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Cited by 97Cardiac Ischemia and ReperfusionHyperglycemia and glycemic control in critically ill and hospitalized patientsAcute Myocardial Infarction Research

Insulin: An endogenous cardioprotector

Das, Undurti N.·2003·Current Opinion in Critical Care
DOI 10.1097/00075198-200310000-00007
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Abstract

This review discusses the myocardial protective property of the insulin/glucose-insulin-potassium regimen and the mechanisms involved in this beneficial action. Several recent studies suggest that insulin not only is useful to control hyperglycemia and maintain glucose homeostasis but also may have the unique property to protect the myocardium from reperfusion injury and ischemia and prevent apoptosis of myocardial cells. The insulin/glucose-insulin-potassium (GIK) regimen suppresses the production of tumor necrosis factor-alpha, interleukin-6, macrophage migration inhibitory factor and other pro-inflammatory cytokines, and free radicals; and enhances the synthesis of endothelial nitric oxide and anti-inflammatory cytokines interleukin-4 and interleukin-10. Thus, the insulin/GIK regimen brings about its cardioprotective action. This may also explain why the insulin/GIK regimen is useful in sepsis and septic shock, myocardial recovery in acute myocardial infarction, and critical illness. It is suggested that the infusion of adequate amounts of insulin to patients with acute myocardial infarction, congestive heart failure, cardiogenic shock, and critical illness preserves myocardial integrity and function and ensures rapid recovery. In view of the suppressive action of insulin on the synthesis of proinflammatory cytokines and free radicals, it is possible that the insulin/GIK regimen, when used in a timely and appropriate fashion, may also protect other tissues and organs and facilitate in the recovery of patients who are critically ill.

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Crossref · 10.1097/00075198-200310000-00007

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67 of 67 references verified0 citation errors · 0 not checkable

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  • The insulin receptor shares a signaling pathway with eNOS activation to regulate postprandial blood flow and efficient nutrient disposition to peripheral tissues.

    “The insulin receptor shares a signaling pathway with the activation of endothelial NOS (eNOS) [19,48,49,50,51,52] to regulate the postprandial blood flow and efficient nutrient disposition to peripheral tissues”

    From NO-Rich Diet for Lifestyle-Related Diseases (2015) · cites this paper as [48]

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Authors
Das, U. N.
Corresponding author
Das, Undurti N.
ORCID
Das, Undurti N.
Venue
Current Opinion in Critical Care
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2003-10
Volume
9
Issue
5
Pages
375-383
ISSN
1070-5295 (ISSN-L)
DOI
10.1097/00075198-200310000-00007
OpenAlex
W3023288245
Cited by
97
References
67
Citations by year
2024: 1 · 2023: 1 · 2022: 3 · 2021: 1 · 2018: 2 · 2017: 3 · 2016: 5 · 2015: 4 · 2014: 2 · 2013: 5 · 2012: 5
FWCI
1.52
Type
journal article
Language
en
Open access
closed
Locations
  • Current Opinion in Critical Care (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hyperglycemia and glycemic control in critically ill and hospitalized patients
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
Keywords
insulin, cardioprotection, myocardial ischemia, ischemia-reperfusion injury, apoptosis, inflammatory cytokines, TNF-α, interleukin-6, IL-10, IL-4, macrophage migration inhibitory factor, free radicals, nitric oxide, sepsis, septic shock, acute myocardial infarction, congestive heart failure, cardiogenic shock, critical illness, hyperglycemia
MeSH terms
Animals, Blood Glucose, Glucose, Humans, Hyperglycemia, Insulin, Insulin Resistance, Macrophage Migration-Inhibitory Factors, Myocardial Infarction, Nitric Oxide, Potassium, Shock, Septic, Tumor Necrosis Factor-alpha, Diabetic Ketoacidosis

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