Prolonged effect of single carnitine administration on fasted carnitine-deficient JVS mice regarding their locomotor activity and energy expenditure

Li, Meng Xian; Yoshida, Goichiro; Horiuchi, Masahisa; Kobayashi, Keiko; Saheki, Takeyori

doi:10.1016/j.bbalip.2006.08.013

Cited by 7 publications

(6 citation statements)

References 45 publications

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“…Actually, FFA in 24h-fasted JVS mice decreased after ip administration of carnitine as previously reported [10]. Accumulated fatty acids in the hypothalamus and peripheral tissues such as liver produce fatty liver, cardiac hypertrophy, and reduced locomotor activity, in…”

Section: Accepted M Manuscriptsupporting

confidence: 83%

“…Icv administration of carnitine failed to improve anorexia of fasted JVS mice, in marked contrast to the ip administration. Ip administration of carnitine increased brain carnitine concentrations very slightly [10,12]. We have reported the effect of ip administration of carnitine on plasma and tissue carnitine levels [10].…”

Section: Accepted M Manuscriptmentioning

confidence: 80%

“…Ip administration of carnitine increased brain carnitine concentrations very slightly [10,12]. We have reported the effect of ip administration of carnitine on plasma and tissue carnitine levels [10]. Ten µmol of ip administration to 24h-fasted JVS mice increased the carnitine levels largely in liver and plasma, but slightly in heart skeletal muscle and brain [10].…”

Section: Accepted M Manuscriptmentioning

confidence: 87%

“…As a proof, the abnormalities are ameliorated by intraperitoneal administration of carnitine. Fatty liver and locomotor activity reduction observed in this animal model are deteriorated under fasting condition [8][9][10] since fatty acids are a major energy source in fasting [10]. Fasting is avoided in the treatment of patients with fatty acid oxidation (FAO) disorders [11,12] in order to prevent accelerated fatty acid metabolism and hypoglycemia.…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

“…We have reported the effect of ip administration of carnitine on plasma and tissue carnitine levels [10]. Ten µmol of ip administration to 24h-fasted JVS mice increased the carnitine levels largely in liver and plasma, but slightly in heart skeletal muscle and brain [10]. Therefore, carnitine should act to suppress the enhanced CRF signaling through decrease in FFA in the blood and the hypothalamus [39] leading to initiation of feeding.…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

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Failure of the feeding response to fasting in carnitine-deficient juvenile visceral steatosis (JVS) mice: Involvement of defective acyl-ghrelin secretion and enhanced corticotropin-releasing factor signaling in the hypothalamus

Sakoguchi

Horiuchi²,

Asakawa³

et al. 2009

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Carnitine-deficient juvenile visceral steatosis (JVS) mice, suffering from fatty acid metabolism abnormalities, have reduced locomotor activity after fasting. We examined whether JVS mice exhibit specific defect in the feeding response to fasting, a key process of anti-famine homeostatic mechanism. Carnitine-deficient JVS mice showed grossly defective feeding response to 24 h-fasting, with almost no food intake in the first 4 h, in marked contrast to control animals. JVS mice also showed defective acyl-ghrelin response to fasting, less suppressed leptin, and seemingly normal corticotropin-releasing factor (CRF) expression in the hypothalamus despite markedly increased plasma corticosterone. The anorectic response was ameliorated by intraperitoneal administration of carnitine or acyl-ghrelin, with decreased CRF expression. Intracerebroventricular treatment of CRF type 2 receptor antagonist, anti-sauvagine-30, recovered the defective feeding response of 24 h-fasted JVS mice. The defective feeding response to fasting in carnitine-deficient JVS mice is due to the defective acyl-ghrelin and enhanced CRF signaling in the hypothalamus through fatty acid metabolism abnormalities. In this animal model, carnitine normalizes the feeding response through an inhibition of CRF.

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Section: Accepted M Manuscriptsupporting

confidence: 83%

Section: Accepted M Manuscriptmentioning

confidence: 80%

Section: Accepted M Manuscriptmentioning

confidence: 87%

Section: Accepted M Manuscriptmentioning

confidence: 99%

Section: Accepted M Manuscriptmentioning

confidence: 99%

See 3 more Smart Citations

Failure of the feeding response to fasting in carnitine-deficient juvenile visceral steatosis (JVS) mice: Involvement of defective acyl-ghrelin secretion and enhanced corticotropin-releasing factor signaling in the hypothalamus

Sakoguchi

Horiuchi²,

Asakawa³

et al. 2009

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

Self Cite

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l-Carnitine is essential to β-oxidation of quarried fatty acid from mitochondrial membrane by PLA2

et al. 2010

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Mitochondrial beta-oxidation is an important system involved in the energy production of various cells. In this system, the function of L-carnitine is essential for the uptake of fatty acids to mitochondria. However, it is unclear whether or not endogenous respiration, ADP-induced O(2) consumption without substrates, is caused by L-carnitine treatment. In this study, we investigated whether L-carnitine is essential to the beta-oxidation of quarried fatty acids from the mitochondrial membrane by phospholipase A(2) (PLA(2)) using isolated mitochondria from the liver of rats. Intact mitochondria were incubated in a medium containing Pi, CoA and L-carnitine. The effect of L-carnitine treatment on ADP-induced mitochondrial respiration was observed without exogenous respiratory substrate. Increase in mitochondrial respiration was induced by treatment with L-carnitine in a concentration-dependent manner. Treatment with rotenone, a complex I blocker, completely inhibited ADP-induced oxygen consumption even in the presence of L-carnitine. Moreover, the L-carnitine dependent ADP-induced mitochondrial oxygen consumption did not increase when PLA(2) inhibitors were treated before ADP treatment. The L-carnitine-dependent ADP-induced oxygen consumption did contribute to ATP productions but not heat generation via an uncoupling system. These results suggest that L-carnitine might be essential to the beta-oxidation of quarried fatty acids from the mitochondrial membrane by PLA(2).

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Inhibition of fatty acid oxidation activates transforming growth factor-beta in cerebrospinal fluid and decreases spontaneous motor activity

Fujikawa

Fujita

Iwaki

et al. 2010

Physiology & Behavior

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We have previously reported that transforming growth factor (TGF)-beta in the cerebrospinal fluid (CSF) is involved in the mechanism underlying the regulation of spontaneous motor activity (SMA) by the central nervous system after exercise. However, it remained unclear what physiological condition triggers the activation of TGF-beta. We hypothesized that the shortage of energy derived from fatty acid (FA) oxidation observed in the early phase of exercise activated TGF-beta in the CSF. To test this hypothesis, we investigated whether mercaptoacetate (MA), an inhibitor of FA oxidation, could induce an activation of TGF-beta in the CSF and a decrease in SMA. Intraperitoneal (i.p.) administration of MA activated TGF-beta in CSF in rats and depressed SMA; 2-deoxyglucose, an inhibitor of carbohydrate oxidation, on the other hand, depressed SMA but failed to activate CSF TGF-beta. Intracisternal administration of anti-TGF-beta antibody abolished the depressive effect of MA on SMA. We also found that the depression of SMA and the activation of TGF-beta in the CSF by i.p. MA administration were eliminated by vagotomy. Our data suggest that TGF-beta in the CSF is activated by the inhibition of FA oxidation via the vagus nerve and that this subsequently induces depression of SMA.

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Prolonged effect of single carnitine administration on fasted carnitine-deficient JVS mice regarding their locomotor activity and energy expenditure

Cited by 7 publications

References 45 publications

Failure of the feeding response to fasting in carnitine-deficient juvenile visceral steatosis (JVS) mice: Involvement of defective acyl-ghrelin secretion and enhanced corticotropin-releasing factor signaling in the hypothalamus

Failure of the feeding response to fasting in carnitine-deficient juvenile visceral steatosis (JVS) mice: Involvement of defective acyl-ghrelin secretion and enhanced corticotropin-releasing factor signaling in the hypothalamus

l-Carnitine is essential to β-oxidation of quarried fatty acid from mitochondrial membrane by PLA2

Inhibition of fatty acid oxidation activates transforming growth factor-beta in cerebrospinal fluid and decreases spontaneous motor activity

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