E. Renard et al., Syndrome of body fat redistribution in HIV-1-infected patients: relationships to cortisol and catecholamines, CLIN ENDOCR, 51(2), 1999, pp. 223-230
OBJECTIVE Alterations of body fat distribution have been recently reported
in HIV-infected patients. We aimed to investigate whether the hormones modu
lating adipose tissue metabolism could be implicated.
SUBJECTS We investigated twenty-eight HIV-infected patients who had develop
ed abdominal fat, combined with peripheral lipodystrophy in 25 cases and 'b
uffalo hump' in 2 cases, but who had otherwise improved on antiretroviral t
herapies. Twelve patients with no change in body fat, matched for age, dise
ase control and treatment, were studied as controls.
MEASUREMENTS Body composition was assessed by bioelectrical impedance analy
sis. Subcutaneous (SAT) and visceral (VAT) compartments of total abdominal
adipose tissue (TAT) were measured by computed tomography. Resting metaboli
c rate (RMR) was assessed by indirect calorimetry. Endocrine investigations
included plasma thyroid hormones, cortisol, testosterone, oestradiol and 2
4-hour urinary free cortisol (UFC) and catecholamines.
RESULTS Despite similar body mass index, the patients with body fat alterat
ions showed significantly larger VAT and higher VAT:TAT ratio than controls
(P = 0.002 and 0.0001, respectively). In these patients, RMR was significa
ntly higher than estimated according to the Harris-Benedict formula (+ 19.7
+/- 11.6 %, P = 0.0001) and correlated with VAT (r = 0.58, P = 0.003) and
24-hour urinary output of catecholamines (r = 0.67, P = 0.002), that was si
gnificantly increased in comparison with controls (1737 +/- 1228 vs 476 +/-
292 nmol, P = 0.013). We also found a significant correlation between VAT
and UFC (r = 0.41, P = 0.442) that was absent in controls, although levels
of UFC were similar in the two groups.
CONCLUSIONS Our data suggest that body fat redistribution may involve corti
sol and catecholamine actions. While high release of catecholamines may enh
ance RMR through increased lipolysis, cortisol may promote central fat stor
age. These effects might be related both to persistent hormonal responses t
o stress becoming inappropriate while disease control improved and to an in
creased sensitivity of visceral adipose tissue to cortisol in affected pati
ents.