Update on glucose in critical care

Lheureux, Olivier; Prevedello, Danielle; Preiser, Jean‐Charles

doi:10.1016/j.nut.2018.06.027

Cited by 20 publications

(33 citation statements)

References 72 publications

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“…Adequate glycemic control is believed to decrease systemic inflammation, reduce the risk of AKI and need for dialysis, improve the immune response, and attenuate the catabolic effect of stress‐induced hyperglycemia 27,129,133 . Initial studies of tight glycemic control suggested mortality benefit and demonstrated decreases in EGP; however, mortality benefits were not replicated in subsequent studies, potentially because of an increased incidence of hypoglycemia 20,55,128,134,135 …”

Section: Discussionmentioning

confidence: 99%

“…Dysglycemia in critical illness includes hyperglycemia, hypoglycemia, and glycemic variability, all of which are independent risk factors for higher mortality. 20,25,27,28,55,128 Hyperglycemia depresses the immune system, causes osmotic diuresis and electrolyte abnormalities, worsens catabolic thinning of skeletal muscles, and increases risk of infections. 20,22,26,27,128,129 IR and hyperglycemia in critical illness contribute to a positive-feedback loop of metabolic stress and inflammation.…”

Section: Dysglycemia In Critical Illnessmentioning

confidence: 99%

“…27,129,133 Initial studies of tight glycemic control suggested mortality benefit and demonstrated decreases in EGP; however, mortality benefits were not replicated in subsequent studies, potentially because of an increased incidence of hypoglycemia. 20,55,128,134,135 Although the optimal role for exogenous insulin in the ICU remains unclear, insulin does have beneficial effects against abnormally increased EGP. Insulin (1) protects against the depletion of glycogen and triglycerides, (2) prevents liver injury by reducing hepatic inflammation, and (3) prevents the phosphorylation of STAT3, thus restoring physiologic hepatic gluconeogenesis.…”

Section: Dysglycemia In Critical Illnessmentioning

confidence: 99%

“…Glycogenolysis is primarily triggered by catecholamines and is sustained under the influence of epinephrine and cortisol. Gluconeogenesis is stimulated largely by glucagon and, to a lesser extent, by epinephrine and cortisol 20,26 . The ebb phase begins immediately after injury, peaking within 3 hours and lasting for 12–24 hours, and results in increased EGP that is proportional to the severity of illness and to plasma epinephrine concentrations.…”

Section: Egp In Critical Illness: An Overviewmentioning

confidence: 99%

“…GLUT2 regulates the flow of glucose across hepatocytes and pancreatic β cells. GLUT4 is the primary transporter for IMGU in adipose tissue and skeletal muscle 20 . Critical illness is associated with a downregulation of GLUT4 translocation and a decrease in its avidity for glucose, resulting in peripheral IR 24 .…”

Section: Substrate Utilization In Critical Illnessmentioning

confidence: 99%

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Endogenous Glucose Production in Critical Illness

et al. 2021

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Regulation of endogenous glucose production (EGP) by hormonal, neuronal, and metabolic signaling pathways contributes to the maintenance of euglycemia under normal physiologic conditions. EGP is defined by the generation of glucose from substrates through glycogenolysis and gluconeogenesis, usually in fasted states, for local and systemic use. Abnormal increases in EGP are noted in patients with diabetes mellitus type 2, and elevated EGP may also impact the pathogenesis of nonalcoholic fatty liver disease and congestive heart failure. In this narrative review, we performed a literature search in PubMed to identify recently published English language articles characterizing EGP in critical illness. Evidence from preclinical and clinical studies demonstrates that critical illness can disrupt EGP through multiple mechanisms including increased systemic inflammation, counterregulatory hormone and catecholamine release, alterations in the hypothalamic-pituitary axis, insulin resistance, lactic acidosis, and iatrogenic insults such as vasopressors and glucocorticoids administered as part of clinical care. EGP contributes to hyperglycemia in critical illness when abnormally elevated and to hypoglycemia when abnormally depressed, each of which has been independently associated with increased mortality. Increased EGP may also promote protein catabolism that could worsen critical illness myopathy and impede recovery. Better understanding of the mechanisms and factors contributing to dysregulated EGP in critical illness may help in the development of therapeutic strategies that promote euglycemia, reduce intensive care unit-associated catabolism, and improve patient outcomes.

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Section: Discussionmentioning

confidence: 99%