# Alcohol-induced skeletal muscle dysregulation in SIV/HIV: Mitochondrial-mediated mechanisms

> **NIH NIH F32** · LSU HEALTH SCIENCES CENTER · 2021 · $43,665

## Abstract

Project Summary/Abstract
The primary purpose of this Ruth L. Kirschstein NRSA F32 application is to enhance the postdoctoral training of
a promising young alcohol researcher and to provide research training required to conduct High Priority
HIV/AIDS-related research. The applicant will gain skills to conduct basic and translational research focused on
alcohol-mediated metabolic complications prevalent among people living with HIV (PLWH), which directly
supports a High Priority research area designated by the NIAAA Research Program on HIV/AIDS. The applicant
has a strong track record of human subjects alcohol research in the field of applied exercise physiology, which
she will integrate with basic preclinical research and state-of-the-art molecular techniques to develop her
research niche in alcohol-induced skeletal muscle (SKM) mitochondrial dysregulation. At-risk alcohol use among
PLWH is nearly twice that in the general population. Chronic at-risk alcohol use and HIV/SIV are independently
associated with metabolic comorbidities including SKM dysfunction. Previous work from our laboratory using a
simian model indicates that chronic binge alcohol (CBA) administration decreases oxidative enzyme activity and
maximal oxygen consumption rate in asymptomatic male macaques. Preliminary data demonstrate generated
for this application show that CBA reduces mRNA expression of PGC-1β and TFAM, a downstream target of
PGC-1β, in SKM of CBA-administered, asymptomatic, SIV+/ART+ female rhesus macaques. PGC-1β and TFAM
are essential for mitochondrial biogenesis and homeostasis. However, the CBA-induced functional changes in
SKM mitochondria and the mechanism by which CBA reduces SKM mitochondrial biogenesis and function in
the context of HIV is not known. Therefore, the global hypothesis of the proposed work is that decreased PGC-
1β underlies CBA-mediated decreases in mitochondrial biogenesis and function in SKM of SIV+ female rhesus
macaques and that PGC-1β is a potential therapeutic target to improve mitochondrial homeostasis. We also
hypothesize that at-risk alcohol consumption decreases SKM mitochondrial biogenesis and function in PLWH.
The hypothesis will be systematically tested with the following specific aims: 1) Test the hypothesis that chronic
alcohol decreases mitochondrial biogenesis and function in a PGC-1β dependent manner in myoblasts from
SIV+ female rhesus macaques; 2) Test the hypothesis that pharmacologically promoting PGC-1 expression will
rescue CBA-mediated decreases in mitochondrial biogenesis and function in myoblasts from SIV+ female rhesus
macaques; and 3) Establish that findings from non-human primates translate to PLWH with at-risk alcohol use.
Data generated from the proposed application will provide a more comprehensive molecular understanding of
mitochondrial dysfunction in the context of HIV and alcohol and will provide a foundation for future mechanistic
and translational studies. Additionally, completing the proposed research ...

## Key facts

- **NIH application ID:** 10120504
- **Project number:** 5F32AA027982-02
- **Recipient organization:** LSU HEALTH SCIENCES CENTER
- **Principal Investigator:** Danielle E Levitt
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $43,665
- **Award type:** 5
- **Project period:** 2019-12-01 → 2021-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10120504

## Citation

> US National Institutes of Health, RePORTER application 10120504, Alcohol-induced skeletal muscle dysregulation in SIV/HIV: Mitochondrial-mediated mechanisms (5F32AA027982-02). Retrieved via AI Analytics 2026-06-11 from https://api.ai-analytics.org/grant/nih/10120504. Licensed CC0.

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