Associations of adiponectin and leptin with brain natriuretic peptide in African Americans: the Jackson Heart Study

Abstract

Background Brain natriuretic peptide (BNP) is elevated in decompensated systolic and diastolic heart failure. The plasma levels of adipokines, such as adiponectin and leptin, may provide evidence for mechanistic differences in BNP concentrations. African-American-specific associations are limited in the literature. The objective of this study was to evaluate the associations of adiponectin and leptin with BNP among African Americans. Methods Linear and logistic regressions were used to test the associations between adiponectin, leptin, and plasma BNP in 3738 participants of the Jackson Heart Study (JHS), a single-site prospective cohort study of African Americans in Jackson, Mississippi.Results A direct relationship of adiponectin was observed in multiple multivariate-adjusted linear models: in men (β = 0.41-0.47), and in women (β = 0.32-0.38). Those in the highest quartile of adiponectin expression were twice as likely to have elevated BNP levels after adjustment [odds ratio 2.66 (95% confidence interval, 1. 66-4.34)]. An inverse relationship of leptin with BNP was observed (β = −0.15) but attenuated after adjustment for aldosterone, renin, and adiponectin.Conclusions Different linear associations of adiponectin and leptin with BNP were observed. Odds of elevated adiponectin were observed with elevated BNP in multivariate-adjusted models. This paradoxical relationship of adiponectin and plasma BNP is possibly explained through adiponectin resistance. Cardiovasc Endocrinol Metab 9: 49-

Selected adipocytokine concentrations in patients hospitalized for exacerbated chronic heart failure

“…The obtained results corroborate data presented in recent publications showing that increased blood ADP concentration is a factor in the poor prognosis in CHF patients [12][13][14][15][16][17]. The association of poor prognosis in CHF patients with higher blood ADP concentration, which should, theoretically, exert cardioprotective action, is known as the "ADP paradox", and is recognized as the result of ADP resistance [16]. On the other hand, our results are inconsistent with those of a study by Mayer et al [19], who showed that the associations between higher blood ADP concentration and patient mortality and risk of CHF disappeared after data adjustment for blood NT-proBNP concentration.…”

“…6). The obtained results corroborate data presented in recent publications showing that increased blood ADP concentration is a factor in the poor prognosis in CHF patients [12][13][14][15][16][17]. The association of poor prognosis in CHF patients with higher blood ADP concentration, which should, theoretically, exert cardioprotective action, is known as the "ADP paradox", and is recognized as the result of ADP resistance [16].…”

“…4). In the available articles, data concerning those relationships with regard to ADP, leptin, and TNF-alpha are ambiguous [4,5,[12][13][14][15][16][17]. Despite potential cardioprotective effects of ADP, Mado et al [12] summarize in their review that the adiponectin level gradually increases with the severity of CHF.…”

“…Nevertheless, in patients with CHF, the ADP level gradually increases with the severity of the disease and a higher ADP level is a factor of poor prognosis (the "adiponectin paradox"). Nevertheless, as with leptin and TNF-alpha, the outcomes of clinical studies concerning the relationship between blood ADP concentration and cardiovascular risk are ambiguous [12][13][14][15][16][17]. The adiponectin paradox, defined as an increased cardiovascular risk despite cardioprotective ADP properties, can be explained with reference to ADP resistance [16].…”

“…Nevertheless, as with leptin and TNF-alpha, the outcomes of clinical studies concerning the relationship between blood ADP concentration and cardiovascular risk are ambiguous [12][13][14][15][16][17]. The adiponectin paradox, defined as an increased cardiovascular risk despite cardioprotective ADP properties, can be explained with reference to ADP resistance [16].…”