Open AccessAcute Exercise Stimulates Carnitine Biosynthesis and OCTN2 Expression in Mouse Kidney
Author(s) -
Broderick Tom L.,
Cusimano Frank A.,
Carlson Chelsea,
Tamura Leslie K.
Publication year - 2017
Publication title -
kidney and blood pressure research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.806
H-Index - 51
eISSN - 1423-0143
pISSN - 1420-4096
DOI - 10.1159/000478737
Subject(s) - original paper
Background/Aims: Carnitine is essential for the transport of long-chain FAs (FA) into the mitochondria for energy production. During acute exercise, the increased demand for FAs results in a state of free carnitine deficiency in plasma. The role of kidney in carnitine homeostasis after exercise is not known. Methods: Swiss Webster mice were sacrificed immediately after a 1-hour moderate intensity treadmill run, and at 4-hours and 8-hours into recovery. Non-exercising mice served as controls. Plasma was analyzed for carnitine using acetyltransferase and [<sup>14</sup>C] acetyl-CoA. Kidney was removed for gene and protein expression of butyrobetaine hydroxylase (γ-BBH), organic cation transporter (OCTN2), and peroxisome proliferator-activated receptor (PPARα), a regulator of fatty acid oxidation activated by FAs. Results: Acute exercise caused a decrease in plasma free carnitine levels. Rapid return of free carnitine to control levels during recovery was associated with increased γ-BBH expression. Both mRNA and protein levels of OCTN2 were detected in kidney after exercise and during recovery, suggesting renal transport mechanisms were stimulated. These changes were accompanied with a reciprocal increase in PPARα protein expression. Conclusions: Our results show that the decrease in free carnitine after exercise rapidly activates carnitine biosynthesis and renal transport mechanism in kidney to establish carnitine homeostasis.