MCP-1and IL-1β expression in the myocardia of two young patients with Type 1 diabetes mellitus and fatal diabetic ketoacidosis.
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 (T1DM) 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) chemokine and the interleukin (IL)-1β 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-1β was seen in the myocardia of the T1DM/DKA 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.
Burnett School of Biomedical Sciences, College of medicine, University of Central Florida, Orlando, FL, USA.
Jianli
J
Niu
Department of Pathology and Laboratory Medicine, The Brody School of Medicine, East Carolina University, Greenville, NC, USA.
M G F
MG
Gilliland
School of Basic Medicine, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, China.
Zhuqing
Z
Jin
Burnett School of Biomedical Sciences, College of medicine, University of Central Florida, Orlando, FL, USA.
Pappachan E
PE
Kolattukudy
Department of Pediatrics, Section of Pediatric Endocrinology, Georgia Regents University, Augusta, GA, USA. Electronic address: whoffman@gru.edu.
William H
WH
Hoffman
D000293:Adolescent; D000328:Adult; D017209:Apoptosis; D018932:Chemokine CCL2 / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D016883:Diabetic Ketoacidosis / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D017809:Fatal Outcome; D006801:Humans; D006984:Hypertrophy / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D007124:Immunoenzyme Techniques; D020287:In Situ Nick-End Labeling; D007249:Inflammation / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D053583:Interleukin-1beta / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D018384:Oxidative Stress; D055815:Young Adult
C111835:CCL2 protein, human; D018932:Chemokine CCL2; D053583:Interleukin-1beta
Diabetic cardiomyopathy; Diabetic ketoacidosis; IL-1β; MCP-1; Obesity; Type 1 diabetes mellitus