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dc.contributor.authorClary, Caroline R
dc.contributor.authorGuidot, Daniel M
dc.contributor.authorBratina, Margaux A
dc.contributor.authorOtis, Jeffrey S
dc.date.accessioned2013-06-12T14:58:06Z
dc.date.available2013-06-12T14:58:06Z
dc.date.issued2011-08-16
dc.identifier.citationAIDS Research and Therapy. 2011 Aug 16;8(1):30
dc.identifier.urihttp://dx.doi.org/10.1186/1742-6405-8-30
dc.identifier.urihttp://hdl.handle.net/10724/19628
dc.description.abstractAbstract Background Separately, chronic alcohol ingestion and HIV-1 infection are associated with severe skeletal muscle derangements, including atrophy and wasting, weakness, and fatigue. One prospective cohort study reported that 41% of HIV-infected patients met the criteria for alcoholism, however; few reports exist on the co-morbid effects of these two disease processes on skeletal muscle homeostasis. Thus, we analyzed the atrophic effects of chronic alcohol ingestion in HIV-1 transgenic rats and identified alterations to several catabolic and anabolic factors. Findings Relative plantaris mass, total protein content, and fiber cross-sectional area were reduced in each experimental group compared to healthy, control-fed rats. Alcohol abuse further reduced plantaris fiber area in HIV-1 transgenic rats. Consistent with previous reports, gene levels of myostatin and its receptor activin IIB were not increased in HIV-1 transgenic rat muscle. However, myostatin and activin IIB were induced in healthy and HIV-1 transgenic rats fed alcohol for 12 weeks. Catabolic signaling factors such as TGFβ1, TNFα, and phospho-p38/total-p38 were increased in all groups compared to controls. There was no effect on IL-6, leukemia inhibitory factor (LIF), cardiotrophin-1 (CT-1), or ciliary neurotrophic factor (CNTF) in control-fed, transgenic rats. However, the co-morbidity of chronic alcohol abuse and HIV-1-related protein expression decreased expression of the two anabolic factors, CT-1 and CNTF. Conclusions Consistent with previous reports, alcohol abuse accentuated skeletal muscle atrophy in an animal model of HIV/AIDS. While some catabolic pathways known to drive alcoholic or HIV-1-associated myopathies were also elevated in this co-morbid model (e.g., TGFβ1), consistent expression patterns were not apparent. Thus, specific alterations to signaling mechanisms such as the induction of the myostatin/activin IIB system or reductions in growth factor signaling via CT-1- and CNTF-dependent mechanisms may play larger roles in the regulation of muscle mass in alcoholic, HIV-1 models.
dc.titleChronic alcohol ingestion exacerbates skeletal muscle myopathy in HIV-1 transgenic rats
dc.typeJournal Article
dc.date.updated2013-06-07T14:53:42Z
dc.description.versionPeer Reviewed
dc.language.rfc3066en
dc.rights.holderCaroline R Clary et al.; licensee BioMed Central Ltd.


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