Mechanism of Insulin Resistance in Infection

Lang, Charles H.

doi:10.1007/978-3-642-76736-4_44

Cited by 6 publications

(4 citation statements)

References 67 publications

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“…Nevertheless, some other mechanism also must contribute to the observed effects, as even the intravenous administration of glipizide sodium salt, which resulted in high plasma concentrations, failed to reduce blood glucose concentrations during HS. We think that part of the answer is the relatively well-characterized phenomenon of "insulin resistance" occurring during shock and trauma, that is, a reduced ability of the organs to respond to insulin and to mobilize glucose (26,27). The mechanisms and mediators of insulin resistance are multiple and likely to involve cytokines as well as a ␤-adrenoceptormediated pathway (27).…”

Section: Discussionmentioning

confidence: 97%

“…We think that part of the answer is the relatively well-characterized phenomenon of "insulin resistance" occurring during shock and trauma, that is, a reduced ability of the organs to respond to insulin and to mobilize glucose (26,27). The mechanisms and mediators of insulin resistance are multiple and likely to involve cytokines as well as a ␤-adrenoceptormediated pathway (27). In the current therapeutic scenario, insulin resistance works to our advantage, as it does not allow hypoglycemia to develop during the initial phase of the pharmacologic resuscitation.…”

Section: Discussionmentioning

confidence: 99%

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Parenteral administration of glipizide sodium salt, an inhibitor of adenosine triphosphate-sensitive potassium channels, prolongs short-term survival after severe controlled hemorrhage in rats*

Evgenov

Pacher

Williams

et al. 2003

Critical Care Medicine

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Parenteral administration of glipizide sodium salt, an inhibitor of adenosine triphosphate-sensitive potassium channels, prolongs short-term survival after severe controlled hemorrhage in rats*

Evgenov

Pacher

Williams

et al. 2003

Critical Care Medicine

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“…In skeletal muscle, cytokines decrease the activity of glycogen synthase, and catecholamines act on adrenergic β2 cell receptors to reduce IMGU 86 . In adipocytes, catecholamines decrease IMGU by blunting the insulin‐induced increase in tyrosine autophosphorylation of the insulin receptor kinase 26,87 . Peripheral IR is exacerbated by immobility and by decreases in muscle protein synthesis 88,89 …”

Section: Modulation Of Egp In Critical Illnessmentioning

confidence: 99%

“…86 In adipocytes, catecholamines decrease IMGU by blunting the insulininduced increase in tyrosine autophosphorylation of the insulin receptor kinase. 26,87 Peripheral IR is exacerbated by immobility and by decreases in muscle protein synthesis. 88,89 Central IR is characterized by a defect in the inability of physiological concentrations of insulin to suppress hepatic glucose production.…”

Section: Insulin Resistancementioning

confidence: 99%

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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Sepsis‐induced Changes in Pancreatic Hormone Secretion

Lang

2001

Comprehensive Physiology

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The sections in this article are: Alterations in Insulin Concentration, Secretion, and Clearance Hemorrhage and Acute Blood Loss Thermal Injury Traumatic Injury Bacterial Infection Endotoxin and Related Insults Summary Alterations in Glucagon Concentration, Secretion, and Clearance Hemorrhage and Acute Blood Loss Thermal Injury Traumatic Injury Bacterial Infection Endotoxin and Related Insults Summary Stress‐Induced Changes in Other Pancreatic Hormones Amylin Somatostatin Pancreatic Polypeptide Impact of Trauma‐Induced Changes in Glucagon and Insulin on Metabolism

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Mechanism of Insulin Resistance in Infection

Cited by 6 publications

References 67 publications

Parenteral administration of glipizide sodium salt, an inhibitor of adenosine triphosphate-sensitive potassium channels, prolongs short-term survival after severe controlled hemorrhage in rats*

Parenteral administration of glipizide sodium salt, an inhibitor of adenosine triphosphate-sensitive potassium channels, prolongs short-term survival after severe controlled hemorrhage in rats*

Endogenous Glucose Production in Critical Illness

Sepsis‐induced Changes in Pancreatic Hormone Secretion

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