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Obesity Studies

Lipoprotein Lipase Overexpression in Skeletal Muscle Attenuates Weight Regain by Potentiating Energy Expenditure

  1. David M. Presby1,
  2. Michael C. Rudolph2,
  3. Vanessa D. Sherk3,
  4. Matthew R. Jackman1,
  5. Rebecca M. Foright4,
  6. Kenneth L. Jones5,
  7. Julie A. Houck3,
  8. Ginger C. Johnson3,
  9. Janine A. Higgins5,
  10. P. Darrell Neufer6,
  11. Robert H. Eckel3 and
  12. Paul S. MacLean3⇑
  1. 1Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA
  2. 2Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK
  3. 3Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO
  4. 4Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS
  5. 5Department of Pediatrics, University of Colorado Denver Anschutz Medical Campus, Aurora, CO
  6. 6East Carolina Diabetes and Obesity Institute and the Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC
  1. Corresponding author: Paul S. MacLean, paul.maclean{at}cuanschutz.edu
Diabetes 2021 Apr; 70(4): 867-877. https://doi.org/10.2337/db20-0763
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Abstract

Moderate weight loss improves numerous risk factors for cardiometabolic disease; however, long-term weight loss maintenance (WLM) is often thwarted by metabolic adaptations that suppress energy expenditure and facilitate weight regain. Skeletal muscle has a prominent role in energy homeostasis; therefore, we investigated the effect of WLM and weight regain on skeletal muscle in rodents. In skeletal muscle of obesity-prone rats, WLM reduced fat oxidative capacity and downregulated genes involved in fat metabolism. Interestingly, even after weight was regained, genes involved in fat metabolism were also reduced. We then subjected mice with skeletal muscle lipoprotein lipase overexpression (mCK-hLPL), which augments fat metabolism, to WLM and weight regain and found that mCK-hLPL attenuates weight regain by potentiating energy expenditure. Irrespective of genotype, weight regain suppressed dietary fat oxidation and downregulated genes involved in fat metabolism in skeletal muscle. However, mCK-hLPL mice oxidized more fat throughout weight regain and had greater expression of genes involved in fat metabolism and lower expression of genes involved in carbohydrate metabolism during WLM and regain. In summary, these results suggest that skeletal muscle fat oxidation is reduced during WLM and regain, and therapies that improve skeletal muscle fat metabolism may attenuate rapid weight regain.

Footnotes

  • This article contains supplementary material online at https://doi.org/10.2337/figshare.13652960.

  • Received July 22, 2020.
  • Accepted January 27, 2021.
  • © 2021 by the American Diabetes Association
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Lipoprotein Lipase Overexpression in Skeletal Muscle Attenuates Weight Regain by Potentiating Energy Expenditure
David M. Presby, Michael C. Rudolph, Vanessa D. Sherk, Matthew R. Jackman, Rebecca M. Foright, Kenneth L. Jones, Julie A. Houck, Ginger C. Johnson, Janine A. Higgins, P. Darrell Neufer, Robert H. Eckel, Paul S. MacLean
Diabetes Apr 2021, 70 (4) 867-877; DOI: 10.2337/db20-0763

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Lipoprotein Lipase Overexpression in Skeletal Muscle Attenuates Weight Regain by Potentiating Energy Expenditure
David M. Presby, Michael C. Rudolph, Vanessa D. Sherk, Matthew R. Jackman, Rebecca M. Foright, Kenneth L. Jones, Julie A. Houck, Ginger C. Johnson, Janine A. Higgins, P. Darrell Neufer, Robert H. Eckel, Paul S. MacLean
Diabetes Apr 2021, 70 (4) 867-877; DOI: 10.2337/db20-0763
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