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

Exp Mol Pathol. 2014 Feb;96(1):71-9. doi: 10.1016/j.yexmp.2013.11.001. Epub 2013 Nov 16.

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 (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.

Keywords: Diabetic cardiomyopathy; Diabetic ketoacidosis; IL-1β; MCP-1; Obesity; Type 1 diabetes mellitus.

Publication types

  • Case Reports
  • Research Support, N.I.H., Extramural

MeSH terms

  • Adolescent
  • Adult
  • Apoptosis
  • Chemokine CCL2 / metabolism*
  • Diabetes Mellitus, Type 1 / complications*
  • Diabetes Mellitus, Type 1 / metabolism
  • Diabetes Mellitus, Type 1 / pathology
  • Diabetic Ketoacidosis / complications*
  • Diabetic Ketoacidosis / metabolism
  • Diabetic Ketoacidosis / pathology
  • Fatal Outcome
  • Humans
  • Hypertrophy / etiology*
  • Hypertrophy / metabolism
  • Hypertrophy / pathology
  • Immunoenzyme Techniques
  • In Situ Nick-End Labeling
  • Inflammation / etiology*
  • Inflammation / metabolism
  • Inflammation / pathology
  • Interleukin-1beta / metabolism*
  • Male
  • Myocardium / metabolism
  • Myocardium / pathology*
  • Oxidative Stress
  • Young Adult

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • Interleukin-1beta