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Original Studies |
Expression in Human Skeletal Muscle1
Metabolism and Diabetes Research Group, The Garvan Institute of Medical Research, Sydney, New South Wales 2010, Australia
Address all correspondence and requests for reprints to: Dr. Naras Lapsys, Metabolism and Diabetes Research Group, The Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, New South Wales 2010, Australia. E-mail: n.lapsys{at}garvan.unsw.edu.au
Peroxisome proliferator-activated receptor
(PPAR-
) activation in
adipose tissue is known to regulate genes involved in adipocyte
differentiation and lipid metabolism. However, the role of PPAR-
in
muscle remains unclear. To examine the potential regulation of genes by
PPAR-
in human skeletal muscle, we used semiquantitative RT-PCR to
determine the expression of PPAR-
, lipoprotein lipase (LPL), muscle
carnitine palmitoyl transferase-1 (mCPT1), fatty acid-binding protein
(FABP), carnitine acylcarnitine transferase (CACT), and glucose
transporter-4 (GLUT4) in freeze-dried muscle samples from 14 male
subjects. These samples were dissected free of adipose and other tissue
contamination, as confirmed by minimal or absent adipsin expression.
Between individuals, the messenger ribonucleic acid concentration of
PPAR-
varied up to 3-fold, whereas LPL varied up to 6.5-fold, mCPT1
13-fold, FABP 4-fold, CACT 4-fold, and GLUT4 up to 3-fold. The
expression of LPL (r2 = 0.54; P =
0.003), mCPT1 (r2 = 0.42; P =
0.012), and FABP (r2 = 0.324; P =
0.034) all correlated significantly with PPAR-
expression in the
same samples. No significant correlation was observed between the
expression of CACT and PPAR-
or between GLUT4 and PPAR-
. These
findings demonstrate a relationship between PPAR-
expression and the
expression of other genes of lipid metabolism in muscle and support the
hypothesis that PPAR-
activators such as the antidiabetic
thiazolidinediones may regulate fatty acid metabolism in skeletal
muscle as well as in adipose tissue.
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