Objective: Cardiovascular risk significantly increases after menopause. Lipoprotein lipase (LPL) is a key enzyme in the metabolism of triglyceride (TG)-rich lipoproteins, which contributes to cardiometabolic homeostasis. Adiponectin is an adipocytokine, which also influences the cardiometabolic status. The objective of this study was to evaluate the contribution of plasma adiponectin to the cardiometabolic status of women with loss-of-function LPL gene variants (LPLD).
Methods: A total of 568 white women (127 women with partial LPL deficiency and 441 controls) were included. The association of plasma adiponectin with LPLD was assessed using multiple regression models. Cardiometabolic covariates included anthropometrics, lipids (TG, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B), fasting glucose, and smoking status.
Results: Plasma adiponectin concentration was significantly lower in women with LPLD (8.69 ± 5.13 vs 6.50 ± 4.66 μg/mL; P < 0.001). Women with LPLD also presented a significantly higher risk of coronary artery disease (P = 0.013). After menopause, adiponectin explained a significant (P < 0.01) proportion of the variance in cardiometabolic covariates in both groups. This effect was more pronounced in women with LPLD: 13% versus 8% for high-density lipoprotein cholesterol, 8% versus 4% for waist circumference, 9% versus 5% for fasting TG, and 6% versus 2% for fasting glucose. When controlling for cardiometabolic covariates, low adiponectin values independently contributed to the clinical expression of LPLD in postmenopausal women (odds ratio, 5.55; 95% CI, 0.04-0.81; P = 0.025).
Conclusions: In conclusion, these results suggest that a low plasma adiponectin level significantly contributes to the cardiometabolic risk profile of postmenopausal women with LPLD, independently of anthropometrics, lipids, and other covariates.
From the Department of Medicine, Université de Montréal, Montréal, and ECOGENE-21 Clinical Research Center, Chicoutimi Hospital, Chicoutimi, Quebec, Canada.
Received August 9, 2010; revised and accepted September 14, 2010.
Funding/support: This work was supported by a Canadian Institutes of Health Research Team grant (CTP-82941) and by the ECOGENE-21 Clinical Research Center. D. Gaudet is the holder of the Canada Research Chair in Preventive Genetics and Community Genomics (www.chairs.gc.ca). K. Tremblay is a Université de Montréal postdoctoral and CCRP fellow and receives support from the Canadian Heart and Stroke Foundation. J. Méthot is a Université de Montréal postdoctoral fellow and received support from the Canadian Institutes of Health Research.
Financial disclosure/conflicts of interest: None reported.
Address correspondence to: Daniel Gaudet, MD, PhD, Department of Medicine, Université de Montréal, ECOGENE-21 Clinical Research Center, Chicoutimi Hospital, Pavillon des Augustines (5th Floor), 225 Rue St-Vallier, Chicoutimi, Quebec, Canada G7H 7P2. E-mail: firstname.lastname@example.org