Korean J Physiol Pharmacol.  2021 Mar;25(2):167-175. 10.4196/kjpp.2021.25.2.167.

Far-infrared rays enhance mitochondrial biogenesis and GLUT3 expression under low glucose conditions in rat skeletal muscle cells

Affiliations
  • 1Departments of Physiology, College of Medicine, Chung-Ang University, Seoul 06974, Korea,
  • 2Departments of Medicine, College of Medicine, Chung-Ang University, Seoul 06974, Korea,
  • 3Cardiovascular and Metabolic Disease Center, SMART Marine Therapeutics Center, Inje University, Busan 47392, Korea,
  • 4Department of Family Medicine, College of Medicine, Chung-Ang University Hospital, Seoul 06973, Korea,
  • 5Department of Physiology and Cell Biology, University of Nevada, Reno School of Medicine, Reno, NV 89557, USA

Abstract

Far-infrared rays (FIR) are known to have various effects on atoms and molecular structures within cells owing to their radiation and vibration frequencies. The present study examined the effects of FIR on gene expression related to glucose transport through microarray analysis in rat skeletal muscle cells, as well as on mitochondrial biogenesis, at high and low glucose conditions. FIR were emitted from a bio-active material coated fabric (BMCF). L6 cells were treated with 30% BMCF for 24 h in medium containing 25 or 5.5 mM glucose, and changes in the expression of glucose transporter genes were determined. The expression of GLUT3 (Slc2a3) increased 2.0-fold (p < 0.05) under 5.5 mM glucose and 30% BMCF. In addition, mitochondrial oxygen consumption and membrane potential (ΔΨm) increased 1.5- and 3.4-fold (p < 0.05 and p < 0.001), respectively, but no significant change in expression of Pgc-1a, a regulator of mitochondrial biogenesis, was observed in 24 h. To analyze the relationship between GLUT3 expression and mitochondrial biogenesis under FIR, GLUT3 was down-modulated by siRNA for 72 h. As a result, the ΔΨm of the GLUT3 siRNA-treated cells increased 3.0-fold (p < 0.001), whereas that of the control group increased 4.6-fold (p < 0.001). Moreover, Pgc-1a expression increased upon 30% BMCF treatment for 72 h; an effect that was more pronounced in the presence of GLUT3. These results suggest that FIR may hold therapeutic potential for improving glucose metabolism and mitochondrial function in metabolic diseases associated with insufficient glucose supply, such as type 2 diabetes.

Keyword

Glucose; Glucose transporter type 3; Infrared rays; Mitochondrial biogenesis; Radiation

Figure

  • Fig. 1 Gene ontology (GO) enrichment analysis. The bar graph indicates the number of differently expressed genes in GO terms associated with glucose from bio-active materials coated fabric-worn rat skeletal muscle. The nine GO biological process terms ranked with the highest p-value are shown. GO functional analysis was based on gomap stat. *p < 0.05, **p < 0.01, ***p < 0.001 vs. control group.

  • Fig. 2 Far-infrared rays (FIR) alter the mRNA expression of glucose transporter class 1 members. (A) GLUT1 (Slc2a1) (B) GLUT3 (Slc2a3), and (C) GLUT4 (Slcea4) expression was analyzed under 25 and 5.5 mM glucose conditions, and upon bio-active materials coated fabric treatment for 24 h by quantitative real-time polymerase chain reaction. *p < 0.05 vs. control group.

  • Fig. 3 Far-infrared rays (FIR) effectively activate mitochondrial biogenesis. Changes in (A) mitochondrial DNA copy number (mtDNA-CN) and (B) respiratory control ratio (RCR) per mtDNA-CN ratio under 25 mM and 5.5 mM glucose conditions. (C) Mitochondrial membrane potential (ΔΨm) was determined by measuring TMRE (tetramethylrhodamine, ethyl ester) fluorescence under 5.5 mM glucose conditions by confocal microscopy (scale bar = 50 μm). (D) TMRE region of interest fluorescence intensity per cell area ratio measurement using Image J. (E) Pgc-1a expression was analyzed by reverse transcription polymerase chain reaction. *p < 0.05, **p < 0.01, ***p < 0.001 vs. control group.

  • Fig. 4 Far-infrared rays (FIR) activate mitochondrial biogenesis at low glucose concentrations via GLUT3. The control and GLUT3 siRNA groups were treated with bio-active materials coated fabric for 72 h under 25 or 5.5 mM glucose conditions. (A) Mitochondrial membrane potential (ΔΨm) as determined by TMRE (tetramethylrhodamine, ethyl ester) fluorescence and (B) confirmation of mitochondrial mass by measurements of NAO (acridine orange 10-nonyl bromide) fluorescence using confocal microscopy (scale bar = 50 μm). (C) TMRE and (D) NAO region of interest fluorescence intensity per cell area ratio. (E) Pgc-1a expression was performed by reverse transcription polymerase chain reaction. ***p < 0.001 vs. control group; ##p < 0.01 vs. experimental group.


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