Abstract:
:Recently, the marked decline in renal carnitine reabsorption has been thought to account fotr the systemic carnitine deficiency in juvenile visceral steatosis (JVS) mice. We have conducted a kinetic analysis using embryonic fibroblasts derived from normal, heterozygous, and homozygous jvs mice and found that the high-affinity carnitine transporter (Km = 5.5 microM), which shows Na+ and temperature dependency and stereospecificity, is defective in homozygous jvs mice. Moreover, a gene dose-dependent decrease of carnitine transport activity, which was due to a decrease in the number of the transporter molecules, was found in heterozygous jvs mice. Similar phenomena have been observed in human primary carnitine deficiency. Therefore, JVS mice may be useful for understanding this extremely rare human hereditary disorder.
journal_name
Biochem Pharmacoljournal_title
Biochemical pharmacologyauthors
Hashimoto N,Suzuki F,Tamai I,Nikaido H,Kuwajima M,Hayakawa J,Tsuji Adoi
10.1016/s0006-2952(97)00670-9subject
Has Abstractpub_date
1998-05-15 00:00:00pages
1729-32issue
10eissn
0006-2952issn
1873-2968pii
S0006295297006709journal_volume
55pub_type
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