Plasma adiponectin levels are markedly elevated in imatinib-treated chronic myeloid leukemia (CML) patients: A mechanism for improved insulin sensitivity in Type 2 diabetic CML patients?

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dc.contributor.authorFitter, S.
dc.contributor.authorVandyke, K.
dc.contributor.authorSchultz, C.
dc.contributor.authorWhite, D.
dc.contributor.authorHughes, T.
dc.contributor.authorZannettino, A.
dc.date.issued2010
dc.description.abstractContext: The mechanism(s) by which imatinib improves glycemic control in chronic myeloid leukemia (CML) patients with type 2 diabetes remains unclear. Objective: Adiponectin is an important regulator of insulin sensitivity that is secreted exclusively by adipocytes. We previously reported that imatinib promotes adipocytic differentiation of mesenchymal stromal cells. We therefore hypothesized that imatinib therapy would be associated with an increase in peripheral and intramedullary adiposity and elevated plasma adiponectin levels. Research Design and Methods: Adiponectin levels in CML patient plasma, at diagnosis and then during imatinib mesylate therapy, was measured using an ELISA. Adiponectin multimers in plasma were analyzed using nondenaturing PAGE and immunoblotting. Intramedullary adiposity and adipose tissue mass was determined using histomorphometry and dual-energy X-ray absorptiometry, respectively. Results: In CML patients, an increase in intramedullary and peripheral adiposity was observed after 6 months of imatinib therapy and plasma adiponectin levels, in the form of high- and low-molecular-weight complexes, were elevated 3-fold, compared with pretreatment levels, after 3, 6, and 12 months of therapy. Conclusions: Elevated adiponectin levels in imatinib-treated CML patients provide a possible mechanism for improved glucose and lipid metabolism reported for some imatinib-treated patients.
dc.description.statementofresponsibilityStephen Fitter, Kate Vandyke, Christopher G. Schultz, Deborah White, Timothy P. Hughes, and Andrew C. W. Zannettino
dc.identifier.citationJournal of Clinical Endocrinology and Metabolism, 2010; 95(8):3763-3767
dc.identifier.doi10.1210/jc.2010-0086
dc.identifier.issn0021-972X
dc.identifier.issn0021-972X
dc.identifier.orcidFitter, S. [0000-0003-1663-6807]
dc.identifier.orcidVandyke, K. [0000-0002-1033-849X]
dc.identifier.orcidWhite, D. [0000-0003-4844-333X]
dc.identifier.orcidHughes, T. [0000-0002-0910-3730] [0000-0002-7990-4509]
dc.identifier.orcidZannettino, A. [0000-0002-6646-6167]
dc.identifier.urihttp://hdl.handle.net/2440/64089
dc.language.isoen
dc.publisherEndocrine Society
dc.rightsCopyright © 2010 by The Endocrine Society
dc.source.urihttps://doi.org/10.1210/jc.2010-0086
dc.subjectHumans
dc.subjectInsulin Resistance
dc.subjectBenzamides
dc.subjectPiperazines
dc.subjectPyrimidines
dc.subjectProtein Kinase Inhibitors
dc.subjectAbsorptiometry, Photon
dc.subjectBlotting, Western
dc.subjectEnzyme-Linked Immunosorbent Assay
dc.subjectTreatment Outcome
dc.subjectAnalysis of Variance
dc.subjectFemale
dc.subjectMale
dc.subjectAdiposity
dc.subjectAdiponectin
dc.subjectLeukemia, Myelogenous, Chronic, BCR-ABL Positive
dc.subjectImatinib Mesylate
dc.titlePlasma adiponectin levels are markedly elevated in imatinib-treated chronic myeloid leukemia (CML) patients: A mechanism for improved insulin sensitivity in Type 2 diabetic CML patients?
dc.typeJournal article
pubs.publication-statusPublished

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