Bench-to-bedside review: Glucose and stress conditions in the intensive care unit

Abstract

The physiological response to blood glucose elevation is the pancreatic release of insulin, which blocks hepatic glucose production and release, and stimulates glucose uptake and storage in insulin-dependent tissues. When this first regulatory level is overwhelmed (that is, by exogenous glucose supplementation), persistent hyperglycaemia occurs with intricate consequences related to the glucose acting as a metabolic substrate and as an intracellular mediator. It is thus very important to unravel the glucose metabolic pathways that come into play during stress as well as the consequences of these on cellular functions. During acute injuries, activation of serial hormonal and humoral responses inducing hyperglycaemia is called the 'stress response'. Central activation of the nervous system and of the neuroendocrine axes is involved, releasing hormones that in most cases act to worsen the hyperglycaemia. These hormones in turn induce profound modifications of the inflammatory response, such as cytokine and mediator profiles. The hallmarks of stress-induced hyperglycaemia include 'insulin resistance' associated with an increase in hepatic glucose output and insufficient release of insulin with regard to glycaemia. Although both acute and chronic hyperglycaemia may induce deleterious effects on cells and organs, the initial acute endogenous hyperglycaemia appears to be adaptive. This acute hyperglycaemia participates in the maintenance of an adequate inflammatory response and consequently should not be treated aggressively. Hyperglycaemia induced by an exogenous glucose supply may, in turn, amplify the inflammatory response such that it becomes a disproportionate response. Since chronic exposure to glucose metabolites, as encountered in diabetes, induces adverse effects, the proper roles of these metabolites during acute conditions need further elucidation.

Using Blood Glucose Estimation to Interpret Stress in Patients Undergoing Minor Oral Surgery Procedures

“…Following this, the ability of anaesthetic agents and neural blockade to modify stress responses has been studied. Although it seems that the stress response developed to allow injured animals to survive by catabolising their own body fuels, it has been argued that the response is unnecessary in current clinical practise (Figure1 ) [1][2][3][4][5][6][7][8][9][10].…”

“…The circulating catecholamines, cortisol and growth hormone result in elevated blood glucose levels. Consequently, synthesis and release of insulin is stimulated to maintain blood glucose levels within normal range [1][2][3][4][5][6][7][8][9][10][11][12][13]. In the pancreas glucagon is released and insulin secretion may be diminished.…”

“…In the pancreas glucagon is released and insulin secretion may be diminished. The overall metabolic effect of hormonal changes is increased catabolism that mobilizes substrates to provide energy sources and a mechanism to retain salt and water and maintain fluid volume and cardiovascular homeostasis [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16].…”

“…It is defined as a state of disharmony or disturbances in homeostasis provoked by psychological, environmental or physiological stressor situations [1,2]. These situations promote immunoinflammatory and metabolic responses that are entangled in an intricate way, as the cells involved in these key events ontogenetically originate from a unique primordial organ combining both immune and metabolic functions [3][4][5][6][7][8][9][10][11][12]. In 1932 Cubberston documented and quantified the time course of stress response and introduced the terms "ebb" and "flow" to describe an initial decrease and subsequent increase in metabolic activity due to stress [1].…”

Dynamic change of glycemic status during the early phase after allogeneic hematopoietic stem cell transplantation

“…Post-HSCT inflammation is a possible cause of elevated IR. 10 Several studies demonstrated that levels of inflammatory cytokines were elevated even during the conditioning regimen, 11,12 suggesting that these cytokines could cause increased IR quite early after HSCT. Our finding that the HOMA-IR score was higher in patients who received a myeloablative conditioning regimen than a reducedintensity conditioning regimen also supported this idea.…”