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Physiol Rep. 2016 Aug;4(15). pii: e12890. doi: 10.14814/phy2.12890.

Mitochondrial function assessed by 31P MRS and BOLD MRI in non-obese type 2 diabetic rats.

Author information

1
Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio Case Center for Imaging Research, Case Western Reserve University, Cleveland, Ohio.
2
Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio.
3
Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio Department of Electrical and Computer Engineering and Biomedical Engineering Institute, Old Dominion University, Norfolk, Virginia.
4
Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio Case Center for Imaging Research, Case Western Reserve University, Cleveland, Ohio Department of Radiology, Case Western Reserve University, Cleveland, Ohio Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio xin.yu@case.edu.

Abstract

The study aims to characterize age-associated changes in skeletal muscle bioenergetics by evaluating the response to ischemia-reperfusion in the skeletal muscle of the Goto-Kakizaki (GK) rats, a rat model of non-obese type 2 diabetes (T2D). (31)P magnetic resonance spectroscopy (MRS) and blood oxygen level-dependent (BOLD) MRI was performed on the hindlimb of young (12 weeks) and adult (20 weeks) GK and Wistar (control) rats. (31)P-MRS and BOLD-MRI data were acquired continuously during an ischemia and reperfusion protocol to quantify changes in phosphate metabolites and muscle oxygenation. The time constant of phosphocreatine recovery, an index of mitochondrial oxidative capacity, was not statistically different between GK rats (60.8 ± 13.9 sec in young group, 83.7 ± 13.0 sec in adult group) and their age-matched controls (62.4 ± 11.6 sec in young group, 77.5 ± 7.1 sec in adult group). During ischemia, baseline-normalized BOLD-MRI signal was significantly lower in GK rats than in their age-matched controls. These results suggest that insulin resistance leads to alterations in tissue metabolism without impaired mitochondrial oxidative capacity in GK rats.

KEYWORDS:

31P magnetic resonance spectroscopy; blood oxygen level‐dependent MRI; ischemia reperfusion; mitochondrial oxidative capacity

PMID:
27511984
PMCID:
PMC4985553
DOI:
10.14814/phy2.12890
[Indexed for MEDLINE]
Free PMC Article

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