Abstract: FR-PO174
Skeletal Muscle Mitochondrial Function and Dynamics in Patients on Maintenance Hemodialysis
Session Information
- Mitochondriacs and More
November 03, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nutrition, Inflammation, and Metabolism
- 1401 Nutrition, Inflammation, Metabolism
Authors
- Gamboa, Jorge, Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Falck, Aaron M., Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Keller, Chad Alexander, Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Roshanravan, Baback, University of Washington, Seattle, Washington, United States
- Ikizler, Talat Alp, Vanderbilt University Medical Center, Nashville, Tennessee, United States
Background
Patients on maintenance hemodialysis (MHD) commonly suffer of frailty and sarcopenia, which increase the risk of morbidity and mortality. The loss of muscle power is one of the components of the frailty phenotype, and poor muscle function is recognized as a major cause of frailty. Mitochondria are the main source of energy in skeletal muscle and are important for muscle function. Proper mitochondrial function depends on the balance between fission and fusion (mitochondrial dynamics). Thus, we evaluated changes in mitochondrial function and dynamics in skeletal muscle in patients on MHD.
Methods
We evaluated 20 patients on MHD and 19 controls with no history of CKD that were matched by age, gender, history of diabetes, BMI, and race. We measured in vivo mitochondrial function by 31-phosphorus magnetic resonance spectroscopy (31P-MRS) in the quadriceps muscle. We used the half time recovery of phosphocreatine (P-Cr) after a brief exercise as the measure of mitochondrial function. A faster recovery correlates with better mitochondrial function. We also measured markers of mitochondrial fusion and fission by western blot in skeletal muscle biopsies from the vastus lateralis.
Results
Controls and patients on MHD were similar in terms of age (47.0±9.5 vs. 47.7±12.3) and BMI (30.0±6.0 vs. 30.4±7.8). We found that the half time recovery of P-Cr was faster in controls compared to patients on MHD (Figure 1A). We found an increase in the abundance of dynamin related protein 1 (DRP-1), a marker of mitochondrial fission, in patients on MHD (Figure 1B). We did not find changes in other marker of mitochondrial dynamics.
Conclusion
Our data suggest that in vivo mitochondrial function is impaired in patients on MHD. The increase in mitochondrial fission marker DRP-1 in MHD patients could be a mechanism for segregation and elimination of damaged mitochondria.
Funding
- NIDDK Support