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. 2022 Dec;11(1):143-152.
doi: 10.1080/21623945.2022.2042962.

Adipose tissue aging partially accounts for fat alterations in HIV lipodystrophy

Affiliations

Adipose tissue aging partially accounts for fat alterations in HIV lipodystrophy

Pere Domingo et al. Adipocyte. 2022 Dec.

Abstract

Lipodystrophy is a major disturbance in people living with HIV-1 (PLWH). Several systemic alterations in PLWH are reminiscent of those that occur in ageing. It is unknown whether the lipodystrophy in PLWH is the consequence of accelerated ageing in adipose tissue. We compared systemic and adipose tissue disturbances in PLWH with those in healthy elderly individuals (~80 y old). We observed similarly enhanced expression of inflammation-related genes and decreased autophagy in adipose tissues from elderly individuals and PLWH. Indications of repressed adipogenesis and mitochondrial dysfunction were found specifically in PLWH, whereas reduced telomere length and signs of senesce were specific to elderly individuals. We conclude that ageing of adipose tissue accounts only partially for the alterations in adipose tissues of PLWH.

Keywords: HIV; Lipodystrophy; adipose; ageing; autophagy; inflammation.

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Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

Figure 1.
Figure 1.
Circulating and transcript levels of inflammatory and adipose cytokines in elderly healthy and PLWH individuals with lipodystrophy, compared to healthy young controls. (a) Circulating levels of pro-inflammatory and metabolism-related cytokines in plasma from controls (n = 34), elderly (n = 28), and people living with HIV with lipodystrophy (PLWH-LD) (n = 60). (b) Proinflammatory and adipose metabolism-related mRNA levels in adipose tissue samples from the same three groups. The bars represent means ± SEM. Dotted line and grey bar represent mean ± SEM in healthy controls. (*p < 0.05, **p < 0.01, ***p < 0.001 compared with controls; #p < 0.05, ##p < 0.01 comparing PLWH-LD with elderly).
Figure 2.
Figure 2.
Senescence markers in elderly healthy and PLWH individuals with lipodystrophy, compared to healthy young controls. (a) mRNA levels of CDKN1A, CDKN2A, and MDM2 in adipose tissue samples from controls (n = 10), elderly (n = 12), and PLWH-LD (n = 18). (b) Representative image and quantification of P53 protein levels in control, elderly, and PLWH-LD adipose tissue samples (n = 3–4). C: Coomassie blue staining. (c) Telomere length measurements in adipose tissue samples from the same three groups, also including a subset of neonate samples (n = 5). The bars represent means ± SEM. Dotted line and grey bar represent mean ± SEM in healthy controls. (*p < 0.05, **p < 0.01 compared with controls).
Figure 3.
Figure 3.
Autophagy markers in elderly healthy and PLWH individuals with lipodystrophy, compared to healthy young controls. (a) Gene expression levels of autophagy markers in adipose tissue samples from controls (n = 10), elderly (n = 12), and PLWH-LD (n = 18). (b) Representative image and quantification of LC3B-II protein levels in control, elderly, and PLWH-LD adipose tissue samples (n = 3–6). C: Coomassie blue staining. The bars represent means ± SEM. Dotted line and grey bar represent mean ± SEM in healthy controls. (*p < 0.05, **p < 0.01 compared with controls).

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