scholarly journals Structural Basis and Genotype–Phenotype Correlations of INSR Mutations Causing Severe Insulin Resistance

Diabetes ◽  
2017 ◽  
Vol 66 (10) ◽  
pp. 2713-2723 ◽  
Author(s):  
Jun Hosoe ◽  
Hiroko Kadowaki ◽  
Fuyuki Miya ◽  
Katsuya Aizu ◽  
Tomoyuki Kawamura ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Structural Basis ◽  
Severe Insulin Resistance

In vivo chloroquine-induced inhibition of insulin degradation in a diabetic patient with severe insulin resistance

Diabetes ◽  
1984 ◽  
Vol 33 (12) ◽  
pp. 1133-1137 ◽  
Author(s):  
B. R. Blazar ◽  
C. B. Whitley ◽  
A. E. Kitabchi ◽  
M. Y. Tsai ◽  
J. Santiago ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Diabetic Patient ◽  
Insulin Degradation ◽  
Severe Insulin Resistance

Digenic inheritance of severe insulin resistance in a human pedigree

10.1038/ng926 ◽  
2002 ◽  
Vol 31 (4) ◽  
pp. 379-384 ◽  
Author(s):  
David B. Savage ◽  
Maura Agostini ◽  
Inês Barroso ◽  
Mark Gurnell ◽  
Jian'an Luan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Severe Insulin Resistance ◽  
Digenic Inheritance

Insulin action and resistance in obesity and noninsulin-dependent type II diabetes mellitus

1982 ◽  
Vol 243 (1) ◽  
pp. E15-E30 ◽  
Author(s):  
J. M. Olefsky ◽  
O. G. Kolterman ◽  
J. A. Scarlett
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Insulin Receptor ◽  
Insulin Action ◽  
Insulin Receptors ◽  
Tissue Level ◽  
Dependent Diabetes Mellitus ◽  
Target Tissue ◽  
Severe Insulin Resistance ◽  
Glucose Clamp Technique

Resistance to the action of insulin can result from a variety of causes, including the formation of abnormal insulin or proinsulin molecules, the presence of circulating antagonists to insulin or the insulin receptor, or defects in insulin action at the target tissue level. Defects of the latter type are characteristic of obesity and of noninsulin-dependent diabetes mellitus. Analysis of the nature of the insulin resistance in those disorders has been investigated in intact subjects with the use of the euglycemic glucose clamp technique, and both insulin receptors and insulin-mediated glucose metabolism have been studied in adipocytes and monocytes from affected individuals. In both conditions, the cause of insulin resistance is heterogeneous. In some, insulin resistance appears to be due to a defect in the insulin receptor, whereas others have a defect both in the receptor and at the postreceptor level. In both groups, more severe insulin resistance is due to the postreceptor lesion and is correctable with appropriate therapy.

scholarly journals SEVERE INSULIN RESISTANCE DUE TO C.576C>G (P.I119M) MUTATION IN THE INSR GENE: CASE REPORT

2017 ◽  
Vol 3 (1) ◽  
pp. e17-e21
Author(s):  
Raya A. Almazrouei ◽  
Juma Alkaabi ◽  
Fatima M. Alkaabi ◽  
Hanan Alshamsi
Keyword(s):  
Insulin Resistance ◽  
Case Report ◽  
Severe Insulin Resistance ◽  
Insr Gene

Effects of exercise on insulin distribution and action in testosterone-treated oophorectomized female rats

2000 ◽  
Vol 88 (6) ◽  
pp. 2116-2122 ◽  
Author(s):  
Maria Niklasson ◽  
Peter Daneryd ◽  
Peter Lönnroth ◽  
Agneta Holmäng
Keyword(s):  
Insulin Resistance ◽  
Physical Exercise ◽  
Insulin Action ◽  
Female Rats ◽  
Control Group ◽  
Free Access ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Severe Insulin Resistance ◽  
Ovx Rats ◽  
Running Wheels

Administration of testosterone (T) to oophorectomized (Ovx) female rats is followed by severe insulin resistance, localized to postreceptor cellular events in the muscle. In this study, intervention by exercise was introduced to examine whether circulatory adaptations are involved in insulin resistance. Two groups of Ovx rats were studied: one group was given T (Ovx+T); another group had free access to running wheels (Ovx+T+Ex). In addition, one control group (sham operated) was studied. Insulin sensitivity was measured with the euglycemic hyperinsulinemic clamp technique (submaximal) for 150 min. Muscle interstitial glucose and insulin concentrations were measured by microdialysis. The measurements showed that, in Ovx+T rats, the onset of insulin action was significantly ( P < 0.05) slower during the first 95 min of the clamp compared with that in Ovx+T+Ex and controls. Muscle interstitial concentrations of insulin but not glucose were lower in both Ovx+T and Ovx+T+Ex rats than in controls throughout the clamp. It was concluded that physical exercise prevented the slow onset of insulin action in Ovx+T rats without changing the distribution time of muscle interstitial insulin. The results indicate that hyperandrogenicity is characterized by delayed muscle insulin action. Physical exercise reverses these defects without any beneficial effect on muscle interstitial insulin concentrations.

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