Minimal alteration in muscle lipid genes following stabilized weight loss

Robert H. Coker, Leizleigh Robinette, Philip A. Kern

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Variations in skeletal muscle peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1), carntine palmitoyltransferase-1 (CPT-1), perilipin protein 2 (PLIN2), and adipose tissue triglyceride lipase (ATGL), and comparative gene identification-58 (CGI-58) have been described as playing 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 with weight loss (CWL) compared with exercise training with weight loss (EWL) on the abovementioned parameters has not been fully elucidated. Using a combination of metabolic feeding and/or supervised exercise training, we evaluated the influence of stabilized weight loss elicited by CWL compared with 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. There were no significant changes in PGC-1α, CPT-1, PLIN2, ATGL and, CGI-58 messenger RNA (mRNA) in CWL and EWL. While there were no changes in ATGL mRNA in CWL, there was a strong trend (P = 0.05) for the ΔATGL mRNA in EWL with stabilized weight loss. There were no significant changes in IMCL or LDS within skeletal muscle in CWL or EWL, respectively. In 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.

Original languageEnglish
Pages (from-to)1277-1282
Number of pages6
JournalApplied Physiology, Nutrition and Metabolism
Volume42
Issue number12
DOIs
StatePublished - 2017

Bibliographical note

Funding Information:
Funding was provided by National Institutes of Health (NIH), National Institute of Diabetes, Digestive, and Kidney Diseases K01 DK 64716-01, NIH grants P30 AG28718 and UL1TR001998, and American Heart Association Grant 0335172N. We would like to thank Rick Williams, Bradley Hogate, and Bounleut Phanavanh for expert technical analysis.

Funding Information:
Dr. Coker is a Managing Partner and Co-Owner of Essential Blends LLC, which has received funding from the National Institutes of Health Small Business Innovations in Research program to develop clinical nutrition products. The data presented in this manuscript are unrelated. We declare that the results of the study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation.

Publisher Copyright:
© 2017, Canadian Science Publishing. All rights reserved.

Keywords

  • Fat metabolism
  • Metabolic syndrome
  • Mitochondrial metabolism
  • Nutrition
  • Obesity

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Nutrition and Dietetics
  • Physiology (medical)

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