Injury-induced insulin resistance in adipose tissue
► A rodent model of critical illness diabetes was used. ► Adipose tissue became acutely insulin resistant in this model. ► Within minutes, there was a reduction in insulin-induced phosphorylation of IR, IRS-1, Akt and GSK-3β. ► Insulin resistance occurred rapidly in adipose tissue, prior to the insu...
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Published in | Biochemical and biophysical research communications Vol. 421; no. 3; pp. 442 - 448 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
11.05.2012
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Subjects | |
Online Access | Get full text |
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Summary: | ► A rodent model of critical illness diabetes was used. ► Adipose tissue became acutely insulin resistant in this model. ► Within minutes, there was a reduction in insulin-induced phosphorylation of IR, IRS-1, Akt and GSK-3β. ► Insulin resistance occurred rapidly in adipose tissue, prior to the insulin resistance in skeletal muscle.
Hyperglycemia and insulin resistance are common findings in critical illness. Patients in the surgical ICU are frequently treated for this ‘critical illness diabetes’ with intensive insulin therapy, resulting in a substantial reduction in morbidity and mortality. Adipose tissue is an important insulin target tissue, but it is not known whether adipose tissue is affected by critical illness diabetes. In the present study, a rodent model of critical illness diabetes was used to determine whether adipose tissue becomes acutely insulin resistant and how insulin signaling pathways are being affected. There was a reduction in insulin-induced phosphorylation of IR, IRS-1, Akt and GSK-3β. Since insulin resistance occurs rapidly in adipose tissue, but before the insulin resistance in skeletal muscle, it may play a role in the initial development of critical illness diabetes. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These two individuals contributed equally to this work. |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2012.03.146 |