Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: UNIPROT:P56851 (
epididymal
)
11,273
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
This study was designed to examine whether short- and long-term treatments by a low level of dietary L-carnitine are capable of altering enzyme activities related to fatty acid oxidation in normal Wistar rats. Under controlled feeding, ten days of treatment changed neither body weights nor liver and gastrocnemius weights, but succeeded in reducing the weight of peri-
epididymal
adipose tissues. Triacylglycerol contents were lowered in liver and ketone body concentrations were found slightly more elevated in blood. In the liver, mitochondrial carnitine palmitoyltransferase I (CPT I) exhibited a slightly higher specific activity and a lower sensitivity to malonyl-CoA inhibition, while peroxisomal fatty acid oxidizing system (PFAOS) was found to be less active. Carnitine supplied for one month reduced the mass of the periepididymal fat tissue, but not those of the other studied organs, and produced a slight but non-significant gain in body weight after ten days of treatment. In the liver,
CPTI
characteristics were comparable in control and treated groups, while PFAOS activity was less in rats receiving carnitine. Data show that L-carnitine at a low level in the diet exerted two paradoxical effects before and after ten days of treatment. Results are discussed in regard to fatty acid oxidation in mitochondria and peroxisomes, and to the possible altered acyl-CoA/acylcarnitine ratio with increased concentrations of L-carnitine in the liver.
...
PMID:Effect of short- and long-term treatments by a low level of dietary L-carnitine on parameters related to fatty acid oxidation in Wistar rat. 855 64
Muscle-type carnitine palmitoyltransferase I (M-CPTI) is the key enzyme for fatty acid beta-oxidation in heart and skeletal muscles and in adipose tissue. So far, M-
CPTI
mRNA has been detected in white adipocytes from
epididymal
fat pads of rats and humans, but not in mouse adipocytes. To characterize the gene expression of M-
CPTI
in mice, we isolated the genomic DNA encoding mouse M-
CPTI
and determined its transcription initiation site. As a result, the mouse M-
CPTI
gene seemed to have multiple initiation sites, as in the case of the rat and human genes. Furthermore, the conserved nucleotide sequence of the response element for peroxisome proliferators was shown to exist in the upstream of the mouse gene as in that of the rat and human genes. From these observations, we suggest that the anomalous expression of M-
CPTI
in mouse adipocytes reported previously may be regulated by factors other than peroxisome proliferators. Previously, we reported that there were transcripts containing regions of both CK/EK-beta and M-
CPTI
genes in humans. In this study, we found that such transcripts also exist in rodents and that the amounts of the transcripts containing regions of both of these genes did not depend on the expression level of CK/EK-beta.
...
PMID:The gene encoding muscle-type carnitine palmitoyltransferase I: comparison of the 5'-upstream region of human and rodent genes. 1276 1