WFRF:(Madsbad S.)
Sökning: WFRF:(Madsbad S.) > IRS-1 serine phosph...
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03106naa a2200313 4500 | |
| 001 | oai:prod.swepub.kib.ki.se:111830646 | |
| 003 | SwePub | |
| 008 | 240913s2006 | |||||||||||000 ||eng| | |
| 024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1118306462 URI |
| 024 | 7 | a https://doi.org/10.2337/diabetes.55.03.06.db05-07962 DOI |
| 040 | a (SwePub)ki | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Bouzakri, K4 aut |
| 245 | 1 0 | a IRS-1 serine phosphorylation and insulin resistance in skeletal muscle from pancreas transplant recipients |
| 264 | 1 | b American Diabetes Association,c 2006 |
| 520 | a 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. | |
| 700 | 1 | a Karlsson, HKRu Karolinska Institutet4 aut |
| 700 | 1 | a Vestergaard, H4 aut |
| 700 | 1 | a Madsbad, S4 aut |
| 700 | 1 | a Christiansen, E4 aut |
| 700 | 1 | a Zierath, JRu Karolinska Institutet4 aut |
| 710 | 2 | a Karolinska Institutet4 org |
| 773 | 0 | t Diabetesd : American Diabetes Associationg 55:3, s. 785-791q 55:3<785-791x 0012-1797x 1939-327X |
| 856 | 4 | u http://diabetes.diabetesjournals.org/content/55/3/785.full.pdf |
| 856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:111830646 |
| 856 | 4 8 | u https://doi.org/10.2337/diabetes.55.03.06.db05-0796 |
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- Bouzakri, K
- Karlsson, HKR
- Vestergaard, H
- Madsbad, S
- Christiansen, E
- Zierath, JR
- Artiklar i publikationen
- Diabetes
- Av lärosätet
- Karolinska Institutet
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