Health consequences of obesity/Bibliography

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Revision as of 11:13, 9 October 2009 by imported>Amelia Sheldon (→‎Primary Research Papers)
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A list of key readings about Health consequences of obesity.
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Review Articles

  1. Magni P. et al. (2009) Feeding behavior in mammals including humans. Ann.N.Y.Acad.Sci. 1163:221-232. PMID 19456343
  2. Gaal L.F.V. et al. (2006) Mechanisms linking obesity with cardiovascular disease. Nature. 444:875-879. PMID 17167476 (“Obesity increases the risk of cardiovascular disease and premature death. Adipose tissue releases a large number of bioactive mediators that influence not only body weight homeostasis but also insulin resistance — the core feature of type 2 diabetes — as well as alterations in lipids, blood pressure, coagulation, fibrinolysis and inflammation, leading to endothelial dysfunction and atherosclerosis.”)
  3. Kopelman P.G. (2000) Obesity as a medical problem. Nature. 404:635-642. PMID 10766250
  4. Mathew B. et al. (2008) Obesity: effects on cardiovascular disease and its diagnosis. J Am Board Fam Med. 21:562-568. PMID 18988724 (“The higher prevalence of cardiovascular disease in obese individuals is indirectly mediated, to a large extent, by the increased frequency of various well known risk factors like hypertension, diabetes, and dyslipidemia, either individually or as part of the metabolic syndrome. However, there are several ways in which obesity directly affects the cardiovascular system; these will be discussed in detail.”)

Primary Research Papers

  1. Terao S. et al. (2008) Inflammatory and injury responses to ischemic stroke in obese mice. Stroke, Journal of the American Heart Association. 39:943-950. The adhesion of leukocytes and platelets in cerebral venules, blood– brain barrier permeability, brain water content, and infarct volume were measured in wild-type, obese (ob/ob), and leptin-reconstituted ob/ob mice subjected to 30 minutes middle cerebral artery occlusion and reperfusion. Obesity worsens the inflammatory and injury responses to middle cerebral artery occlusion and reperfusion by a mechanism independent of leptin deficiency. Monocyte chemoattractant protein-1 appears to contribute to the exaggerated responses to ischemic stroke in obese mice.
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