ABSTRACT
BACKGROUND: Plasma adiponectin is a significant correlate of the pro-inflammatory cardiometabolic risk profile associated with obesity and type 2 diabetes. Salivary pH is influenced by several cardiometabolic risk components such as inflammation, oxidation and numerous oral and systemic health modulators, including the menopausal status. This study aimed to assess the association between plasma adiponectin concentrations and salivary pH in women according to the menopausal status. METHOD: Unstimulated saliva collection was performed in 151 Caucasian women of French-Canadian origin (53 premenopausal women (PMW) and 98 menopausal women (MW)). Student's t test, ANOVA and linear regression models were used to assess the association between plasma adiponectin concentrations and salivary pH. RESULTS: Plasma adiponectin levels increased as a function of salivary pH in the whole sample and among MW (r = 0.29 and r = 0.36, p < 0.001). The proportion of the variance of plasma adiponectin levels explained by the salivary pH (R2) was 10.8% (p < 0.001). Plasma adiponectin levels progressively increased across salivary pH quartiles (p = 0.005). CONCLUSIONS: These results suggest that salivary pH is a significant correlate of plasma adiponectin levels in women. With the increasing prevalence of type 2 diabetes and obesity, new technologies should be developed to more easily monitor health status, disease onset and progression. Salivary pH, a simple, inexpensive and non-invasive measure, could be a very promising avenue.
ABSTRACT
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.
