PMID- 29232696
OWN - NLM
STAT- MEDLINE
DCOM- 20180104
LR  - 20181113
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 12
DP  - 2017
TI  - Effect of temperature on fatty acid metabolism in skeletal muscle mitochondria of 
      untrained and endurance-trained rats.
PG  - e0189456
LID - 10.1371/journal.pone.0189456 [doi]
LID - e0189456
AB  - We studied the effects of various assay temperatures, representing hypothermia 
      (25 degrees C), normothermia (35 degrees C), and hyperthermia (42 degrees C), on the oxidation of 
      lipid-derived fuels in rat skeletal muscle mitochondria of untrained and 
      endurance-trained rats. Adult 4-month-old male Wistar rats were assigned to a 
      training group (rats trained on a treadmill for 8 weeks) or a sedentary control 
      group. In skeletal muscle mitochondria of both control and trained rats, an 
      increase in the assay temperature from 25 degrees C to 42 degrees C was accompanied by a 
      consistent increase in the oxidation of palmitoylcarnitine and 
      glycerol-3-phosphate. Moreover, endurance training increased mitochondrial 
      capacity to oxidize the lipid-derived fuels at all studied temperatures. The 
      endurance training-induced increase in mitochondrial capacity to oxidize fatty 
      acids was accompanied by an enhancement of mitochondrial biogenesis, as shown by 
      the elevated expression levels of Nrf2, PGC1alpha, and mitochondrial marker and by 
      the elevated expression levels of mitochondrial proteins involved in fatty acid 
      metabolism, such as fatty acid transporter CD36, carnitine palmitoyltransferase 
      1A (CPT1A), and acyl-CoA dehydrogenase (ACADS). We conclude that hyperthermia 
      enhances but hypothermia attenuates the rate of the oxidation of fatty acids and 
      glycerol-3-phosphate in rat skeletal muscle mitochondria isolated from both 
      untrained and trained rats. Moreover, our results indicate that endurance 
      training up-regulates mitochondrial biogenesis markers, lipid-sustained oxidative 
      capacity, and CD36 and CPT1A proteins involved in fatty acid transport, possibly 
      via PGC1alpha and Nrf2 signaling pathways.
FAU - Zoladz, Jerzy A
AU  - Zoladz JA
AUID- ORCID: 0000-0002-1143-5590
AD  - Department of Muscle Physiology, Faculty of Rehabilitation, University School of 
      Physical Education, Krakow, Poland.
FAU - Koziel, Agnieszka
AU  - Koziel A
AD  - Department of Bioenergetics, Adam Mickiewicz University, Poznan, Poland.
FAU - Broniarek, Izabela
AU  - Broniarek I
AD  - Department of Bioenergetics, Adam Mickiewicz University, Poznan, Poland.
FAU - Woyda-Ploszczyca, Andrzej M
AU  - Woyda-Ploszczyca AM
AD  - Department of Bioenergetics, Adam Mickiewicz University, Poznan, Poland.
FAU - Ogrodna, Karolina
AU  - Ogrodna K
AD  - Department of Bioenergetics, Adam Mickiewicz University, Poznan, Poland.
FAU - Majerczak, Joanna
AU  - Majerczak J
AD  - Department of Muscle Physiology, Faculty of Rehabilitation, University School of 
      Physical Education, Krakow, Poland.
FAU - Celichowski, Jan
AU  - Celichowski J
AD  - Department of Neurobiology, University School of Physical Education, Poznan, 
      Poland.
FAU - Szkutnik, Zbigniew
AU  - Szkutnik Z
AD  - Faculty of Applied Mathematics, AGH University of Science and Technology, Krakow, 
      Poland.
FAU - Jarmuszkiewicz, Wieslawa
AU  - Jarmuszkiewicz W
AD  - Department of Bioenergetics, Adam Mickiewicz University, Poznan, Poland.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20171212
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Fatty Acids)
SB  - IM
MH  - Animals
MH  - Fatty Acids/*metabolism
MH  - Male
MH  - Mitochondria, Muscle/*metabolism
MH  - Muscle, Skeletal/*metabolism
MH  - Oxidation-Reduction
MH  - *Physical Conditioning, Animal
MH  - Rats
MH  - Rats, Wistar
MH  - *Temperature
PMC - PMC5726737
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2017/12/13 06:00
MHDA- 2018/01/05 06:00
PMCR- 2017/12/12
CRDT- 2017/12/13 06:00
PHST- 2017/05/04 00:00 [received]
PHST- 2017/11/28 00:00 [accepted]
PHST- 2017/12/13 06:00 [entrez]
PHST- 2017/12/13 06:00 [pubmed]
PHST- 2018/01/05 06:00 [medline]
PHST- 2017/12/12 00:00 [pmc-release]
AID - PONE-D-17-17232 [pii]
AID - 10.1371/journal.pone.0189456 [doi]
PST - epublish
SO  - PLoS One. 2017 Dec 12;12(12):e0189456. doi: 10.1371/journal.pone.0189456. 
      eCollection 2017.