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Background : Abdominal obesity is an essential component of metabolic syndrome and it causes insulin resistance. In contrast to women, the serum testosterone level has an inverse relationship with the visceral fat mass in men. Therefore, we investigated the relation of the serum testosterone concent...

Background : Abdominal obesity is an essential component of metabolic syndrome and it causes insulin resistance. In contrast to women, the serum testosterone level has an inverse relationship with the visceral fat mass in men. Therefore, we investigated the relation of the serum testosterone concentration with metabolic syndrome and coronary artery disease in Korean middle-aged and elderly men. Methods : 211 male subjects who were admitted to the cardiology department due to chest pain at Hanyang University Hospital from January to December, 2005 (mean age: 59.1±10.7 yrs) were enrolled in this study. All the blood samplings for laboratory tests, including the testosterone and estradiol tests, were done between 6 AM to 8 AM. Coronary artery disease was defined when there was more than 50% narrowing of the vascular lumen on the coronary angiography. Metabolic syndrome was defined according to the NCEP-ATP III guidelines. Results : Among the other cardiovascular risk factors, metabolic syndrome was the most important contributor to coronary artery disease (adjusted OR=4.32, 95% CI: 1.96-9.52). Even after adjustment for age, BMI, smoking, alcohol consumption and hypertension, lower testosterone was associated with a higher fasting glucose level (p<0.01) and higher insulin resistance (p<0.05). Each SD (1.88 ng/mL) increase in the total testosterone was associated with a 51% reduced risk of having metabolic syndrome (OR=0.49; 95% CI, 0.36-0.68). Although men with coronary artery disease tended to have lower testosterone levels, there was no statistical significance. Conclusions : Lower testosterone levels might have a causative role in the development of metabolic syndrome and possibly coronary artery disease through the induction of insulin resistance.

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