Type 2 diabetes as an inflammatory cardiovascular disorder.
Type 2 diabetes carries a 2-6-fold increased risk of cardiovascular disease (CVD) and death. Indeed, the risk of major cardiovascular events in Type 2 diabetic patients without history of coronary heart disease (CHD) is equivalent to that observed in non-diabetic subjects with CHD. However, atherosclerosis may also precede the development of diabetes, suggesting that both disorders share common genetic and environmental antecedent factors ("common soil" hypothesis). One such a possible ancestor is insulin resistance which constitutes both a major feature of Type 2 diabetes and an independent risk factor for CHD. It is well documented that inflammatory processes play an important role in the causation of atherosclerotic CVD. Inflammatory mediators play a paramount role in the initiation, progression, and rupture of atherosclerotic plaques. Thus, markers of inflammation and endothelial dysfunction may provide additional information about a patient's risk of developing CVD and may become new targets for treatment. On the other hand, evidence has emerged suggesting that inflammation is also involved in the development of Type 2 diabetes. Prospective studies have demonstrated that increased levels of pro-inflammatory markers such as CRP or reduced levels of anti-inflammatory markers such as adiponectin predict the development of Type 2 diabetes. Thus, there is accumulating evidence suggesting that inflammation is the bridging link between atherosclerosis and the metabolic syndrome. Interventions by lifestyle modification or agents with anti-inflammatory properties may reduce the risk of both conditions. Drugs exerting anti-inflammatory and vascular effects have future potential to be used within an array of interventions aimed at reducing the enormous cardiovascular burden associated with Type 2 diabetes.
Ziegler
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German Diabetes Clinic, German Diabetes Center, Leibniz Institute at the Heinrich Heine University, WHO Collaborating Center in Diabetes, European Training Center in Endocrinology and Metabolism, Düsseldorf, Germany. dan.ziegler@ddz.uni-duesseldorf.de
D052242:Adiponectin; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001161:Arteriosclerosis / Q000175:diagnosis* / Q000473:pathology; D002318:Cardiovascular Diseases / Q000175:diagnosis* / Q000378:metabolism; D048909:Diabetes Complications / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis* / Q000378:metabolism; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D007333:Insulin Resistance; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D007962:Leukocytes / Q000378:metabolism; D011446:Prospective Studies; D045162:Thiazolidinediones / Q000494:pharmacology
D052242:Adiponectin; D000893:Anti-Inflammatory Agents; D036341:Intercellular Signaling Peptides and Proteins; D045162:Thiazolidinediones; C089946:2,4-thiazolidinedione