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 adiponectin’s 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.

1.
Kobayashi J, Murase Y, Kawashiri M, Nohara A, Inazu A, Mabuchi H: Low plasma adiponectin levels are associated with increased hepatic lipase activity in vivo (Letter).
Diabetes Care
29
:
181
,
2006
2.
von Eynatten M, Schneider JG, Humpert PM, Rudofsky G, Schmidt N, Barosch P, Hamann A, Morcos M, Kreuzer J, Bierhaus A, Nawroth PP, Dugi KA: Decreased plasma lipoprotein lipase in hypoadiponectinemia: an association independent of systemic inflammation and insulin resistance.
Diabetes Care
27
:
2925
–2929,
2004
3.
Schneider JG, von Eynatten M, Schiekofer S, Nawroth PP, Dugi KA: Low plasma adiponectin levels are associated with increased hepatic lipase activity in vivo.
Diabetes Care
28
:
2181
–2186,
2005
4.
Tan KCB, Xu A, Shiu SWM, Lam KSL: Association between adiponectin and hepatic lipase activity (Abstract).
Diabetes
53 (Suppl. 2)
:
A353
,
2004
5.
Finley KB, Considine RV, Genovese DJ, Vega GL, Sumner AE: In African Americans the effect of adiponectin on HDL may be mediated by hepatic lipase (Abstract).
Diabetes
54 (Suppl. 1)
:
A238
,
2005
6.
Yabu Y, Noma K, Nakatani K, Nishioka J, Suematsu M, Katsuki A, Hori Y, Yano Y, Sumida Y, Wada H, Nobori T: C-514T polymorphism in hepatic lipase gene promoter is associated with elevated triglyceride levels and decreasing insulin sensitivity in nondiabetic Japanese subjects.
Int J Mol Med
16
:
421
–425,
2005
7.
Kobayashi J, Kusunoki M, Murase Y, Kawashiri M, Higashikata T, Miwa K, Katsuda S, Takata M, Asano A, Nohara A, Inazu A, Mabuchi H: Relationship of lipoprotein lipase and hepatic triacylglycerol lipase activity to serum adiponectin levels in Japanese hyperlipidemic men.
Horm Metab Res
37
:
505
–509,
2005