Plasma adiponectin and the risk of hypertension in white and black postmenopausal women.

Division of Preventive Medicine, Brigham and Women's Hospital, Boston, MA
Clinical Chemistry (Impact Factor: 7.77). 08/2012; 58(10):1438-45. DOI: 10.1373/clinchem.2012.191080
Source: PubMed

ABSTRACT Adiponectin may have a protective role in the development of obesity-related metabolic and vascular disorders, including hypertension. We conducted a prospective, nested case control study to investigate the relation between baseline plasma adiponectin, measures of adiposity, and subsequent risk of hypertension.
We selected 400 white and 400 black postmenopausal women, age <70 years, who developed incident hypertension during 5.9-year follow-up and an equal number of age- and race-matched controls in the Women's Health Initiative Observational Study. We measured plasma concentrations of total adiponectin in their baseline blood samples.
In crude matched models, plasma adiponectin was inversely associated with risk of hypertension among both white and black women. The association appeared to be nonlinear in white women but dose related in black women. Adjustment for lifestyle factors, measures of obesity, and obesity-related clinical factors attenuated these associations. The multivariable relative risk (95% CI) of hypertension across increasing quartiles of plasma adiponectin were 1.00, 0.98 (0.66-1.46), 0.63 (0.41-0.97), and 0.92 (0.60-1.42) in white women (P(trend): 0.38) and 1.00, 0.96 (0.64-1.46), 0.83 (0.53-1.29), and 0.58 (0.36-0.94) in black women (P(trend): 0.02). Further adjustment for inflammatory markers and endothelial markers eliminated the association in white, but not black, women.
In this prospective, nested case control study, we found an inverse association between plasma adiponectin and risk of hypertension in white and black postmenopausal women. The reduced risk of hypertension was limited to only intermediate concentrations of adiponectin in white women whereas it was graded across quartiles of adiponectin in black women.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Animal studies and small controlled studies in humans suggest that adiponectin may regulate blood pressure via brain-mediated and endothelium-mediated mechanisms. We performed a systematic review and meta-analysis to evaluate the epidemiological evidence on plasma adiponectin levels and hypertension in free-living adult population. A systematic search of MEDLINE and EMBASE, up to February 2013, identified 43 nonprospective and 5 prospective studies that included 17 598 adults (8220 with hypertension; mean age 19-69 years; and mean body mass index 22-38 kg/m(2)). Two investigators independently extracted data on adiponectin levels by hypertension status and dose-response relationship. We used a random-effects model to compute the weighted mean difference in adiponectin levels between adults with hypertension and normotensive adults and a 2-stage generalized least-square trend methods to compute the odds ratio of hypertension per 1 µg/mL increase in adiponectin. Adults with hypertension had 1.64 µg/mL (95% confidence interval, -2.07, -1.21) lower adiponectin levels than normotensive adults. Every 1 µg/mL increase in adiponectin levels was associated with 6% reduced risk of hypertension (95% confidence interval, 0.92, 0.97). These findings were consistent across study design and characteristics, including age, sex, and body mass index (P>0.05). However, our meta-analysis was limited by unexplained large between-study heterogeneity, a small number of prospective studies, and selective reporting of dose-response data. In conclusion, epidemiological evidence suggests that plasma adiponectin level is a biomarker and possible mediator in the development of adiposity-related hypertension. The question remains as to adiponectin as a potential therapeutic target and its relationship with other adipokines in blood pressure regulation.
    Hypertension 05/2013; · 7.63 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Adiponectin and leptin are likely involved in the pathophysiology of rheumatoid arthritis (RA) and therefore potential new therapeutic targets. Adiponectin inhibition could be expected to enhance cardiovascular metabolic risk. However, it is unknown whether RA changes the influence of adipokines on cardiovascular metabolic risk. We determined whether RA impacts on the independent relationships of circulating leptin and adiponectin concentrations with cardiovascular risk factors and carotid intima-media thickness (cIMT) in 277 black African subjects from a developing population; 119 had RA. RA impacted on the relationships of adiponectin concentrations with lipid concentrations and blood pressure, independent of confounders including adiposity (interaction P < 0.05). This translated into an association of adiponectin concentrations with more favorable lipid variables including HDL cholesterol (P = 0.0005), non-HDL cholesterol (P = 0.007), and triglyceride (P = 0.005) concentrations, total cholesterol-HDL cholesterol (P = 0.0002) and triglycerides-HDL cholesterol (P = 0.0003) ratios, and higher systolic (P = 0.0006), diastolic (P = 0.0004), and mean blood pressure (P = 0.0007) in RA but not non-RA subjects. Leptin was not associated with metabolic risk after adjustment for adiposity. The cIMT did not differ by RA status, and adipokine concentrations were unrelated to atherosclerosis. This study suggests that leptin and adiponectin inhibition may not alter overall cardiovascular risk and disease in RA.
    Mediators of Inflammation 01/2013; 2013:461849. · 2.42 Impact Factor