MCP-1 and IL-1 beta expression in the myocardia of two young patients with Type 1 diabetes mellitus and fatal diabetic ketoacidosis

    Authors

    J. L. Niu; M. G. F. Gilliland; Z. Q. Jin; P. E. Kolattukudy;W. H. Hoffman

    Comments

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    Abbreviated Journal Title

    Exp. Mol. Pathol.

    Keywords

    Diabetic cardiomyopathy; Diabetic ketoacidosis; IL-1 beta; MCP-1; Obesity; Type 1 diabetes mellitus; MONOCYTE CHEMOATTRACTANT PROTEIN-1; EXPERIMENTAL AUTOIMMUNE MYOCARDITIS; MICROVASCULAR ENDOTHELIAL-CELLS; FREE FATTY-ACIDS; OXIDATIVE STRESS; INFLAMMATORY CYTOKINES; CARDIOVASCULAR-DISEASE; DILATED CARDIOMYOPATHY; LIPID-PEROXIDATION; HEART-FAILURE; Pathology

    Abstract

    Convincing evidence exists for the early onset of diabetic cardiomyopathy and coronary artery disease (CAD) as distinct forms of cardiac disease in young patients with Type 1 diabetes mellitus (TI DM) and the pre-stages of T2DM, forms of dysregulated insulin signaling. Progression of both chronic cardiac conditions is mediated by oxidative stress and low grade inflammation. This study reports the expression of monocyte chemotactic protein-1 (MCP-1) chemoldne and the interleukin (IL)-1 beta inflammatory cytokine in two young patients with suboptimal metabolic control and fatal diabetic ketoacidosis (DKA), two age-matched overweight/obesity cases and two age-matched controls. In addition, markers of oxidative stress, apoptosis, collagen deposition and cardiomyocyte hypertrophy were studied. Significant expression of MCP-1 and IL-beta was seen in the myocardia of the T1DM/DNA cases, with lesser amounts expressed in the overweight/obesity myocardia. All of the other markers except cardiomyocyte hypertrophy were expressed to a significantly greater extent in the T1DM/DKA and overweight/obesity cases in comparison to the age-matched controls. Cardiomyocyte hypertrophy was significantly greater in the overweight/obesity cases than in the T1DM/DKA or the control cases. (C) 2013 Elsevier Inc. All rights reserved.

    Journal Title

    Experimental and Molecular Pathology

    Volume

    96

    Issue/Number

    1

    Publication Date

    1-1-2014

    Document Type

    Article

    Language

    English

    First Page

    71

    Last Page

    79

    WOS Identifier

    WOS:000332143000010

    ISSN

    0014-4800

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