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1 Department of Medicine, Division of Diabetes, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine, Division of Infectious Diseases, Helsinki University Central Hospital, Helsinki, Finland
2 Department of Medicine, Atherosclerosis Research Unit, King Gustav V Research Institute, Karolinska Institutet, Stockholm, Sweden
3 Minerva Research Institute, Helsinki, Finland
4 Department of Internal Medicine and Molecular Science, Osaka University Graduate School of Medicine, Osaka, Japan
5 Faculte de Medecine R Laennec, INSERM U.449, Lyon, France
6 Department of Medicine, Division of Diabetes, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine, Atherosclerosis Research Unit, King Gustav V Research Institute, Karolinska Institutet, Stockholm, Sweden
* To whom correspondence should be addressed. E-mail: jussi.sutinen{at}hus.fi.
Highly active antiretroviral therapy (HAART) has improved the prognosis of HIV-infected patients,
but is associated with severe adverse events, such as lipodystrophy and insulin resistance.
Rosiglitazone did not increase subcutaneous fat in patients with HAART-associated lipodystrophy
(HAL) in a randomized, double-blind, placebo-controlled trial, although it attenuated insulin
resistance and decreased liver fat content. The aim of this study was to examine effects of
rosiglitazone on gene expression in subcutaneous adipose tissue in 30 patients with HAL. The
mRNA concentrations in subcutaneous adipose tissue were measured using real time PCR. 24-week
treatment with rosiglitazone (8 mg/d) compared to placebo, significantly increased the expression of
adiponectin, PPAR
and the PPAR co-activator 1, and decreased IL-6 expression. Expression of
other genes involved in lipogenesis, fatty acid metabolism or glucose transport, such as ACS,
ALBP, CD45, FATP-1, FATP-4, GLUT1, GLUT4, KLBP, LPL, PPAR
, SREBP-1c remained
unchanged. Rosiglitazone also significantly increased serum adiponectin concentration. The change
in serum adiponectin concentration was inversely correlated with the change in fasting serum
insulin concentration and liver fat content. In conclusion, rosiglitazone induced significant changes
in gene expression in subcutaneous adipose tissue and ameliorated insulin resistance in patients
with HAL. Increased expression of adiponectin might have mediated most of the favourable insulin-sensitizing
effects of rosiglitazone in these patients.
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