DOI: 10.2337/diacare.29.01.06.dc05-1962 © 2006 by the American Diabetes Association
Low Plasma Adiponectin Levels Are Associated With Increased Hepatic Lipase Activity In VivoResponse to Kobayashi et al.From the Department of Medicine I (Endocrinology and Metabolism), Ruprecht-Karls-University of Heidelberg, Heidelberg, Germany Address correspondence to Jochen G. Schneider, Washington University School of Medicine, Department of Endocrinology, Metabolism and Lipid Research, Campus Box 8127, St. Louis, MO 63110. E-mail: schneider.jg{at}gmail.com or js{at}mailbox-js.de We thank Kobayashi et al. (1) for their interest in our work on the relationship between adiponectin and human plasma lipases (2, 3). These authors raise the question of whether differences in genetic background, BMI, or insulin levels of the studied populations could help to explain the differences with regard to statistical significance between their and our results. Although we exclusively studied Caucasian subjects, other authors have recently reported an independent influence of adiponectin on hepatic lipase activity in Chinese and African-American populations (4, 5). Therefore, the genetic background does not appear to play a major role in the association of adiponectin and hepatic lipase. However, we cannot rule out that the association may be different in a Japanese population. This could be due to the fact that the T-allele frequency of the functional 514C/T polymorphism in the hepatic lipase promoter has been reported to be much higher in Japanese than in Caucasian subjects (6). In addition, population-based studies do not as yet consider factors such as adiponectins oligomer composition and possible resistance to its action, which may contribute to variances of the results among different subject cohorts. The association between adiponectin and lipoprotein lipase activity still awaits further clarification in populations other than Caucasians. We performed additional analyses of our data regarding a potential influence of BMI and/or insulin levels on the association of adiponectin and hepatic lipase. When we divided the patients into groups below or above the median BMI and insulin levels, respectively, we observed no significant difference with regard to the association of adiponectin with hepatic lipase (nondiabetic male coronary artery disease subjects: BMI >27.4 kg/m2, n = 115, r = 0.29, P < 0.01; BMI <27.4 kg/m2, n = 91, r = 0.28, P < 0.01; insulin <21 µU/ml, n = 131, r = 0.36, P < 0.01; insulin >21 µU/ml, n = 75, r = 0.2, P = 0.1; similar results were seen in the diabetic subjects). Therefore, differences in BMI and insulin levels between the studied populations are unlikely to be the cause of divergent results. We believe that the difference in statistical significance of the results of our studies and that of Kobayashi et al. (7) is likely due to the larger sample size in our studies. References
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