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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 alteration of plasma adiponectin concentration after i.c.v. injection of M617 in rats (n = 8). The plasma adiponectin concentration was higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The adiponectin contents were lower in D-M617 and DC groups compared with N-M617 and NC groups, respectively. All data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●●P < 0.01 versus N-M617; ○P < 0.05 versus DC.
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fig3: The alteration of plasma adiponectin concentration after i.c.v. injection of M617 in rats (n = 8). The plasma adiponectin concentration was higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The adiponectin contents were lower in D-M617 and DC groups compared with N-M617 and NC groups, respectively. All data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●●P < 0.01 versus N-M617; ○P < 0.05 versus DC.

Mentions: In this experiment, we observed the impact of central GalR1 on plasma adiponectin levels in fat cells. As shown in Figure 3, the central administration of M617 elevated the adiponectin contents (F[3,32] = 124.7, P < 0.001). The adiponectin contents in the diabetic M617 group were enhanced by 7.2% (P < 0.05) compared with the diabetic controls but reduced by 22.7% (P < 0.01) compared with the nondiabetic M617 group. As compared with nondiabetic controls, the levels were increased by 5.5% (P < 0.05) in the nondiabetic M617 group but reduced by 23.9% (P < 0.01) in the diabetic control group. These results suggest that activation of GalR1 in brain may increase adiponectin release to ameliorate insulin resistance.


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 alteration of plasma adiponectin concentration after i.c.v. injection of M617 in rats (n = 8). The plasma adiponectin concentration was higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The adiponectin contents were lower in D-M617 and DC groups compared with N-M617 and NC groups, respectively. All data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●●P < 0.01 versus N-M617; ○P < 0.05 versus DC.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4835658&req=5

fig3: The alteration of plasma adiponectin concentration after i.c.v. injection of M617 in rats (n = 8). The plasma adiponectin concentration was higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The adiponectin contents were lower in D-M617 and DC groups compared with N-M617 and NC groups, respectively. All data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●●P < 0.01 versus N-M617; ○P < 0.05 versus DC.
Mentions: In this experiment, we observed the impact of central GalR1 on plasma adiponectin levels in fat cells. As shown in Figure 3, the central administration of M617 elevated the adiponectin contents (F[3,32] = 124.7, P < 0.001). The adiponectin contents in the diabetic M617 group were enhanced by 7.2% (P < 0.05) compared with the diabetic controls but reduced by 22.7% (P < 0.01) compared with the nondiabetic M617 group. As compared with nondiabetic controls, the levels were increased by 5.5% (P < 0.05) in the nondiabetic M617 group but reduced by 23.9% (P < 0.01) in the diabetic control group. These results suggest that activation of GalR1 in brain may increase adiponectin release to ameliorate insulin resistance.

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