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DiaComp Funded Abstracts

Program Application Abstract

Liver fat is related to aldosterone in HIV-­infected patients with lipodystrophy
Quadri, Nabiha   (Massachusetts General Hospital)
Individuals with HIV infection have an increased prevalence of lipodystrophy. These changes in fat redistribution are linked to an increased risk of fatty liver and insulin resistance, and the exact mechanism for these metabolic abnormalities remains unclear. Recent data show that HIV-­ infected individuals with excess visceral adiposity have increased renin-­angiotensin-­aldosterone system (RAAS) activation in association with impaired glucose homeostasis and inflammation. In addition to its traditional role in regulating sodium balance and blood volume, emerging evidence suggests that this system plays a part in mediating inflammatory processes. In this regard, we hypothesized that HIV-­infected participants with increased aldosterone would demonstrate excess ectopic fat deposition in the liver and decreased insulin sensitivity. Forty-­ four participants with clinical evidence of lipohypertrophy were prospectively recruited for this study, and RAAS parameters were characterized under identical controlled conditions and similar time points. Participants were assessed for liver fat using 1H magnetic resonance spectroscopy and for insulin sensitivity via the euglycemic hyperinsulinemic clamp technique. 24-­hour urinary aldosterone excretion was significantly associated with increased liver fat (?=0.39, P= 0.01). In addition, HIV-­infected participants with radiological evidence of fatty liver (lipid fat fraction> 5%) had significantly higher levels of urinary aldosterone compared to those without evidence of fatty liver (26.3±8.5 vs. 7.9±2.0 µg/24hr, P=0.02). 24-­hour urinary aldosterone excretion (?=0.16, P= 0.32) and serum aldosterone (?=0.13, P= 0.40) did not relate to insulin sensitivity assessed by insulin clamp. In further analyses, participants were substratified into those with and without evidence of metabolic syndrome. Those with metabolic syndrome had a significantly higher percentage of liver fat (11.5±2.1 vs. 5.1±1.2 %, P=0.003). 24-­hour urinary aldosterone excretion (?=0.56, p=0.02) and serum aldosterone (?=0.63, p=0.007) were both strongly correlated to liver fat among the HIV group with metabolic syndrome. Multivariate modeling demonstrated that serum aldosterone (ß estimate=0.007, P=0.04) and presence of metabolic syndrome (ß estimate =0.035, P=0.003) were both significant and independent predictors of liver fat (overall model r=0.52, p=0.003). These novel data show that increased aldosterone is associated with liver fat in HIV lipodystrophy and may suggest further investigation into the potential use of mineralocorticoid receptor blockade as a therapeutic strategy to reduce metabolic complications in HIV.