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Intramuscular fat and endocrine signaling in muscular dystrophy

Award Number: R01AR088153
ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/10/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2030

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Intramuscular fat and endocrine signaling in muscular dystrophy - Project Summary Progressive replacement of skeletal muscle with intramuscular adipose tissue (IMAT) is a defining feature of the dystrophinopathies, Duchenne (DMD) and Becker muscular dystrophy (BMD). Although IMAT accumulation is also observed in obesity and aging, in muscular dystrophy it arises through a distinct, non-metabolic mechanism and can replace entire muscles, creating a uniquely large adipose depot. Subcutaneous and visceral fat are well-established endocrine tissues whose adipokine secretion contributes to systemic metabolic dysfunction. However, the endocrine activity of IMAT, particularly in muscular dystrophy where its volume is massive, remains virtually unstudied. This represents a fundamental gap in understanding how muscle degeneration may influence whole-body metabolic health. Preliminary data from our group indicate that several circulating adipokines, including leptin and fatty acid binding protein 4, increase with disease severity in DMD and correlate strongly with MRI-based measures of muscle fat independent of age, BMI, and corticosteroid use. These findings suggest IMAT may function as an active endocrine tissue and a major source of circulating adipokines. Therefore, the aim of this project is to define the endocrine role of IMAT in dystrophinopathy and determine its potential systemic consequences. We hypothesize progressive IMAT accumulation secretes adipokines into systemic circulation and contributes to metabolic dysfunction, including hepatic steatosis. Leveraging two ongoing parent studies, we will integrate IMAT biopsies, quantitative MRI, and serum analyses in children and adults with dystrophinopathy. Aim 1 will establish that IMAT in dystrophinopathy secretes adipokines that enter systemic circulation by performing proteomics on IMAT biopsies from adults with BMD. Aim 2 will quantify the contribution of IMAT burden to circulating adipokine levels in DMD and BMD, determining whether IMAT expansion drives proportional increases in IMAT-derived adipokines. Exploratory Aim 3 will define relationships between IMAT, circulating adipokines, and hepatic steatosis using quantitative MRI to determine whether endocrine IMAT activity contributes to liver fat accumulation in dystrophinopathy. Establishing IMAT as an endocrine tissue would represent a paradigm shift in understanding metabolic dysfunction in muscular dystrophy, identifying a previously unrecognized mechanism linking muscle degeneration to systemic metabolism. Findings may reveal IMAT- derived adipokines as biomarkers or therapeutic targets and improve risk stratification for gene therapy–related hepatic toxicity.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $381,527 )
2026	2026	UNIVERSITY OF FLORIDA	1523 UNION RD RM 207	GAINESVILLE	FL	32611	ALACHUA	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	1	9/11/2026	NEW	$381,527
														Subtotal = $381,527

Grand Total All Awards = $381,527

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Intramuscular fat and endocrine signaling in muscular dystrophy

Award Number: R01AR088153

ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/10/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2030

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