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- May 9, 2008 |
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CME on Diabetes is a website built to transmit top-level CME conferences given by international experts in endocrinology, insulin resistance, prediabetes, metabolic syndrome and type 2 diabetes. More than 2.6 million slides have been viewed since the website launch. Thank you for your continued support and commitment!
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| Presentation |
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"Inflammation, insulin resistance and CHD"Prof. Steven M. Haffner (biography)
English - 2003-03-28 - 69 minutes
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 | (41 slides) |
Summary :
Type 2 diabetes is associated with a marked increase in coronary heart disease; however, the severity of glycemia during the diabetic phase is only modestly related to the risk of coronary heart disease. Because of this observation, most interest is focused on the pre-diabetic state. Many studies have shown increased cardiovascular risk factors prior to the onset of type 2 diabetes. In the San Antonio Heart Study, increased cardiovascular risk factors were attributed to increased insulin resistance rather than decreased insulin secretion in the pre-diabetic subjects.
Ridker and others have shown that subclinical inflammation (usually assessed by increased levels of C-reactive protein) is strongly related to the risk of CHD. More recently numerous studies have shown that increased CRP levels are related to insulin resistance and the metabolic syndrome. Furthermore, CRP levels may predict the developpement of type 2 diabetes. Rosiglitazone and insulin sensitizers decrease CRP levels by about 25%, a magnitude similar to the effect of statins in other studies. Subclinical inflammation is thought by some to be part of the basis for both the development of type 2 diabetes and cardiovascular disease.
More information is available about C-Reactive Protein.
Learning objectives :
- The effect of insulin resistance on coronary heart disease in the pre-type 2 diabetic state
- The interrelationships between the risk of CHD, CRP levels, insulin resistance and metabolic syndrome
- The influence of rosiglitazone and insulin sensitizers on CRP levels
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