RAAS Activation Is Associated With Visceral Adiposity and Insulin Resistance Among HIV-infected Patients

J Clin Endocrinol Metab. 2015 Aug;100(8):2873-82. doi: 10.1210/jc.2015-1461. Epub 2015 Jun 18.

Abstract

Context: Little is known about renin-angiotensin-aldosterone system (RAAS) activation in relationship to visceral adipose tissue (VAT) accumulation in HIV-infected patients, a population at significant risk for insulin resistance and other metabolic disease.

Design: Twenty HIV and 10 non-HIV-infected subjects consumed a standardized low sodium or liberal sodium diet to stimulate or suppress the RAAS, respectively. RAAS parameters were evaluated in response to each diet and a graded angiotensin II infusion. Further analyses were performed after groups were substratified by median VAT measured by magnetic resonance imaging.

Results: Aldosterone concentrations during the low-sodium diet were higher in HIV than non-HIV-infected subjects [13.8 (9.7, 30.9) vs 9.2 (7.6, 13.6) ng/dL, P = .03] and increased across groups stratified by visceral adipose tissue (VAT) [8.5 (7.1, 12.8), 9.2 (8.1, 21.5), 11.4 (9.4, 13.8), and 27.2 (13.0, 36.9) ng/dL in non-HIV-infected without increased VAT, non-HIV-infected with increased VAT, HIV-infected without increased VAT, HIV-infected with increased VAT, respectively, overall trend P = .02]. Under this condition, plasma renin activity [3.50 (2.58, 4.65) vs 1.45 (0.58, 2.33) ng/mL · h, P = .002] was higher among the HIV-infected subjects with vs without increased VAT. Differences in the suppressibility of plasma renin activity by graded angiotensin infusion were seen stratifying by VAT among the HIV-infected group (P < .02 at each dose). In addition, aldosterone (P = .007) was an independent predictor of insulin resistance in multivariate modeling, controlling for VAT and adiponectin.

Conclusion: These data suggest excess RAAS activation in relationship to visceral adiposity in HIV-infected patients that may independently contribute to insulin resistance. Mineralocorticoid blockade may have therapeutic potential to reduce metabolic complications in HIV-infected patients with increased visceral adiposity.

Trial registration: ClinicalTrials.gov NCT01407237.

Publication types

  • Controlled Clinical Trial
  • Multicenter Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiposity / physiology*
  • Adolescent
  • Adult
  • Aged
  • Aldosterone / metabolism
  • Angiotensin II / pharmacology
  • Diet, Sodium-Restricted
  • Female
  • HIV Infections / complications
  • HIV Infections / metabolism*
  • HIV Infections / pathology
  • HIV Infections / physiopathology
  • HIV-1
  • Humans
  • Inflammation / complications
  • Inflammation / metabolism
  • Inflammation / pathology
  • Inflammation / physiopathology
  • Insulin Resistance / physiology*
  • Intra-Abdominal Fat / drug effects
  • Intra-Abdominal Fat / metabolism
  • Intra-Abdominal Fat / pathology*
  • Intra-Abdominal Fat / physiopathology
  • Male
  • Middle Aged
  • Obesity, Abdominal / complications
  • Obesity, Abdominal / metabolism
  • Obesity, Abdominal / pathology
  • Obesity, Abdominal / physiopathology
  • Renin-Angiotensin System / drug effects
  • Renin-Angiotensin System / physiology*
  • Young Adult

Substances

  • Angiotensin II
  • Aldosterone

Associated data

  • ClinicalTrials.gov/NCT01407237