Effect of magnesium sulfate administration to improve insulin resistance in type 2 diabetes animal model: using the hyperinsulinemic-euglycemic clamp technique

2018 ◽  
Vol 32 (6) ◽  
pp. 603-616 ◽  
Author(s):  
Shahla Sohrabipour ◽  
Mohammad Reza Sharifi ◽  
Mohammadreza Sharifi ◽  
Ardeshir Talebi ◽  
Nepton Soltani
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Animal Model ◽  
Magnesium Sulfate ◽  
Euglycemic Clamp ◽  
Clamp Technique ◽  
Hyperinsulinemic Euglycemic Clamp ◽  
Improve Insulin Resistance

scholarly journals Endocrine regulation of G-protein subunit production in an animal model of type 2 diabetes mellitus

2001 ◽  
Vol 168 (3) ◽  
pp. 509-515 ◽  
Author(s):  
BD Rodgers ◽  
M Bernier ◽  
MA Levine
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Animal Model ◽  
Type 2 Diabetes Mellitus ◽  
Animal Models ◽  
G Protein ◽  
Dependent Manner ◽  
Protein Subunit

Adipocyte beta-adrenergic sensitivity is compromised in animal models of obesity and type 2 diabetes. Although changes in the membrane concentrations of G-protein alpha subunits (Galpha) have been implicated, it remains to be determined how these changes are affected by insulin resistance in the different animal models. Because previous studies used young animals, we measured the concentrations of Galpha and Gbeta subunits in epididymal fat from aged (48 weeks old) db/db mice and from their lean littermates to more closely reproduce the model of type 2 diabetes mellitus. Levels of immunoreactive Galphas, Galphai(1/2), Galphao and Galphaq/11 were all significantly greater in adipocyte membranes from the db/db mice than in membranes from their lean non-diabetic littermate controls. Levels of Galphai(1) and Galphai(2) were also individually determined and although they appeared to be slightly higher in db/db membranes, these differences were not significant. Although the levels of both Galphas isoforms were elevated, levels of the 42 and 46 kDa proteins rose by approximately 42% and 20% respectively, indicating differential protein processing of Galphas. By contrast, levels of Galphai3 were similar in the two groups. The levels of common Gbeta and Gbeta2 were also elevated in db/db mice, whereas Gbeta1 and Gbeta4 levels were not different. To determine whether these changes were due to insulin resistance per se or to elevated glucocorticoid production, G-protein subunit levels were quantified in whole cell lysates from 3T3-L1 adipocytes that were stimulated with different concentrations of either insulin or corticosterone. Although none of the subunit levels was affected by insulin, the levels of both Galphas isoforms were increased equally by corticosterone in a concentration-dependent manner. Since glucocorticoids are known regulators of Galphas gene expression in many cell types and in adipocytes from diabetic rodents, the results presented herein appear to more accurately reflect diabetic pathophysiology than do those of previous studies which report a decrease in Galphas levels. Taken together, these results indicate that most of the selective changes in G-protein subunit production in adipocytes from this animal model of type 2 diabetes may not be due to diminished insulin sensitivity, but may be due to other endocrine or metabolic abnormalities associated with the diabetic phenotype.

β-Cell tropin- and glucose-induced hypersecretion of insulin and amylin from perfused fatty rat pancreas

1993 ◽  
Vol 137 (3) ◽  
pp. 375-381 ◽  
Author(s):  
S. J. Dunmore ◽  
M. A. Cawthorne ◽  
D. C. J. Hislop ◽  
J. L. Morton ◽  
A. Beloff-Chain
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Animal Model ◽  
High Glucose ◽  
Perfused Pancreas ◽  
Β Cell ◽  
Rat Pancreas ◽  
Obesity And Diabetes ◽  
High Insulin

ABSTRACT The neurointermediate pituitary peptide β-cell tropin (BCT) has potent insulin-releasing and lipogenic properties and is elevated in obesity and type-2 diabetes. The effects of BCT and glucose on the release of insulin and amylin from the perfused pancreas of obese 'fatty' (fa/fa) rats and lean (Fa/?) controls were measured. Pancreata were perfused, sequentially, with buffer containing: 5·6 mmol glucose/l (basal); basal glucose±0·5 nmol BCT/l; 16·7 mmol glucose/l (high). Insulin and amylin release during basal glucose treatment was eight to nine times greater from pancreata from fatty than from lean rats. BCT induced a fivefold greater monophasic insulin and amylin release from fatty compared with lean pancreata. When not preceded by BCT there was a twofold greater high glucose-induced amylin release from fatty pancreata but no difference in insulin secretion. When preceded by BCT stimulation, high glucose induced twofold greater insulin and fourfold larger amylin release from fatty compared with lean pancreata. Molar secretion ratios of insulin: amylin varied between 30:1 and 50:1. In view of the elevated levels of BCT found in the fatty rat and in the light of the above findings, it is concluded that the peptide may have a role in the development of hyperinsulinaemia, hyperamylinaemia and insulin resistance in this animal model of obesity and diabetes. Journal of Endocrinology (1993) 137, 375–381

Effective gene delivery of shBMP-9 using polyethyleneimine-based core–shell nanoparticles in an animal model of insulin resistance

Nanoscale ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 2008-2016 ◽  
Author(s):  
Yanjun Jia ◽  
Dechao Niu ◽  
Qiujin Li ◽  
Hong Huang ◽  
Xinrun Li ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Animal Model ◽  
Type 2 Diabetes Mellitus ◽  
Core Shell ◽  
Shell Nanoparticles ◽  
Morphogenetic Protein ◽  
Core Shell Nanoparticles

Bone morphogenetic protein (BMP)-9 has been associated with insulin resistance and type 2 diabetes mellitus.

Sign in / Sign up

Export Citation Format

Share Document