Effect of voluntary exercise upon the metabolic syndrome and gut microbiome composition in mice

Physiol Rep. 2021 Nov;9(21):e15068. doi: 10.14814/phy2.15068.

Abstract

The metabolic syndrome is a cluster of conditions that increase an individual's risk of developing diseases. Being physically active throughout life is known to reduce the prevalence and onset of some aspects of the metabolic syndrome. Furthermore, previous studies have demonstrated that an individual's gut microbiome composition has a large influence on several aspects of the metabolic syndrome. However, the mechanism(s) by which physical activity may improve metabolic health are not well understood. We sought to determine if endurance exercise is sufficient to prevent or ameliorate the development of the metabolic syndrome and its associated diseases. We also analyzed the impact of physical activity under metabolic syndrome progression upon the gut microbiome composition. Utilizing whole-body low-density lipoprotein receptor (LDLR) knockout mice on a "Western Diet," we show that long-term exercise acts favorably upon glucose tolerance, adiposity, and liver lipids. Exercise increased mitochondrial abundance in skeletal muscle but did not reduce liver fibrosis, aortic lesion area, or plasma lipids. Lastly, we observed several changes in gut bacteria and their novel associations with metabolic parameters of clinical importance. Altogether, our results indicate that exercise can ameliorate some aspects of the metabolic syndrome progression and alter the gut microbiome composition.

Keywords: LDLR; exercise; metabolic syndrome; microbiome; obesity.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adiposity
  • Animals
  • Gastrointestinal Microbiome*
  • Glucose / metabolism
  • Liver / metabolism
  • Male
  • Metabolic Syndrome / metabolism
  • Metabolic Syndrome / physiopathology*
  • Metabolic Syndrome / therapy
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria, Liver / metabolism
  • Physical Conditioning, Animal / methods*
  • Receptors, LDL / genetics
  • Receptors, LDL / metabolism
  • Running

Substances

  • Receptors, LDL
  • Glucose