Higher levels of ATGL are associated with exercise-induced enhancement of lipolysis in rat epididymal adipocytes

In adipose cells, adipose triglyceride lipase (ATGL) catalyzes the first step in adipocyte triacylglyceride hydrolysis, thereby regulating both basal and hormone-stimulated lipolysis. However, little is known about the molecular mechanism(s) underlying habitual exercise-induced adaptive modulation o...

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Veröffentlicht in:PloS one 2012-07, Vol.7 (7), p.e40876
Hauptverfasser: Ogasawara, Junetsu, Sakurai, Takuya, Kizaki, Takako, Ishibashi, Yoshinaga, Izawa, Tetsuya, Sumitani, Yoshikazu, Ishida, Hitoshi, Radak, Zsolt, Haga, Shukoh, Ohno, Hideki
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creator Ogasawara, Junetsu
Sakurai, Takuya
Kizaki, Takako
Ishibashi, Yoshinaga
Izawa, Tetsuya
Sumitani, Yoshikazu
Ishida, Hitoshi
Radak, Zsolt
Haga, Shukoh
Ohno, Hideki
description In adipose cells, adipose triglyceride lipase (ATGL) catalyzes the first step in adipocyte triacylglyceride hydrolysis, thereby regulating both basal and hormone-stimulated lipolysis. However, little is known about the molecular mechanism(s) underlying habitual exercise-induced adaptive modulation of ATGL in white adipocytes via alteration in transcription regulator and lipolytic cofactors. Male Wistar rats were randomly divided into 2 groups a sedentary control group (CG) and a habitual exercise group (EG). The EG was subjected to running on a treadmill set at 5 days per week for 9 weeks. The CG was not subjected to running on a treadmill. In the EG, levels of ATGL mRNA and protein were elevated with a significant increase in lipolysis compared with the CG, accompanied by a significant increase in associations of CGI-58 with ATGL protein. Under these conditions, an upregulation of peroxisome proliferation-activated receptorg-2 (PPARg-2) was observed. In the EG, the addition of rosiglitazone further significantly increased the levels of ATGL protein compared with the CG. However, attenuated levels of the ATGL protein in adipocytes were obtained by the addition of insulin, which is known to inhibit the expression of ATGL, in both types of groups. Actually, levels of plasma insulin were significantly reduced in the EG compared with the CG. These data suggest that elevated levels of ATGL are involved in the exercise-induced enhancement of lipolysis in primary adipocytes. The exact mechanism(s) underlying this phenomenon is associated, at least in part, with upregulated transcriptional activation of PPARg-2. In addition, exercise-induced lower circulation levels of insulin also correlate with habitual exercise-induced higher levels of ATGL in primary adipocytes.
doi_str_mv 10.1371/journal.pone.0040876
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subjects Acyltransferases
Adipocytes
Adipocytes - drug effects
Adipocytes - enzymology
Animals
Biology
Body Weight - drug effects
Carrier Proteins - metabolism
Cofactors
DNA - metabolism
Epididymis - cytology
Exercise
Fatty acids
Gene Expression Regulation, Enzymologic - drug effects
Glycerol
HeLa Cells
Hormones
Humans
Hydrolysis
Insulin
Insulin - blood
Insulin - pharmacology
Insulin resistance
Internal medicine
Kinases
Laboratory animals
Lipase
Lipase - genetics
Lipase - metabolism
Lipids
Lipolysis
Lipolysis - drug effects
Male
Medicine
Metabolism
Organ Size - drug effects
Perilipin-1
Peroxisome proliferator-activated receptors
Phosphoproteins - metabolism
Physical Conditioning, Animal
Physical training
PPAR gamma - genetics
PPAR gamma - metabolism
Protein Binding - drug effects
Proteins
Rats
Rats, Wistar
RNA
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rosiglitazone
Sport science
Sterol Esterase - metabolism
Thiazolidinediones - pharmacology
Transcription activation
Triglycerides
title Higher levels of ATGL are associated with exercise-induced enhancement of lipolysis in rat epididymal adipocytes
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