Discovering the Impact of T1D on Sphingolipid Profiles

Discovering the Impact of T1D on Sphingolipid Profiles

Discovering the Impact of T1D on Sphingolipid Profiles


Dr. Matthew Krause

University of Windsor

Megan Noble

Schulich School of Medicine & Dentistry

 

FUNDER: Schulich-UWindsor Opportunities for Research Excellence Program (SWORP)

GRANT DURATION: 2022-2023

 

 

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Skeletal muscle mass and strength play a vital role in healthy aging; anabolic impairments in skeletal muscle and reduced repair processes contribute to mortality and morbidity. Type 1 diabetes (T1D) is a disease that causes intrinsic differences in skeletal muscle repair and regeneration, contributing to a major diabetic complication termed diabetic myopathy. Sphingolipids constitute an important class of lipids that that act as structural components of cells and drive diverse receptor-mediated intracellular signalling pathways, including glucose homeostasis and muscle recovery pathways. Preliminary findings in the Krause Lab suggest that in vivo, regulation of sphingolipid metabolites in skeletal muscle is impaired in T1D mouse models; however, little is understood about the contribution of blood sphingolipids to the regulation of skeletal muscle regeneration.

Exercise training appears to modulate skeletal muscle sphingolipid content associated with improved muscle strength, mass, and metabolism. While some studies have suggested exercise can modulate sphingolipid levels in skeletal muscle and improve muscle repair and regeneration capacities, the impact of exercise on sphingolipid levels in T1D skeletal muscle and plasma remains unknown. Given the many uncertainties regarding sphingolipid levels in T1D patients and exercise, this study aims to quantify the sphingolipid profile of T1D patients. This information will be subsequently used to analyze changes in sphingolipid profiles pre- and post-exercise in both plasma and skeletal muscle samples from a T1D mouse model, the Akita mouse. This work will help generate new hypotheses aimed at filling major knowledge gaps in the role of circulating sphingolipids in T1D.

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