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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. administration of M617 enhanced GLUT4 contents and trafficking to plasma membranes of fat cells (n = 8). (a) The GLUT4 immunoreactivity in total cell membranes and plasma membranes was higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups as compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The GLUT4 immunoreactivity in D-M617 and DC was lower as compared with N-M617 and NC, respectively, in total cell membranes and plasma membranes of adipose cells. (b) The central treatment with M617 enhanced the ratios of GLUT4 levels in plasma membranes to total cell membranes in D-M617 and N-M617 compared with each control, respectively. As compared with the diabetic controls, the ratio in N-M617 was increased, but in DC it was reduced. The 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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fig5: The i.c.v. administration of M617 enhanced GLUT4 contents and trafficking to plasma membranes of fat cells (n = 8). (a) The GLUT4 immunoreactivity in total cell membranes and plasma membranes was higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups as compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The GLUT4 immunoreactivity in D-M617 and DC was lower as compared with N-M617 and NC, respectively, in total cell membranes and plasma membranes of adipose cells. (b) The central treatment with M617 enhanced the ratios of GLUT4 levels in plasma membranes to total cell membranes in D-M617 and N-M617 compared with each control, respectively. As compared with the diabetic controls, the ratio in N-M617 was increased, but in DC it was reduced. The 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: The central administration of M617 significantly elevated GLUT4 protein levels in both total cell membranes (F[3,32] = 108.3, P < 0.0001) and plasma membranes (F[3,32] = 132.8, P < 0.0001) of adipose cells (Figure 5(a)). The GLUT4 immunoreactivities in the diabetic M617 group were elevated by 7.2% (P < 0.05) in total cell membranes and 66.9% (P < 0.01) in plasma membranes compared with the diabetic controls but reduced by 22.2% (P < 0.01) in total cell membranes and 29.9% (P < 0.01) in plasma membranes compared with the nondiabetic M617 group. As compared with the nondiabetic control group the GLUT4 levels in the diabetic control group were reduced by 23.4% (P < 0.01) in total cell membranes and 42.2% (P < 0.01) in plasma membranes but were elevated by 5.6% (P < 0.05) in total cell membranes and 37.8% (P < 0.01) in plasma membranes in the nondiabetic M617 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. administration of M617 enhanced GLUT4 contents and trafficking to plasma membranes of fat cells (n = 8). (a) The GLUT4 immunoreactivity in total cell membranes and plasma membranes was higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups as compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The GLUT4 immunoreactivity in D-M617 and DC was lower as compared with N-M617 and NC, respectively, in total cell membranes and plasma membranes of adipose cells. (b) The central treatment with M617 enhanced the ratios of GLUT4 levels in plasma membranes to total cell membranes in D-M617 and N-M617 compared with each control, respectively. As compared with the diabetic controls, the ratio in N-M617 was increased, but in DC it was reduced. The 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.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig5: The i.c.v. administration of M617 enhanced GLUT4 contents and trafficking to plasma membranes of fat cells (n = 8). (a) The GLUT4 immunoreactivity in total cell membranes and plasma membranes was higher in diabetic M617 (D-M617) and nondiabetic M617 (N-M617) groups as compared with diabetic controls (DC) and nondiabetic controls (NC), respectively. The GLUT4 immunoreactivity in D-M617 and DC was lower as compared with N-M617 and NC, respectively, in total cell membranes and plasma membranes of adipose cells. (b) The central treatment with M617 enhanced the ratios of GLUT4 levels in plasma membranes to total cell membranes in D-M617 and N-M617 compared with each control, respectively. As compared with the diabetic controls, the ratio in N-M617 was increased, but in DC it was reduced. The 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: The central administration of M617 significantly elevated GLUT4 protein levels in both total cell membranes (F[3,32] = 108.3, P < 0.0001) and plasma membranes (F[3,32] = 132.8, P < 0.0001) of adipose cells (Figure 5(a)). The GLUT4 immunoreactivities in the diabetic M617 group were elevated by 7.2% (P < 0.05) in total cell membranes and 66.9% (P < 0.01) in plasma membranes compared with the diabetic controls but reduced by 22.2% (P < 0.01) in total cell membranes and 29.9% (P < 0.01) in plasma membranes compared with the nondiabetic M617 group. As compared with the nondiabetic control group the GLUT4 levels in the diabetic control group were reduced by 23.4% (P < 0.01) in total cell membranes and 42.2% (P < 0.01) in plasma membranes but were elevated by 5.6% (P < 0.05) in total cell membranes and 37.8% (P < 0.01) in plasma membranes in the nondiabetic M617 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