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Endogenous Glucose Production in Critical Illness.
Nameer Al-Yousif1, Sagar Rawal2, Michael Jurczak3
1Department of Internal Medicine, UPMC Mercy Hospital, Pittsburgh, Pennsylvania, USA.
Summary
Critical illness disrupts endogenous glucose production (EGP), leading to hyperglycemia or hypoglycemia, both linked to increased mortality. Understanding these disruptions is key to improving patient outcomes in critical care.
Area of Science:
- Endocrinology
- Metabolism
- Critical Care Medicine
Background:
- Endogenous glucose production (EGP) maintains normal blood sugar levels through glycogenolysis and gluconeogenesis.
- Dysregulated EGP is implicated in type 2 diabetes, nonalcoholic fatty liver disease, and heart failure.
- Critical illness presents unique challenges to EGP regulation.
Purpose of the Study:
- To review recent literature on the mechanisms disrupting EGP in critical illness.
- To understand the impact of critical illness on glucose homeostasis.
- To identify potential therapeutic targets for managing EGP in critically ill patients.
Main Methods:
- A narrative review of English language articles.
- Literature search conducted in PubMed.
- Focus on preclinical and clinical studies characterizing EGP in critical illness.
Main Results:
- Critical illness disrupts EGP via inflammation, hormone release, hypothalamic-pituitary axis alterations, insulin resistance, lactic acidosis, and iatrogenic factors.
- Abnormal EGP in critical illness can cause hyperglycemia or hypoglycemia, both associated with increased mortality.
- Elevated EGP may exacerbate protein catabolism, worsening critical illness myopathy and hindering recovery.
Conclusions:
- Dysregulated EGP is a significant factor in critical illness, contributing to adverse outcomes.
- Further research into EGP mechanisms in critical illness is needed.
- Targeting EGP may offer novel therapeutic strategies to improve outcomes in critically ill patients.
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