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- Bouzakri, K (author)
IRS-1 serine phosphorylation and insulin resistance in skeletal muscle from pancreas transplant recipients
- Article/chapterEnglish2006
Publisher, publication year, extent ...
- American Diabetes Association,2006
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- LIBRIS-ID:oai:prod.swepub.kib.ki.se:111830646
- http://kipublications.ki.se/Default.aspx?queryparsed=id:111830646URI
- https://doi.org/10.2337/diabetes.55.03.06.db05-0796DOI
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- Language:English
- Summary in:English
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- Insulin-dependent diabetic recipients of successful pancreas allografts achieve self-regulatory insulin secretion and discontinue exogenous insulin therapy; however, chronic hyperinsulinemia and impaired insulin sensitivity generally develop. To determine whether insulin resistance is accompanied by altered signal transduction, skeletal muscle biopsies were obtained from pancreas-kidney transplant recipients (n = 4), nondiabetic kidney transplant recipients (receiving the same immunosuppressive drugs; n = 5), and healthy subjects (n = 6) before and during a euglycemic-hyperinsulinemic clamp. Basal insulin receptor substrate (IRS)-1 Ser (312) and Ser (616) phosphorylation, IRS-1–associated phosphatidylinositol 3-kinase activity, and extracellular signal–regulated kinase (ERK)-1/2 phosphorylation were elevated in pancreas-kidney transplant recipients, coincident with fasting hyperinsulinemia. Basal IRS-1 Ser (312) and Ser (616) phosphorylation was also increased in nondiabetic kidney transplant recipients. Insulin increased phosphorylation of IRS-1 at Ser (312) but not Ser (616) in healthy subjects, with impairments noted in nondiabetic kidney and pancreas-kidney transplant recipients. Insulin action on ERK-1/2 and Akt phosphorylation was impaired in pancreas-kidney transplant recipients and was preserved in nondiabetic kidney transplant recipients. Importantly, insulin stimulation of the Akt substrate AS160 was impaired in nondiabetic kidney and pancreas-kidney transplant recipients. In conclusion, peripheral insulin resistance in pancreas-kidney transplant recipients may arise from a negative feedback regulation of the canonical insulin-signaling cascade from excessive serine phosphorylation of IRS-1, possibly as a consequence of immunosuppressive therapy and hyperinsulinemia.
Added entries (persons, corporate bodies, meetings, titles ...)
- Karlsson, HKRKarolinska Institutet (author)
- Vestergaard, H (author)
- Madsbad, S (author)
- Christiansen, E (author)
- Zierath, JRKarolinska Institutet (author)
- Karolinska Institutet (creator_code:org_t)
Related titles
- In:Diabetes: American Diabetes Association55:3, s. 785-7910012-17971939-327X
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