scholarly journals STAT3 Sensitizes Insulin Signaling by Negatively Regulating Glycogen Synthase Kinase-3 

Diabetes ◽  
2008 ◽  
Vol 57 (5) ◽  
pp. 1227-1235 ◽  
Author(s):  
A. Moh ◽  
W. Zhang ◽  
S. Yu ◽  
J. Wang ◽  
X. Xu ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3

Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium–potassium pump in the hearts of male rats

2020 ◽  
Vol 11 (2) ◽  
pp. 1455-1466 ◽  
Author(s):  
Snjezana Romic ◽  
Ana Djordjevic ◽  
Snezana Tepavcevic ◽  
Tijana Culafic ◽  
Mojca Stojiljkovic ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Insulin Signaling ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Male Rats ◽  
Glycogen Synthase Kinase 3 ◽  
Sodium Potassium ◽  
Sodium Potassium Pump

This study provides new insights into the effects of chronic stress and a combination of a fructose diet and chronic stress on the studied molecules in the heart.

scholarly journals Kinome Analysis Reveals Nongenomic Glucocorticoid Receptor-Dependent Inhibition of Insulin Signaling

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3555-3562 ◽  
Author(s):  
Mark Löwenberg ◽  
Jurriaan Tuynman ◽  
Meike Scheffer ◽  
Auke Verhaar ◽  
Louis Vermeulen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protein Kinase ◽  
Molecular Mechanism ◽  
Insulin Signaling ◽  
Glycogen Synthase ◽  
Immunosuppressive Agents ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3 ◽  
Short Term Treatment ◽  
Dependent Inhibition

Glucocorticoids (GCs) are powerful immunosuppressive agents that control genomic effects through GC receptor (GR)-dependent transcriptional changes. A common complication of GC therapy is insulin resistance, but the underlying molecular mechanism remains obscure. Evidence is increasing for rapid genomic-independent GC action on cellular physiology. Here, we generate a comprehensive description of nongenomic GC effects on insulin signaling using peptide arrays containing 1176 different kinase consensus substrates. Reduced kinase activities of the insulin receptor (INSR) and several downstream INSR signaling intermediates (i.e. p70S6k, AMP-activated protein kinase, glycogen synthase kinase-3, and Fyn) were detected in adipocytes and T lymphocytes due to short-term treatment with dexamethasone (DEX), a synthetic fluorinated GC. Western blot analysis confirmed suppressed phosphorylation of the INSR and a series of downstream INSR targets (i.e. INSR substrate-1, p70S6k, protein kinase B, phosphoinositide-dependent protein kinase, Fyn, and glycogen synthase kinase-3) after DEX treatment. DEX inhibited insulin signaling through a GR-dependent (RU486 sensitive) and transcription-independent (actinomycin D insensitive) mechanism. Overall, we postulate here a molecular mechanism for GC-induced insulin resistance based on nongenomic GR-dependent inhibition of insulin signaling.

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