NDLI: PPARδ agonism inhibits skeletal muscle PDC activity, mitochondrial ATP production and force generation during prolonged contraction

Content Provider	PubMed Central
Author	Dumitru, Constantin-teodosiu Baker, David J. Constantin, Despina Greenhaff, Paul L.
Copyright Year	2009
Abstract	We have recently shown that PPARδ agonism, used clinically to treat insulin resistance, increases fat oxidation and up-regulates mitochondrial PDK4 mRNA and protein expression in resting skeletal muscle. We hypothesized that PDK4 up-regulation, which inhibits pyruvate dehydrogenase complex (PDC)-dependent carbohydrate (CHO) oxidation, would negatively affect muscle function during sustained contraction where the demand on CHO is markedly increased. Three groups of eight male Wistar rats each received either vehicle or a PPARδ agonist (GW610742X) at two doses (5 and 100 mg (kg body mass (bm))−1 orally for 6 days. On the seventh day, the gastrocnemius–soleus–plantaris muscle group was isolated and snap frozen, or underwent 30 min of electrically evoked submaximal intensity isometric contraction using a perfused hindlimb model. During contraction, the rate of muscle PDC activation was significantly lower at 100 mg (kg bm)−1 compared with control (P < 0.01). Furthermore, the rates of muscle PCr hydrolysis and lactate accumulation were significantly increased at 100 mg (kg bm)−1 compared with control, reflecting lower mitochondrial ATP generation. Muscle tension development during contraction was significantly lower at 100 mg (kg bm)−1 compared with control (25%; P < 0.05). The present data demonstrate that PPARδ agonism inhibits muscle CHO oxidation at the level of PDC during prolonged contraction, and is paralleled by the activation of anaerobic metabolism, which collectively impair contractile function.
Related Links	http://dx.doi.org/10.1113/jphysiol.2008.164210
Ending Page	239
Page Count	9
Starting Page	231
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 1
Volume Number	587
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2009-01-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

PPARδ agonism inhibits skeletal muscle PDC activity, mitochondrial ATP production and force generation during prolonged contraction

Skeletal muscle metabolism, contraction force and glycogen utilization during prolonged electrical stimulation in humans.

PPARδ agonism induces a change in fuel metabolism and activation of an atrophy programme, but does not impair mitochondrial function in rat skeletal muscle

Skeletal muscle metabolism, contraction force and glycogen utilization during prolonged electrical stimulation in humans.

ATP and heat production in human skeletal muscle during dynamic exercise: higher efficiency of anaerobic than aerobic ATP resynthesis

Energy metabolism and contraction force of human skeletal muscle in situ during electrical stimulation.

ATP utilization for calcium uptake and force production in different types of human skeletal muscle fibres

Energy metabolism and contraction force of human skeletal muscle in situ during electrical stimulation.

Regulation of skeletal muscle PPARδ mRNA expression in twins

PPARδ agonism inhibits skeletal muscle PDC activity, mitochondrial ATP production and force generation during prolonged contraction

Similar Documents

PPARδ agonism inhibits skeletal muscle PDC activity, mitochondrial ATP production and force generation during prolonged contraction

Skeletal muscle metabolism, contraction force and glycogen utilization during prolonged electrical stimulation in humans.

PPARδ agonism induces a change in fuel metabolism and activation of an atrophy programme, but does not impair mitochondrial function in rat skeletal muscle

Skeletal muscle metabolism, contraction force and glycogen utilization during prolonged electrical stimulation in humans.

ATP and heat production in human skeletal muscle during dynamic exercise: higher efficiency of anaerobic than aerobic ATP resynthesis

Energy metabolism and contraction force of human skeletal muscle in situ during electrical stimulation.

ATP utilization for calcium uptake and force production in different types of human skeletal muscle fibres

Energy metabolism and contraction force of human skeletal muscle in situ during electrical stimulation.

Regulation of skeletal muscle PPARδ mRNA expression in twins

PPARδ agonism inhibits skeletal muscle PDC activity, mitochondrial ATP production and force generation during prolonged contraction