A mitochondria-targeted vitamin E derivative decreases hepatic oxidative stress and inhibits fat deposition in mice

Gaowei Mao, George A. Kraus, Ikyon Kim, Michael E. Spurlock, Theodore B. Bailey, Qijing Zhang, Donald C. Beitz

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Our objective in this study was to determine whether a mitochondria- targeted vitamin E derivative (MitoVit E) would decrease oxidative stress and associated obesity by preventing a previously proposed aconitase inhibition cascade. Sixty-four mice were fed a high-fat (HF) diet for 5 wk. They were then switched to either a low-fat (LF) or amedium-fat (MF) diet and gavaged with MitoVit E (40 mg MitoVit E . kg body weight-1) or drug vehicle (10% ethanol in 0.9% NaCl solution) every other day for 5 wk. Epididymal fat weight, as well as liver lipid and remaining carcass lipid, were significantly lower in the MF group receiving MitoVit E (MF-E) than in the MF group receiving vehicle only (MF-C). Liver mitochondrial H2O 2 production and the protein carbonyl level were also significantly lower in MF-E than in MF-C mice. In contrast, none of the biochemical variables (aconitase activity, ATP and H2O2 production, and protein carbonyl level) in the muscle mitochondria were modified by MitoVit E in either MF or LF groups. Expression of acetyl-CoA carboxylase and fatty acid synthase in both liver and adipose tissue of MF groups was not affected by MitoVit E. However, expression of carnitine palmitoyltransferase 1a in the liver and uncoupling protein 2 in adipose tissue were significantly enhanced by MitoVit E in both LF and MF groups. In conclusion, MitoVit E attenuates hepatic oxidative stress and inhibits fat deposition in mice but not through alleviation of the aconitase inhibition cascade.

Original languageEnglish
Pages (from-to)1425-1431
Number of pages7
JournalJournal of Nutrition
Volume140
Issue number8
DOIs
Publication statusPublished - 2010 Aug 1

Fingerprint

Vitamin E
Mitochondria
Oxidative Stress
Fats
Aconitate Hydratase
Liver
Adipose Tissue
Muscle Mitochondrion
Carnitine O-Palmitoyltransferase
Lipids
Acetyl-CoA Carboxylase
Fatty Acid Synthases
High Fat Diet
Proteins
Ethanol
Obesity
Adenosine Triphosphate
Body Weight
Diet
Weights and Measures

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

Mao, Gaowei ; Kraus, George A. ; Kim, Ikyon ; Spurlock, Michael E. ; Bailey, Theodore B. ; Zhang, Qijing ; Beitz, Donald C. / A mitochondria-targeted vitamin E derivative decreases hepatic oxidative stress and inhibits fat deposition in mice. In: Journal of Nutrition. 2010 ; Vol. 140, No. 8. pp. 1425-1431.
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abstract = "Our objective in this study was to determine whether a mitochondria- targeted vitamin E derivative (MitoVit E) would decrease oxidative stress and associated obesity by preventing a previously proposed aconitase inhibition cascade. Sixty-four mice were fed a high-fat (HF) diet for 5 wk. They were then switched to either a low-fat (LF) or amedium-fat (MF) diet and gavaged with MitoVit E (40 mg MitoVit E . kg body weight-1) or drug vehicle (10{\%} ethanol in 0.9{\%} NaCl solution) every other day for 5 wk. Epididymal fat weight, as well as liver lipid and remaining carcass lipid, were significantly lower in the MF group receiving MitoVit E (MF-E) than in the MF group receiving vehicle only (MF-C). Liver mitochondrial H2O 2 production and the protein carbonyl level were also significantly lower in MF-E than in MF-C mice. In contrast, none of the biochemical variables (aconitase activity, ATP and H2O2 production, and protein carbonyl level) in the muscle mitochondria were modified by MitoVit E in either MF or LF groups. Expression of acetyl-CoA carboxylase and fatty acid synthase in both liver and adipose tissue of MF groups was not affected by MitoVit E. However, expression of carnitine palmitoyltransferase 1a in the liver and uncoupling protein 2 in adipose tissue were significantly enhanced by MitoVit E in both LF and MF groups. In conclusion, MitoVit E attenuates hepatic oxidative stress and inhibits fat deposition in mice but not through alleviation of the aconitase inhibition cascade.",
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A mitochondria-targeted vitamin E derivative decreases hepatic oxidative stress and inhibits fat deposition in mice. / Mao, Gaowei; Kraus, George A.; Kim, Ikyon; Spurlock, Michael E.; Bailey, Theodore B.; Zhang, Qijing; Beitz, Donald C.

In: Journal of Nutrition, Vol. 140, No. 8, 01.08.2010, p. 1425-1431.

Research output: Contribution to journalArticle

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AU - Kraus, George A.

AU - Kim, Ikyon

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AU - Bailey, Theodore B.

AU - Zhang, Qijing

AU - Beitz, Donald C.

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N2 - Our objective in this study was to determine whether a mitochondria- targeted vitamin E derivative (MitoVit E) would decrease oxidative stress and associated obesity by preventing a previously proposed aconitase inhibition cascade. Sixty-four mice were fed a high-fat (HF) diet for 5 wk. They were then switched to either a low-fat (LF) or amedium-fat (MF) diet and gavaged with MitoVit E (40 mg MitoVit E . kg body weight-1) or drug vehicle (10% ethanol in 0.9% NaCl solution) every other day for 5 wk. Epididymal fat weight, as well as liver lipid and remaining carcass lipid, were significantly lower in the MF group receiving MitoVit E (MF-E) than in the MF group receiving vehicle only (MF-C). Liver mitochondrial H2O 2 production and the protein carbonyl level were also significantly lower in MF-E than in MF-C mice. In contrast, none of the biochemical variables (aconitase activity, ATP and H2O2 production, and protein carbonyl level) in the muscle mitochondria were modified by MitoVit E in either MF or LF groups. Expression of acetyl-CoA carboxylase and fatty acid synthase in both liver and adipose tissue of MF groups was not affected by MitoVit E. However, expression of carnitine palmitoyltransferase 1a in the liver and uncoupling protein 2 in adipose tissue were significantly enhanced by MitoVit E in both LF and MF groups. In conclusion, MitoVit E attenuates hepatic oxidative stress and inhibits fat deposition in mice but not through alleviation of the aconitase inhibition cascade.

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