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Role of Insulin Resistance and Hyperglycemia in the Development of Atherosclerosis

Insulin resistance (IR) is the underlying defect in >90% of patients with type 2 diabetes mellitus and the major pathologic mechanism for the associated susceptibility to premature cardiovascular disease (CVD). The progression of IR to diabetes parallels the progression of endothelial dysfunction to... Full description

Journal Title: The American journal of cardiology 2007, Vol.99 (4), p.6-14
Main Author: Bansilal, Sameer, MD
Other Authors: Farkouh, Michael E., MD, MSc , Fuster, Valentin, MD, PhD
Format: Electronic Article Electronic Article
Language: English
Subjects:
Abridged Index Medicus
Adipose Tissue - metabolism
Animals
Atherosclerosis
Cardiology
Cardiovascular
Cardiovascular disease
Coronary Artery Disease - metabolism
Coronary Artery Disease - physiopathology
Development and progression
Diabetes
Endothelium, Vascular - metabolism
Endothelium, Vascular - physiopathology
Humans
Hyperglycemia
Hyperglycemia - metabolism
Hyperglycemia - physiopathology
Insulin
Insulin resistance
Insulin Resistance - physiology
Monocytes - metabolism
Muscle, Smooth, Vascular - metabolism
Receptor, Insulin - metabolism
T-Lymphocytes - metabolism
Publisher: United States: Elsevier Inc
ID: ISSN: 0002-9149
Link: https://www.ncbi.nlm.nih.gov/pubmed/17307054
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title: Role of Insulin Resistance and Hyperglycemia in the Development of Atherosclerosis
format: Article
creator:
  • Bansilal, Sameer, MD
  • Farkouh, Michael E., MD, MSc
  • Fuster, Valentin, MD, PhD
subjects:
  • Abridged Index Medicus
  • Adipose Tissue - metabolism
  • Animals
  • Atherosclerosis
  • Cardiology
  • Cardiovascular
  • Cardiovascular disease
  • Coronary Artery Disease - metabolism
  • Coronary Artery Disease - physiopathology
  • Development and progression
  • Diabetes
  • Endothelium, Vascular - metabolism
  • Endothelium, Vascular - physiopathology
  • Humans
  • Hyperglycemia
  • Hyperglycemia - metabolism
  • Hyperglycemia - physiopathology
  • Insulin
  • Insulin resistance
  • Insulin Resistance - physiology
  • Monocytes - metabolism
  • Muscle, Smooth, Vascular - metabolism
  • Receptor, Insulin - metabolism
  • T-Lymphocytes - metabolism
ispartof: The American journal of cardiology, 2007, Vol.99 (4), p.6-14
description: Insulin resistance (IR) is the underlying defect in >90% of patients with type 2 diabetes mellitus and the major pathologic mechanism for the associated susceptibility to premature cardiovascular disease (CVD). The progression of IR to diabetes parallels the progression of endothelial dysfunction to atherosclerosis. The downregulation of the antiatherogenic phosphatidylinositol-3-kinase–mediated insulin receptor–signaling pathway, and maintained activity of the proatherogenic mitogenic-activated protein kinase pathway in insulin-resistant states, leads to accelerated atherosclerosis. Efforts to prevent or slow the epidemic of atherothrombotic CVD must focus on the reversal of the disturbances in glucose and lipid homeostasis through the amelioration of IR.
language: eng
source:
identifier: ISSN: 0002-9149
fulltext: no_fulltext
issn:
  • 0002-9149
  • 1879-1913
url: Link


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descriptionInsulin resistance (IR) is the underlying defect in >90% of patients with type 2 diabetes mellitus and the major pathologic mechanism for the associated susceptibility to premature cardiovascular disease (CVD). The progression of IR to diabetes parallels the progression of endothelial dysfunction to atherosclerosis. The downregulation of the antiatherogenic phosphatidylinositol-3-kinase–mediated insulin receptor–signaling pathway, and maintained activity of the proatherogenic mitogenic-activated protein kinase pathway in insulin-resistant states, leads to accelerated atherosclerosis. Efforts to prevent or slow the epidemic of atherothrombotic CVD must focus on the reversal of the disturbances in glucose and lipid homeostasis through the amelioration of IR.
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languageeng
publisherUnited States: Elsevier Inc
subjectAbridged Index Medicus ; Adipose Tissue - metabolism ; Animals ; Atherosclerosis ; Cardiology ; Cardiovascular ; Cardiovascular disease ; Coronary Artery Disease - metabolism ; Coronary Artery Disease - physiopathology ; Development and progression ; Diabetes ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - physiopathology ; Humans ; Hyperglycemia ; Hyperglycemia - metabolism ; Hyperglycemia - physiopathology ; Insulin ; Insulin resistance ; Insulin Resistance - physiology ; Monocytes - metabolism ; Muscle, Smooth, Vascular - metabolism ; Receptor, Insulin - metabolism ; T-Lymphocytes - metabolism
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descriptionInsulin resistance (IR) is the underlying defect in >90% of patients with type 2 diabetes mellitus and the major pathologic mechanism for the associated susceptibility to premature cardiovascular disease (CVD). The progression of IR to diabetes parallels the progression of endothelial dysfunction to atherosclerosis. The downregulation of the antiatherogenic phosphatidylinositol-3-kinase–mediated insulin receptor–signaling pathway, and maintained activity of the proatherogenic mitogenic-activated protein kinase pathway in insulin-resistant states, leads to accelerated atherosclerosis. Efforts to prevent or slow the epidemic of atherothrombotic CVD must focus on the reversal of the disturbances in glucose and lipid homeostasis through the amelioration of IR.
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abstractInsulin resistance (IR) is the underlying defect in >90% of patients with type 2 diabetes mellitus and the major pathologic mechanism for the associated susceptibility to premature cardiovascular disease (CVD). The progression of IR to diabetes parallels the progression of endothelial dysfunction to atherosclerosis. The downregulation of the antiatherogenic phosphatidylinositol-3-kinase–mediated insulin receptor–signaling pathway, and maintained activity of the proatherogenic mitogenic-activated protein kinase pathway in insulin-resistant states, leads to accelerated atherosclerosis. Efforts to prevent or slow the epidemic of atherothrombotic CVD must focus on the reversal of the disturbances in glucose and lipid homeostasis through the amelioration of IR.
copUnited States
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pmid17307054
doi10.1016/j.amjcard.2006.11.002