Circulating resistin levels are not associated with fat redistribution, insulin resistance, or metabolic profile in patients with the highly active antiretroviral therapy-induced metabolic syndrome.
BACKGROUND
The mechanisms underlying the development of the highly active antiretroviral therapy (HAART)-induced metabolic syndrome remain to be fully elucidated.


OBJECTIVE
The objective of this study was to investigate whether the adipocyte-secreted hormone, resistin, is associated with anthropometric and metabolic abnormalities of the HAART-induced metabolic syndrome.


METHODS
We conducted a cross-sectional study of 227 HIV-positive patients (37 women and 190 men) recruited from the infectious diseases clinics. On the basis of history, physical examination, dual-energy x-ray absorptiometry, and single-slice computed tomography, patients were classified into four groups: non-fat redistribution (n = 85), fat accumulation (n = 42), fat wasting (n = 35), and mixed fat redistribution (n = 56).


METHODS
The main outcome measures were serum resistin levels and anthropometric and metabolic variables.


RESULTS
Mean serum resistin levels were not significantly different among subjects with fat accumulation, fat wasting, or mixed fat redistribution or between these groups and the non-fat redistribution group. We found a weak, but significant, positive correlation between resistin and percent total body fat (r = 0.20; P < 0.01), total extremity fat (r = 0.18; P < 0.01), and abdominal sc fat (r = 0.19; P < 0.01), but not abdominal visceral fat (r = -0.10; P = 0.16) or waist to hip ratio (r = -0.05; P = 0.43). When adjustments were made for gender (women, 3.92 +/- 2.71 ng/ml; men, 2.96 +/- 2.61 ng/ml; P = 0.05), correlations between resistin and the above parameters were no longer significant. Importantly, resistin levels were not correlated with fasting glucose, insulin, homeostasis model assessment of insulin resistance index, triglycerides, or cholesterol levels in the whole group.


CONCLUSIONS
Resistin is related to gender, but is unlikely to play a major role in the insulin resistance and metabolic abnormalities of the HAART-induced metabolic syndrome.
Barb
Diana
D
Division of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Stoneman 816, Boston, Massachusetts 02215, USA.
Wadhwa
Sanjivini G
SG
Kratzsch
Juergen
J
Gavrila
Alina
A
Chan
Jean L
JL
Williams
Catherine J
CJ
Karchmer
Adolf W
AW
Mantzoros
Christos S
CS
D000273:Adipose Tissue / Q000473:pathology*; D000328:Adult; D023241:Antiretroviral Therapy, Highly Active / Q000009:adverse effects*; D001823:Body Composition; D003430:Cross-Sectional Studies; D005260:Female; D015658:HIV Infections / Q000188:drug therapy; D006729:Hormones, Ectopic / Q000097:blood*; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008875:Middle Aged; D052243:Resistin
D006729:Hormones, Ectopic; C499624:RETN protein, human; D052243:Resistin