The response of mitochondrial respiration and quantity in skeletal muscle and adipose tissue to exercise in humans with prediabetes
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The response of mitochondrial respiration and quantity in skeletal muscle and adipose tissue to exercise in humans with prediabetes. / Szczerbinski, Lukasz; Taylor, Mark Alan; Puchta, Urszula; Konopka, Paulina; Paszko, Adam; Citko, Anna; Szczerbinski, Karol; Goscik, Joanna; Gorska, Maria; Larsen, Steen; Kretowski, Adam.
In: Cells, Vol. 10, No. 11, 3013, 2021.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - The response of mitochondrial respiration and quantity in skeletal muscle and adipose tissue to exercise in humans with prediabetes
AU - Szczerbinski, Lukasz
AU - Taylor, Mark Alan
AU - Puchta, Urszula
AU - Konopka, Paulina
AU - Paszko, Adam
AU - Citko, Anna
AU - Szczerbinski, Karol
AU - Goscik, Joanna
AU - Gorska, Maria
AU - Larsen, Steen
AU - Kretowski, Adam
N1 - Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021
Y1 - 2021
N2 - Background: Mitochondrial dysfunction has been implicated in the pathogenesis of type 2 diabetes, but its contribution to the early stages of dysglycemia remains poorly understood. By collecting a high-resolution stage-based spectrum of dysglycemia, our study fills this gap by evalu-ating derangement in both the function and quantity of mitochondria. We sampled mitochondria in skeletal muscle and subcutaneous adipose tissues of subjects with progressive advancement of dysglycemia under a three-month exercise intervention. Methods: We measured clinical metabolic parameters and gathered skeletal muscle and adipose tissue biopsies before and after the three-month exercise intervention. We then assayed the number of mitochondria via citrate synthase (CS) activity and functional parameters with high-resolution respirometry. Results: In muscle, there were no differences in mitochondrial quantity or function at baseline between normoglycemics and prediabetics. However, the intervention caused improvement in CS activity, implying an increase in mitochondrial quantity. By contrast in adipose tissue, baseline differences in CS activity were present, with the lowest CS activity coincident with impaired fasting glucose and impaired glucose tolerance (IFG + IGT). Finally, CS activity, but few of the functional metrics, improved under the intervention. Conclusions: We show that in prediabetes, no differences in the function or amount of mitochondria (measured by CS activity) in skeletal muscle are apparent, but in adipose tissue of subjects with IFG + IGT, a significantly reduced activity of CS was observed. Finally, metabolic improvements under the exercise correlate to improvements in the amount, rather than function, of mitochondria in both tissues.
AB - Background: Mitochondrial dysfunction has been implicated in the pathogenesis of type 2 diabetes, but its contribution to the early stages of dysglycemia remains poorly understood. By collecting a high-resolution stage-based spectrum of dysglycemia, our study fills this gap by evalu-ating derangement in both the function and quantity of mitochondria. We sampled mitochondria in skeletal muscle and subcutaneous adipose tissues of subjects with progressive advancement of dysglycemia under a three-month exercise intervention. Methods: We measured clinical metabolic parameters and gathered skeletal muscle and adipose tissue biopsies before and after the three-month exercise intervention. We then assayed the number of mitochondria via citrate synthase (CS) activity and functional parameters with high-resolution respirometry. Results: In muscle, there were no differences in mitochondrial quantity or function at baseline between normoglycemics and prediabetics. However, the intervention caused improvement in CS activity, implying an increase in mitochondrial quantity. By contrast in adipose tissue, baseline differences in CS activity were present, with the lowest CS activity coincident with impaired fasting glucose and impaired glucose tolerance (IFG + IGT). Finally, CS activity, but few of the functional metrics, improved under the intervention. Conclusions: We show that in prediabetes, no differences in the function or amount of mitochondria (measured by CS activity) in skeletal muscle are apparent, but in adipose tissue of subjects with IFG + IGT, a significantly reduced activity of CS was observed. Finally, metabolic improvements under the exercise correlate to improvements in the amount, rather than function, of mitochondria in both tissues.
KW - Adipose tissue
KW - Exercise
KW - Fat
KW - Mitochondria
KW - Muscle
KW - Obesity
KW - Prediabetes
KW - Type 2 diabetes
UR - http://www.scopus.com/inward/record.url?scp=85118345877&partnerID=8YFLogxK
U2 - 10.3390/cells10113013
DO - 10.3390/cells10113013
M3 - Journal article
C2 - 34831236
AN - SCOPUS:85118345877
VL - 10
JO - Cells
JF - Cells
SN - 2073-4409
IS - 11
M1 - 3013
ER -
ID: 284639572