 17.2% (P < 0.05) and 14.9% (P < 0.05), while the ratios of pCREB/CREB were not significantly altered (P > 0.05). These results suggest that activation of GalR1 in brain may increase pAkt and pAS160 contents, but not pCREB in adipose cells.


Central Administration of Galanin Receptor 1 Agonist Boosted Insulin Sensitivity in Adipose Cells of Diabetic Rats.

Zhang Z, Fang P, He B, Guo L, Runesson J, Langel Ü, Shi M, Zhu Y, Bo P - J Diabetes Res (2016)

The i.c.v. injection of M617 significantly elevated ratios of pAkt/Akt and pAS160/AS160, but not ratios of pCREB/CREB in fat cells (n = 8). The ratios of pAkt/Akt (a) and pAS160/AS160 (b) were higher but not pCREB/CREB (c) in diabetic M617 group (D-M617) and nondiabetic M617 group (N-M617) than diabetic controls (DC) and nondiabetic controls (NC), respectively. The ratios of pAkt/Akt and pAS160/AS160 were lower, but pCREB/CREB were higher in D-M617 and DC than N-M617 and NC groups, respectively. All data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●P < 0.05, ●●P < 0.01 versus N-M617; ○P < 0.05, ○○P < 0.01 versus DC.
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Related In: Results  -  Collection

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fig6: The i.c.v. injection of M617 significantly elevated ratios of pAkt/Akt and pAS160/AS160, but not ratios of pCREB/CREB in fat cells (n = 8). The ratios of pAkt/Akt (a) and pAS160/AS160 (b) were higher but not pCREB/CREB (c) in diabetic M617 group (D-M617) and nondiabetic M617 group (N-M617) than diabetic controls (DC) and nondiabetic controls (NC), respectively. The ratios of pAkt/Akt and pAS160/AS160 were lower, but pCREB/CREB were higher in D-M617 and DC than N-M617 and NC groups, respectively. All data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●P < 0.05, ●●P < 0.01 versus N-M617; ○P < 0.05, ○○P < 0.01 versus DC.
Mentions: As shown in Figure 6, the injection of M617 into the brain significantly elevated the ratios of pAkt/Akt (F[3, 32] = 10.8, P < 0.0001) and pAS160/AS160 (F[3, 32] = 18.9, P < 0.0001) but reduced the ratios of pCREB/CREB (F[3, 32] = 17.9, P < 0.0001) in adipose cells. The ratios of pAkt/Akt and pAS160/AS160 in the diabetic M617 group were enhanced by 70.9% (P < 0.01) and 31.8% (P < 0.05) compared with diabetic controls but decreased by 18.4% (P < 0.05) and 24.2% (P < 0.01) compared with the nondiabetic M617 group. The ratios of pCREB/CREB in the diabetic M617 group were increased by 36.1% (P < 0.01) compared with the nondiabetic M617 group, while they are not significantly altered (P > 0.05) compared with diabetic controls. As compared with nondiabetic controls, the ratios of pAkt/Akt and pAS160/AS160 in the diabetic control group were reduced by 43.1% (P < 0.01) and 33.9% (P < 0.01), but the ratios of pCREB/CREB were elevated by 34.6% (P < 0.01). Compared with nondiabetic controls, the ratios of pAkt/Akt and pAS160/AS160 in the nondiabetic M617 group were increased by 17.2% (P < 0.05) and 14.9% (P < 0.05), while the ratios of pCREB/CREB were not significantly altered (P > 0.05). These results suggest that activation of GalR1 in brain may increase pAkt and pAS160 contents, but not pCREB in adipose cells.

Bottom Line: The aim of the study was further to investigate whether central M617, a galanin receptor 1 agonist, can benefit insulin sensitivity.The results showed that central injection of M617 significantly increased plasma adiponectin contents, glucose infusion rates in hyperinsulinemic-euglycemic clamp tests, GLUT4 mRNA expression levels, GLUT4 contents in plasma membranes, and total cell membranes of the adipose cells but reduced the plasma C-reactive protein concentration in nondiabetic and diabetic rats.The ratios of GLUT4 contents were higher in plasma membranes to total cell membranes in both nondiabetic and diabetic M617 groups than each control.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology, Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu 225001, China.

ABSTRACT
Our previous studies testified the beneficial effect of central galanin on insulin sensitivity of type 2 diabetic rats. The aim of the study was further to investigate whether central M617, a galanin receptor 1 agonist, can benefit insulin sensitivity. The effects of intracerebroventricular administration of M617 on insulin sensitivity and insulin signaling were evaluated in adipose tissues of type 2 diabetic rats. The results showed that central injection of M617 significantly increased plasma adiponectin contents, glucose infusion rates in hyperinsulinemic-euglycemic clamp tests, GLUT4 mRNA expression levels, GLUT4 contents in plasma membranes, and total cell membranes of the adipose cells but reduced the plasma C-reactive protein concentration in nondiabetic and diabetic rats. The ratios of GLUT4 contents were higher in plasma membranes to total cell membranes in both nondiabetic and diabetic M617 groups than each control. In addition, the central administration of M617 enhanced the ratios of pAkt/Akt and pAS160/AS160, but not phosphorylative cAMP response element-binding protein (pCREB)/CREB in the adipose cells of nondiabetic and diabetic rats. These results suggest that excitation of central galanin receptor 1 facilitates insulin sensitivity via activation of the Akt/AS160 signaling pathway in the fat cells of type 2 diabetic rats.

No MeSH data available.


Related in: MedlinePlus