Lower Plasma Selenoprotein P Levels in Regularly Exercising Young Adults

J ASEAN Fed Endocr Soc. 2023;38(1):6-12. doi: 10.15605/jafes.037.S4. Epub 2022 Apr 30.

Abstract

Objective: Physical exercise can provide many health benefits in humans. Exercise-induced reactive oxygen species (ROS) formation and its downstream signaling cascades are reported to induce mitochondrial biogenesis in exercising tissues. Selenoprotein P (SELENOP) is the antioxidant hepatokine whose hypersecretion is associated with various metabolic diseases. It was reported to impair exercise-induced reactive oxygen species signaling and inhibit subsequent mitochondrial biogenesis in mice. However, the relationship between selenoprotein P and mitochondrial dynamics in humans has not yet been reported. While reduction of plasma selenoprotein P becomes an attractive therapeutic target for metabolic diseases, the role of regular exercise in this regard is still unknown. This study aimed to analyze the influence of regular habitual exercise on plasma selenoprotein P levels and its association with leucocyte mitochondrial DNA copy number in healthy young adults.

Methodology: Plasma selenoprotein P levels and leucocyte mitochondrial DNA copy numbers were compared in 44 regularly exercising subjects and 44 non-exercising controls, and the correlation between the two parameters was analyzed. Plasma selenoprotein P levels were measured by Enzyme-linked Immunosorbent Assay, and leucocyte mitochondrial DNA copy numbers were measured using the qPCR method.

Results: The regular-exercise group had lower plasma selenoprotein P levels with higher leucocyte mitochondrial DNA copy numbers than the non-exercise group. There was a tendency of negative correlation between the two variables in our studied population.

Conclusion: Regular habitual exercise has a beneficial effect on reducing plasma selenoprotein P levels while raising mitochondrial DNA copy numbers.

Keywords: mitochondria; physical exercise; reactive oxygen species; selenoprotein P.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • DNA, Mitochondrial / genetics
  • Humans
  • Leukocytes / metabolism
  • Mitochondria* / genetics
  • Reactive Oxygen Species / metabolism
  • Selenoprotein P* / genetics
  • Young Adult

Substances

  • DNA, Mitochondrial
  • Reactive Oxygen Species
  • Selenoprotein P