Impaired insulin sensitivity as an underlying mechanism linking hepatitis C and posttransplant diabetes mellitus in kidney recipients

2.50
Hdl Handle:
http://hdl.handle.net/10547/593393
Title:
Impaired insulin sensitivity as an underlying mechanism linking hepatitis C and posttransplant diabetes mellitus in kidney recipients
Authors:
Baid-Agrawal, S.; Frei, U.; Reinke, P.; Schindler, R.; Kopp, M.A.; Martus, P.; Berg, T.; Juergensen, J.S.; Anker, Stefan D.; Doehner, Wolfram
Abstract:
Aim of this study was to investigate the mechanism/s associating hepatitis C virus (HCV) infection and posttransplant diabetes mellitus in kidney recipients. Twenty HCV-positive and 22 HCV-negative kidney recipients, 14 HCV-positive nontransplant patients and 24 HCV-negative nontransplant (healthy) subjects were analyzed. A 3-h intravenous glucose tolerance test was performed; peripheral insulin sensitivity was assessed by minimal modeling. Pancreatic insulin secretion, hepatic insulin uptake, pancreatic antibodies and proinflammatory cytokines in serum (tumor necrosis factor-alpha, intereukin-6, high-sensitive C-reactive protein) were also assessed. HCV-positive recipients showed a significantly lower insulin sensitivity as compared to HCV-negative recipients (3.0 +/- 2.1 vs. 4.9 +/- 3.0 min(-1).microU.mL(- 1).10(4), p = 0.02), however, insulin secretion and hepatic insulin uptake were not significantly different. Pancreatic antibodies were negative in all. HCV status was an independent predictor of impaired insulin sensitivity (multivariate analysis, p = 0.008). The decrease of insulin sensitivity due to HCV was comparable for transplant and non-transplant subjects. No significant correlation was found between any of the cytokines and insulin sensitivity. Our results suggest that impaired peripheral insulin sensitivity is associated with HCV infection irrespective of the transplant status, and is the most likely pathogenic mechanism involved in the development of type 2 diabetes mellitus associated with HCV infection.
Affiliation:
Charité Universitätsmedizin Berlin
Citation:
Baid-Agrawal, S. et al (2009) 'Impaired insulin sensitivity as an underlying mechanism linking hepatitis C and posttransplant diabetes mellitus in kidney recipients' Am. J. Transplant. 9 (12):2777-84
Publisher:
Wiley
Journal:
American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
Issue Date:
Dec-2009
URI:
http://hdl.handle.net/10547/593393
DOI:
10.1111/j.1600-6143.2009.02843.x
PubMed ID:
19845589
Additional Links:
http://onlinelibrary.wiley.com/doi/10.1111/j.1600-6143.2009.02843.x/full
Type:
Article
Language:
en
ISSN:
1600-6143
Appears in Collections:
IHR Institute for Health Research

Full metadata record

DC FieldValue Language
dc.contributor.authorBaid-Agrawal, S.en
dc.contributor.authorFrei, U.en
dc.contributor.authorReinke, P.en
dc.contributor.authorSchindler, R.en
dc.contributor.authorKopp, M.A.en
dc.contributor.authorMartus, P.en
dc.contributor.authorBerg, T.en
dc.contributor.authorJuergensen, J.S.en
dc.contributor.authorAnker, Stefan D.en
dc.contributor.authorDoehner, Wolframen
dc.date.accessioned2016-01-14T12:42:24Zen
dc.date.available2016-01-14T12:42:24Zen
dc.date.issued2009-12en
dc.identifier.citationBaid-Agrawal, S. et al (2009) 'Impaired insulin sensitivity as an underlying mechanism linking hepatitis C and posttransplant diabetes mellitus in kidney recipients' Am. J. Transplant. 9 (12):2777-84en
dc.identifier.issn1600-6143en
dc.identifier.pmid19845589en
dc.identifier.doi10.1111/j.1600-6143.2009.02843.xen
dc.identifier.urihttp://hdl.handle.net/10547/593393en
dc.description.abstractAim of this study was to investigate the mechanism/s associating hepatitis C virus (HCV) infection and posttransplant diabetes mellitus in kidney recipients. Twenty HCV-positive and 22 HCV-negative kidney recipients, 14 HCV-positive nontransplant patients and 24 HCV-negative nontransplant (healthy) subjects were analyzed. A 3-h intravenous glucose tolerance test was performed; peripheral insulin sensitivity was assessed by minimal modeling. Pancreatic insulin secretion, hepatic insulin uptake, pancreatic antibodies and proinflammatory cytokines in serum (tumor necrosis factor-alpha, intereukin-6, high-sensitive C-reactive protein) were also assessed. HCV-positive recipients showed a significantly lower insulin sensitivity as compared to HCV-negative recipients (3.0 +/- 2.1 vs. 4.9 +/- 3.0 min(-1).microU.mL(- 1).10(4), p = 0.02), however, insulin secretion and hepatic insulin uptake were not significantly different. Pancreatic antibodies were negative in all. HCV status was an independent predictor of impaired insulin sensitivity (multivariate analysis, p = 0.008). The decrease of insulin sensitivity due to HCV was comparable for transplant and non-transplant subjects. No significant correlation was found between any of the cytokines and insulin sensitivity. Our results suggest that impaired peripheral insulin sensitivity is associated with HCV infection irrespective of the transplant status, and is the most likely pathogenic mechanism involved in the development of type 2 diabetes mellitus associated with HCV infection.en
dc.language.isoenen
dc.publisherWileyen
dc.relation.urlhttp://onlinelibrary.wiley.com/doi/10.1111/j.1600-6143.2009.02843.x/fullen
dc.rightsArchived with thanks to American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeonsen
dc.subjectHepatitis C virus (HCV)en
dc.subjectinsulin resistanceen
dc.subjectkidney transplantationen
dc.subjectposttransplant diabetes mellitus (PTDM)en
dc.subjectdiabetesen
dc.subject.meshAdulten
dc.subject.meshCross-Sectional Studiesen
dc.subject.meshDiabetes Mellitus, Type 2en
dc.subject.meshFemaleen
dc.subject.meshGlucose Tolerance Testen
dc.subject.meshHepatitis C, Chronicen
dc.subject.meshHumansen
dc.subject.meshInsulinen
dc.subject.meshInsulin Resistanceen
dc.subject.meshKidney Transplantationen
dc.subject.meshMaleen
dc.subject.meshMiddle Ageden
dc.titleImpaired insulin sensitivity as an underlying mechanism linking hepatitis C and posttransplant diabetes mellitus in kidney recipientsen
dc.typeArticleen
dc.contributor.departmentCharité Universitätsmedizin Berlinen
dc.identifier.journalAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeonsen

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