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Transcriptional profiles of inguinal fat of HIV-infected and healthy control patients.

ABSTRACT: Although the survival rate for patients infected with human immunodeﬁciency virus type 1 (HIV-1) has dramatically improved due to recent advancements in antiretroviral therapy, the mechanism of pathogenesis of HIV-associated lipodystrophy remains poorly understood. To elucidate the pathophysiological mechanism of disease, we analyzed gene expression profiles of inguinal adipose tissues from HIV-infected and healthy conrol patients. Genetic analysis revealed that fat tissue from patients with HIV typically had increased immune activation, mitochondrial toxicity, chronic inflammation, progressive fibrosis and adipocyte dysfunction including insulin resistance, inhibited adipocyte differentiation and accelerated apoptosis. Of note, triglyceride synthesis and lipolysis were inhibited in adipose tissue from patients with HIV.

ORGANISM(S): Homo sapiens

PROVIDER: GSE147162 | GEO | 2022/03/09

REPOSITORIES: GEO

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Project description:Background and objective: Combination antiretroviral therapy (cART) is associated with lipodystrophy i.e. loss of subcutaneous adipose tissue in abdomen, limbs and face and its accumulation intra-abdominally. No fat is lost dorsocervically and it can even accumulates in this region (“buffalo hump”). It is unknown how preserved dorsocervical fat differs from abdominal subcutaneous fat in HIV-1-infected cART-treated patients with (cART+LD+) and without (cART+LD-) lipodystrophy. Results: Albeit dorsocervical adipose tissue in cART+LD+ seems spared from lipoatrophy, its mitochondrial DNA (mtDNA, copies/cell) content was significantly lower (by 62%) than that of the corresponding tissue in cART+LD-. Expression of CD68 mRNA, a marker of macrophages, and numerous inflammatory genes in microarray were significantly lower in dorsocervical vs. abdominal subcutaneous adipose tissue. Genes with the greatest difference in expression between the two depots were those involved in regulation of transcription and regionalization (homeobox genes), irrespective of lipodystrophy status. There was negligible mRNA expression of uncoupling protein 1, a gene characteristic of brown adipose tissue, in either depot. Conclusions: As mtDNA is depleted even in the non-atrophic dorsocervical adipose tissue, it is unlikely that the cause of lipoatrophy is loss of mtDNA. Dorsocervical adipose tissue is less inflamed than lipoatrophic adipose tissue. It does not resemble brown adipose tissue. The greatest difference in gene expression between dorsocervical and abdominal s.c. adipose tissue is in expression of homeobox genes. We used histology, microarray, polymerase chain reaction and magnetic resonance imaging to compare dorsocervical and abdominal subcutaneous adipose tissue in cART+LD+ (n=21) and cART+LD- (n=11). The study consists of 17 patients on antiretroviral treatment who have developed lipodystrophy and 11 patients that are on similar treatment but have not developped lipodystrophy. All patients are HIV+ and have 2 adipose tissue samples taken from them (dorsocervical+abdominal).

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Transcriptional profiles of inguinal fat of HIV-infected and healthy control patients.

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