Abdominal Obesity: Role in the Pathophysiology of Metabolic Disease and Cardiovascular Risk

Abdominal Obesity: Role in the Pathophysiology of Metabolic Disease and Cardiovascular Risk Visceral adiposity has been identified as an independent risk factor for cardiovascular disease and the so-called metabolic syndrome. The canine obesity model closely recapitulates the correlation between human visceral adiposity and insulin resistance. A recent canine study indicates that insulin expands the volume of distribution associated with skeletal muscle, and that its ability to enhance macromolecular distribution within this space is blunted in the fat-fed obese canine model. Our canine study supports the portal theory of insulin resistance, in which free fatty acids (FFAs) from visceral fat directly enter the liver and have a detrimental effect on insulin action. The role of adipokines in this condition remains less clear. Sympathetic nervous system hyperactivity in obesity may also contribute to excessive FFA release, hypertension, and insulin resistance. Pathologies interrelated with insulin resistance include β-cell hypersecretion, reduced insulin clearance, and resultant hyperinsulinemia. An observed nocturnal increase in plasma FFA levels may account for both insulin resistance and compensatory hyperinsulinemia and warrants further investigation. The elucidation of these interrelated pathologies may help reveal points where medical intervention can reduce metabolic disease. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The American Journal of Medicine Elsevier

Abdominal Obesity: Role in the Pathophysiology of Metabolic Disease and Cardiovascular Risk

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Publisher
Elsevier
Copyright
Copyright © 2007 Elsevier Inc.
ISSN
0002-9343
D.O.I.
10.1016/j.amjmed.2006.11.012
Publisher site
See Article on Publisher Site

Abstract

Visceral adiposity has been identified as an independent risk factor for cardiovascular disease and the so-called metabolic syndrome. The canine obesity model closely recapitulates the correlation between human visceral adiposity and insulin resistance. A recent canine study indicates that insulin expands the volume of distribution associated with skeletal muscle, and that its ability to enhance macromolecular distribution within this space is blunted in the fat-fed obese canine model. Our canine study supports the portal theory of insulin resistance, in which free fatty acids (FFAs) from visceral fat directly enter the liver and have a detrimental effect on insulin action. The role of adipokines in this condition remains less clear. Sympathetic nervous system hyperactivity in obesity may also contribute to excessive FFA release, hypertension, and insulin resistance. Pathologies interrelated with insulin resistance include β-cell hypersecretion, reduced insulin clearance, and resultant hyperinsulinemia. An observed nocturnal increase in plasma FFA levels may account for both insulin resistance and compensatory hyperinsulinemia and warrants further investigation. The elucidation of these interrelated pathologies may help reveal points where medical intervention can reduce metabolic disease.

Journal

The American Journal of MedicineElsevier

Published: Feb 1, 2007

References

  • Regional adiposity and morbidity
    Kissebah, A.H.; Krakower, G.R.
  • Free fatty acids increase basal hepatic glucose production and induce hepatic insulin resistance at different sites
    Lam, T.K.; van de, W.G.; Giacca, A.
  • Molecular evidence supporting the portal theory: a causative link between visceral adiposity and hepatic insulin resistance
    Kabir, M.; Catalano, K.J.; Ananthnarayan, S.
  • Pancreatic beta-cell loss and preservation in type 2 diabetes
    Buchanan, T.A.

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