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Minimal Alteration in Muscle Lipid Genes Following Stabilized Weight Loss

TitleMinimal Alteration in Muscle Lipid Genes Following Stabilized Weight Loss
Publication TypeJournal Article
Year of Publication2017
AuthorsCoker, RH, Robinette, L, Kern, PA
JournalApplied Physiology, Nutrition and Metabolism
Volume[Epub ahead of print]
Abstract

Purpose: Variations in skeletal muscle peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1µ), carntine palmitoyltransferase (CPT-1), perilipin protein (PLIN2), and adipose tissue triglyceride lipase (ATGL), and comparative gene identification-58 (CGI-58) have been described to play important roles in the metabolic regulation of lipid oxidation, and may influence intramyocellular lipid (IMCL) and muscle lipid droplet size (LDS). While acute changes in caloric balance and/or aerobic capacity may affect lipid metabolism, the influence of sustained weight loss derived from caloric restriction (CWL) compared to exercise training (EWL) on the above mentioned parameters has not been fully elucidated.

Methods: Using a combination of metabolic feeding and/or supervised exercise training, we evaluated the influence of stabilized weight loss elicited by CWL compared to EWL without the confounding influence of acute alterations in caloric balance on molecular markers of mitochondrial metabolism and lipid droplet size in middle-aged overweight individuals with impaired glucose tolerance.

Results: There were no significant changes in PGC-1µ, CPT-1, PLIN2, ATGL and CGI-58 mRNA in CWL and EWL. While there were no changes in ATGL mRNA in CWL, there was a strong upward trend (P=0.05) for the DATGL mRNA in EWL with stabilized weight loss. There were no significant changes in IMCL or LDS within type 1 or type 2 skeletal muscle in CWL or EWL, respectively.

Conclusion: Under the conditions of chronic caloric balance following dietary or exercise-based interventions, mediators of mitochondrial function, IMCL and LDS were largely unaffected. Future studies should focus on intervention-based changes in protein expression and/or phosphorylation, and the relationship to physiological endpoints.

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