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Pathogenesis and pathophysiology of the cardiometabolic syndrome.

Abstract
The cardiometabolic syndrome represents a cluster of metabolic abnormalities that are risk factors for cardiovascular disease. The mechanism(s) responsible for developing the cardiometabolic syndrome is not known, but it is likely that multi-organ insulin resistance, which is a common feature of the cardiometabolic syndrome, is involved. Insulin resistance is an important risk factor for type 2 diabetes and can cause vasoconstriction and renal sodium reabsorption, leading to increased blood pressure. Alterations in adipose tissue fatty acid and adipokine metabolism are involved in the pathogenesis of insulin resistance. Excessive rates of fatty acid release into the bloodstream can impair the ability of insulin to stimulate muscle glucose uptake and suppress hepatic glucose production. Noninfectious systemic inflammation associated with adipocyte and adipose tissue macrophage cytokine production can also cause insulin resistance. In addition, increased free fatty acid delivery to the liver can stimulate hepatic very low-density lipoprotein triglyceride production, leading to dyslipidemia.
AuthorsErik P Kirk, Samuel Klein
JournalJournal of clinical hypertension (Greenwich, Conn.) (J Clin Hypertens (Greenwich)) Vol. 11 Issue 12 Pg. 761-5 (Dec 2009) ISSN: 1751-7176 [Electronic] United States
PMID20021538 (Publication Type: Journal Article, Review)
Chemical References
  • Fatty Acids
Topics
  • Cardiovascular Diseases (epidemiology, etiology, physiopathology)
  • Diabetes Mellitus, Type 2 (complications, epidemiology, etiology)
  • Fatty Acids (metabolism)
  • Humans
  • Hypertension (complications)
  • Insulin Resistance
  • Metabolic Syndrome (complications, epidemiology)
  • Muscle, Skeletal (metabolism)
  • Obesity (complications)
  • Prevalence
  • Risk Factors
  • Vasoconstriction

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