Hypoglycaemia Clinical Trial
Official title:
Mechanisms of Insulin Resistance in Critical Illness: Role of Systemic Inflammation and GLP-1
The purpose of this study is to determine the role of inflammation and the insulin regulating hormone GLP-1 during critical illness.
Critically ill patients often exhibit hyperglycaemia. Although the cause of this
hyperglycaemia is probably multifactorial, peripheral insulin resistance is a major
contributor, similar to type 2 diabetes mellitus (T2D). There are several similarities
between critical illness and T2D, including the presence of systemic inflammation and
increased plasma free fatty acids (FFA), all of which may induce insulin resistance in
healthy volunteers. In critical illness, elevated catecholamines, cortisol, growth hormone
and glucagon may also contribute to insulin resistance.
The degree of hyperglycaemia correlates with mortality in ICU patients. van den Berghe et al.
found that IV infusion of insulin to obtain strict normoglycaemia reduced mortality as well
as morbidity in critically ill surgical patients and in some medical ICU patients.
However, insulin increases the risk of hypoglycaemia; this is a major obstacle to strict
euglycaemia in ICU patients and may explain the inability of others to reproduce the benefits
reported by van den Berghe et al. Thus, alternatives to insulin for controlling plasma
glucose (PG) in ICU patients are warranted.
Aim:
To study the role of the incretin hormone, glucagon-like peptide (GLP)-1 for glycaemic,
metabolic, hormonal and inflammatory profile in
- critically ill patients in the intensive care unit (ICU) and
- healthy volunteers exposed to a standardised systemic inflammation
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