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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 GLUT4 mRNA expression levels in adipose cells (n = 8). The GLUT4 mRNA expression levels were higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups as compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The expression levels were lower in D-M617 and DC groups compared with N-M617 and NC groups, respectively. The data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●●P < 0.01 versus N-M617; ○○P < 0.01 versus DC.
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fig4: The i.c.v. injection of M617 significantly elevated GLUT4 mRNA expression levels in adipose cells (n = 8). The GLUT4 mRNA expression levels were higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups as compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The expression levels were lower in D-M617 and DC groups compared with N-M617 and NC groups, respectively. The data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●●P < 0.01 versus N-M617; ○○P < 0.01 versus DC.

Mentions: In the present study, the central treatment with M617 significantly elevated the GLUT4 mRNA expression in fat cells of rats (F[3,32] = 65.7, P < 0.0001). As shown in Figure 4, the GLUT4 mRNA expression in the diabetic M617 group was increased by 36.3% (P < 0.01) compared with diabetic controls but reduced by 18.6% (P < 0.01) compared with the nondiabetic M617 group. As compared with nondiabetic controls, the GLUT4 gene expression was enhanced by 11.1% (P < 0.05) in the nondiabetic M617 group but significantly decreased by 33.7% (P < 0.01) in the diabetic control group.


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 GLUT4 mRNA expression levels in adipose cells (n = 8). The GLUT4 mRNA expression levels were higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups as compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The expression levels were lower in D-M617 and DC groups compared with N-M617 and NC groups, respectively. The data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●●P < 0.01 versus N-M617; ○○P < 0.01 versus DC.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: The i.c.v. injection of M617 significantly elevated GLUT4 mRNA expression levels in adipose cells (n = 8). The GLUT4 mRNA expression levels were higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups as compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The expression levels were lower in D-M617 and DC groups compared with N-M617 and NC groups, respectively. The data shown are the means ± SEM. △P < 0.05, △△P < 0.01 versus NC; ●●P < 0.01 versus N-M617; ○○P < 0.01 versus DC.
Mentions: In the present study, the central treatment with M617 significantly elevated the GLUT4 mRNA expression in fat cells of rats (F[3,32] = 65.7, P < 0.0001). As shown in Figure 4, the GLUT4 mRNA expression in the diabetic M617 group was increased by 36.3% (P < 0.01) compared with diabetic controls but reduced by 18.6% (P < 0.01) compared with the nondiabetic M617 group. As compared with nondiabetic controls, the GLUT4 gene expression was enhanced by 11.1% (P < 0.05) in the nondiabetic M617 group but significantly decreased by 33.7% (P < 0.01) in the diabetic control group.

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