Key result
Treatment-related increases in plasma adiponectin were not associated with a reduction in urinary albumin excretion in obese dysglycemic subjects, but instead showed a weak direct association (Spearman's rho +0.04).
Why the study?
Does intensive lifestyle intervention or metformin reduce urinary albumin excretion by increasing plasma adiponectin in obese dysglycemic subjects?
Cohort (n=2,553)
Double-blind
Adaptive randomization
Yes
Does intensive lifestyle intervention or metformin reduce urinary albumin excretion by increasing plasma adiponectin in obese dysglycemic subjects?
Answers are grounded in this paper and cite their sources.
Treatment-induced increases in plasma adiponectin do not reduce urinary albumin excretion in obese dysglycemic patients, challenging the hypothesis that raising adiponectin improves this renal biomarker.
BACKGROUND AND OBJECTIVES: Molecular data suggests that adiponectin may directly regulate urinary albumin excretion. In the Diabetes Prevention Program (DPP) we measured adiponectin and albuminuria before and after intervention, and we previously reported increases in adiponectin with interventions. Here we have used the DPP dataset to test the hypothesis that treatment-related increases in adiponectin may reduce albuminuria in obesity. DESIGN, SETTING, PARTICIPANTS AND METHODS: We evaluated cross-sectional correlations between plasma adiponectin and urinary albumin excretion at baseline, and the relationship of treatment-related changes in adiponectin and albuminuria. Baseline and follow-up urine albumin to creatinine ratios (ACR (albumin to creatinine ratio)) and plasma adiponectin concentration were available in 2553 subjects. RESULTS: Adjusting for age, sex and race/ethnicity, we observed a statistically significant but weak inverse relationship between adiponectin and ACR at baseline (conditional Spearman's rho = (-) 0.04, p = 0.04). Although DPP treatments significantly increased plasma adiponectin, there were no treatment effects on ACR and no differences in ACR across treatment groups. There was a weak direct (not inverse) association between change in adiponectin and change in albuminuria (adjusted Spearman's rho = (+) 0.04, p = 0.03). CONCLUSIONS: In a large, well-characterized cohort of obese dysglycemic subjects we observed a weak inverse association between circulating adiponectin concentrations and urinary albumin excretion at baseline. Contrary to the hypothesized effect, treatment-related increases in plasma adiponectin were not associated with a reduction in ACR. The association of change in adiponectin with change in ACR should be assessed in populations with overt albuminuria before excluding a beneficial effect of increasing adiponectin to reduce ACR in obesity.
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Mather et al. (2015) conducted a cohort in Obesity and dysglycemia (n=2,553). Change in plasma adiponectin was evaluated on Association between change in adiponectin and change in albuminuria (ACR) (Spearman's rho +0.04, p=0.03). Treatment-related increases in plasma adiponectin were not associated with a reduction in urinary albumin excretion in obese dysglycemic subjects, but instead showed a weak direct association (Spearman's rho +0.04).
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