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Figure 1

Factors promoting gluconeogenesis in critical illness. Counterregulatory hormones oppose the restraining effect of insulin on lipolysis and proteolysis, thus increasing substrate for gluconeogenesis. Despite hyperinsulinemia, hepatic insulin resistance leads to ongoing glucose production in the face of hyperglycemia. This process occurs under positive control of counterregulatory hormones, in particular glucagon and epinephrine.

Figure 2

Mechanism of glucose uptake into skeletal muscle, cardiomyocyte and adipocyte. Insulin binds its receptor, a transmembrane heterodimeric protein that has autophosphorylation activity that has autophosphorylation activity and becomes phosphorylated (P) when stimulated by insulin. The intrinsic tyrosine kinase is enhanced, leading to phosphorylation of a cascade of insulin receptor substrate molecules. This signaling pathway culminates in translocation of intracellular vesicles containing the transport protein Glut4 to the plasma membrane. Involved is an additional step leading to activation of Glut4, so that glucose uptake is increased several-fold. P-sites of phosphorylation on tyrosine residues.

Stress-induced hyperglycemia is a common problem in patients admitted to the ICU, even when glucose homeostasis has previously been normal. Hyperglycemia is a near-universal finding in diabetic persons suffering catabolic illnesses and may worsen prognosis, although this possibility is controversial. The presence of hyperglycemia is associated with an increased risk of infectious complications in surgical patients, and indirect evidence indicates that maintenance of euglycemia can reduce the risk of infection. The causes of stress hyperglycemia include the presence of excessive counterregulatory hormones (glucagon, growth hormone, catecholamine, and glucocorticoid, either endogenous or exogenous), high circulating or tissue levels of cytokine (in particular tumor necrosis factor-α [TNα] and interleukin-1). This metabolic milieu results in failure of insulin to suppress hepatic gluconeogenesis despite hyperglycemia; in addition, insulin-mediated glucose uptake into skeletal muscle is impaired. Patients given excessive nutritional support, especially by the intravenous route, are particularly likely to encounter hyperglycemia. Insulin remains the obvious treatment for hyperglycemia, although evidence documenting the clinical benefit of aggressive insulin therapy in the ICU is sparse.

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Address reprint requests to Karen McCowen, MD, Department of Medicine/Division of Clinical Nutrition, Beth Isreal Deaconess West Campus, 1 Deaconess Road, Boston, MA 02215. e-mail:

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