Acute hyperglycaemia induces an inflammatory response in young patients with type 1 diabetes

Ann Med. 2008;40(8):627-33. doi: 10.1080/07853890802126547.

Abstract

Background: Patients with type 1 diabetes (T1D) are at a substantially increased risk of cardiovascular disease. Stress-induced hyperglycaemia in turn is shown to worsen the prognosis of patients suffering from an acute myocardial infarction. However, the mechanisms behind these findings are incompletely known.

Aim: To investigate whether markers of chronic inflammation, and oxidative stress respond to acute hyperglycaemia in patients with T1D.

Methods: The plasma glucose concentration was rapidly raised from 5 to 15 mmol/L in 35 males (22 men with T1D and 13 age-matched non-diabetic volunteers) and maintained for 2 h. All participants were young non-smokers without any signs of diabetic or other complications. Markers of chronic inflammation, and oxidative stress were analysed in serum/plasma samples drawn at base-line and after 120 min of hyperglycaemia.

Results: Compared to normoglycaemia, acute hyperglycaemia increased the interleukin (IL)-6 concentrations by 39% in patients with T1D (P<0.01) and 26% in healthy volunteers (P<0.05). During hyperglycaemia the superoxide dismutase concentration was increased by 17% in the healthy volunteers (P<0.01) and 5% in the patients with type 1 diabetes (P=NS). The increase in tumour necrosis factor (TNF)-alpha was larger in patients with type 1 diabetes than in non-diabetic volunteers (35% versus -10%, P<0.05).

Conclusions: This study shows that acute hyperglycaemia induces an inflammatory response in patients with type 1 diabetes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Adult
  • Blood Glucose / metabolism
  • Case-Control Studies
  • Diabetes Mellitus, Type 1 / complications*
  • Diabetes Mellitus, Type 1 / physiopathology
  • Humans
  • Hyperglycemia / physiopathology*
  • Inflammation / etiology*
  • Inflammation / physiopathology
  • Interleukin-6 / blood
  • Interleukin-6 / metabolism
  • Male
  • Oxidative Stress*
  • Superoxide Dismutase / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Young Adult

Substances

  • Blood Glucose
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Superoxide Dismutase