Chronic Alcohol Accentuates Simian Acquired Immunodeficiency Syndrome‐Associated Wasting

Molina, Patricia E.; Lang, Charles H.; McNurlan, Margaret A.; Bagby, Gregory J.; Nelson, Steve

doi:10.1111/j.1530-0277.2007.00549.x

Cited by 59 publications

(78 citation statements)

References 55 publications

(59 reference statements)

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“…All cell-based experiments were performed in BSL2 laboratory facilities at LSUHSC-NO. Animals were administered alcohol or sucrose intragastrically as previously described (5,24). Briefly, animals were administered alcohol (13-14 g of ethanol per kilogram body wt per week; 30% wt/vol water) or sucrose for 19 mo via a surgically implanted catheter.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…These cells are quiescent during adulthood but can enter into cell cycle upon stimulation to repair damaged muscle by proliferation, differentiation, and fusion with existing myofibers (39). Our previous studies with chronic binge alcohol (CBA)-fed, Simian immunodeficiency virus (SIV)-infected rhesus macaques have shown that chronic alcohol consumption promotes a prooxidative and proinflammatory skeletal muscle milieu in SIV-infected animals, and this is associated with accentuated wasting at end-stage SIV infection (21,24). The inflammatory environment in skeletal muscle would be expected to activate quiescent SCs to proliferate and differentiate into myotubes to compensate for enhanced skeletal muscle proteolysis (39,45).…”

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confidence: 97%

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Chronic binge alcohol consumption alters myogenic gene expression and reduces in vitro myogenic differentiation potential of myoblasts from rhesus macaques

Simon

LeCapitaine

Berner

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Chronic alcohol abuse is associated with skeletal muscle myopathy. Previously, we demonstrated that chronic binge alcohol (CBA) consumption by rhesus macaques accentuates skeletal muscle wasting at end-stage of simian immunodeficiency virus (SIV) infection. A proinflammatory, prooxidative milieu and enhanced ubiquitin proteasome activity were identified as possible mechanisms leading to loss of skeletal muscle. The possibility that impaired regenerative capacity, as reflected by the ability of myoblasts derived from satellite cell (SCs) to differentiate into myotubes has not been examined. We hypothesized that the inflammation and oxidative stress in skeletal muscle from CBA animals impair the differentiation capacity of myoblasts to form new myofibers in in vitro assays. We isolated primary myoblasts from the quadriceps femoris of rhesus macaques that were administered CBA or isocaloric sucrose (SUC) for 19 mo. Proliferation and differentiation potential of cultured myoblasts were examined in vitro. Myoblasts from the CBA group had significantly reduced PAX7, MYOD1, MYOG, MYF5, and MEF2C expression. This was associated with decreased myotube formation as evidenced by Jenner-Giemsa staining and myonuclei fusion index. No significant difference in the proliferative ability, cell cycle distribution, or autophagy was detected between myoblasts isolated from CBA and SUC groups. Together, these results reflect marked dysregulation of myoblast myogenic gene expression and myotube formation, which we interpret as evidence of impaired skeletal muscle regenerative capacity in CBA-administered macaques. The contribution of this mechanism to alcoholic myopathy warrants further investigation.

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Section: Experimental Protocolmentioning

confidence: 99%

mentioning

confidence: 97%

Chronic binge alcohol consumption alters myogenic gene expression and reduces in vitro myogenic differentiation potential of myoblasts from rhesus macaques

Simon

LeCapitaine

Berner

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…25,26 More recent simian studies have provided evidence that chronic alcohol intake prior to and during HIV infection results in a higher viral set point, more rapid progression to end-stage disease, and exacerbation of the AIDS wasting syndrome through increased expression of tumor necrosis factor-a and atrogin-1. [27][28][29] Several studies on alcohol and HIV disease progression after the introduction of antiretroviral therapy (ART) have established that alcohol results in reduced viral load response and CD4 þ cell reconstitution, and poorer adherence to ART. [30][31][32] A cross-sectional analysis of HIV-1-infected drug users found that heavy alcohol users (defined as alcohol intake three to four or more times per week), who were receiving highly active antiretroviral therapy (HAART), were four times less likely to achieve undetectable viral load and two times more likely to have CD4 þ cell counts below 500 cells=ml than moderate drinkers or abstainers.…”

Section: Introductionmentioning

confidence: 99%

Alcohol Use Accelerates HIV Disease Progression

Baum

Rafie

Lai

et al. 2010

AIDS Research and Human Retroviruses

241

203

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The effects of alcohol abuse on HIV disease progression have not been definitively established. A prospective, 30-month, longitudinal study of 231 HIV(+) adults included history of alcohol and illicit drug use, adherence to antiretroviral therapy (ART), CD4(+) cell count, and HIV viral load every 6 months. Frequent alcohol users (two or more drinks daily) were 2.91 times (95% CI: 1.23-6.85, p = 0.015) more likely to present a decline of CD4 to

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“…For example, the experimental simian immunodeficiency virus infection of macaque monkeys shows a decrease in body weight gain; however, although it allows for better control of nutritional variables than human studies, its use is limited by its expense (32,33). In contrast, several lines of transgenic (Tg) rodents, both mice and rats, that are noninfectious and express one or more of the HIV-1 viral envelope proteins have been developed (39,41).…”

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confidence: 99%

Skeletal and cardiac myopathy in HIV-1 transgenic rats

Pruznak

Hong-Brown²,

Lantry

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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The mechanism by which human immunodeficiency virus (HIV)-1 infection in humans leads to the erosion of lean body mass is poorly defined. Therefore, the purpose of the present study was to determine whether transgenic (Tg) rats that constitutively overexpress HIV-1 viral proteins exhibit muscle wasting and to elucidate putative mechanisms. Over 7 mo, Tg rats gained less body weight than pair-fed controls exclusively as a result of a proportional reduction in lean, not fat, mass. Fast- and slow-twitch muscle atrophy in Tg rats did not result from a reduction in the in vivo-determined rate of protein synthesis. In contrast, urinary excretion of 3-methylhistidine, as well as the content of atrogin-1 and the 14-kDa actin fragment, was elevated in gastrocnemius of Tg rats, suggesting increased muscle proteolysis. Similarly, Tg rats had reduced cardiac mass, which was independent of a change in protein synthesis. This decreased cardiac mass was associated with a reduction in stroke volume, but cardiac output was maintained by a compensatory increase in heart rate. The HIV-induced muscle atrophy was associated with increased whole body energy expenditure, which was not due to an elevated body temperature or secondary bacterial infection. Furthermore, the atrophic response could not be attributed to the development of insulin resistance, decreased levels of circulating amino acids, or increased tissue cytokines. However, skeletal muscle and, to a lesser extent, circulating insulin-like growth factor I was reduced in Tg rats. Although hepatic injury was implicated by increased plasma levels of aspartate and alanine aminotransferases, hepatic protein synthesis was not different between control and Tg rats. Hence, HIV-1 Tg rats develop atrophy of cardiac and skeletal muscle, the latter of which results primarily from an increased protein degradation and may be related to the marked reduction in muscle insulin-like growth factor I.

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Chronic Alcohol Accentuates Simian Acquired Immunodeficiency Syndrome‐Associated Wasting

Cited by 59 publications

References 55 publications

Chronic binge alcohol consumption alters myogenic gene expression and reduces in vitro myogenic differentiation potential of myoblasts from rhesus macaques

Chronic binge alcohol consumption alters myogenic gene expression and reduces in vitro myogenic differentiation potential of myoblasts from rhesus macaques

Alcohol Use Accelerates HIV Disease Progression

Skeletal and cardiac myopathy in HIV-1 transgenic rats

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