Serum adiponectin levels are increased by pathologically induced left ventricular hypertrophy
Hiromichi Wada, Masaharu Akao, Nobutoyo Masunaga, Tomohide Takaya, Rieko Takanabe-Mori, Mitsuru Abe, Junko Funatsu, Yasuyo Nakajima, Mikihiko Kanasaki, Genta Osakada, Tameo Nakano, Koh Ono, Noriko Satoh-Asahara, Akira Shimatsu, Koji Hasegawa.
Division of Translational Research, National Hospital Organization Kyoto Medical Center, Kyoto, Japan.
American Heart Association Scientific Sessions 2010 (Chicago, USA), 2010/11/13-17 (Poster).
Abstract
Background: The adipocytokine adiponectin is regulated by visceral fat accumulation and is decreased in sera of patients with obesity-linked diseases. In a general population, the adiponectin level is inversely associated with left ventricular hypertrophy (LVH). In contrast, levels of adiponectin increase in proportion to the severity of heart failure (HF), which is associated with pathological LVH. Thus, the relationship between adiponectin and LVH is unclear.
Methods and Results: We carried out a cross-sectional study involving 179 consecutive male outpatients with or without chronic heart failure whose NYHA classes were stable for at least 3 months. We performed echocardiography and calculated the left ventricular mass index (LVMI), and they were divided into two groups: patients with LVH (LVH (+); LVMI > 116 g/m2) and those without LVH. There were no significant differences in the age, body mass index (BMI), lipid and metabolic profiles, and medical treatment including renin-angiotensin system inhibitors, statins, and hypoglycemic drugs between the two groups. Serum levels of high-sensitivity C-reactive protein and leptin were also similar between the groups. However, serum levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and adiponectin were significantly increased in the LVH (+) compared to the LVH (-) group (P = 0.002). Stepwise regression analysis revealed that NT-proBNP, triglycerides (TG), non-HDL-C, the BMI, and HDL-C were independent determinants of the adiponectin level. Excluding NT-proBNP, independent determinants of adiponectin proved to be LVMI, TG, the BMI, and non-HDL-C. To evaluate the effect of pathologically induced LVH on the adiponectin level, male C57Bl6 mice of 20–30 g were subjected to transverse aortic constriction (TAC) surgery or sham operation. Fifteen weeks later, the body weight was similar between TAC and sham mice. However, the ventricle to body weight (V/B) ratio as well as serum adiponectin levels were significantly increased in TAC compared to sham mice. Furthermore, serum levels of adiponectin were closely associated with the V/B ratio (r = 0.93, p < 0.0001).
Conclusions: The adiponectin level seems to be regulated not only by visceral fat accumulation, but also by pathologically induced LVH.