Coenzyme Q10 increases the fatty acid oxidation through AMPK-mediated PPARα induction in 3T3-L1 preadipocytes

Soo Kyung Lee, Jung Ok Lee, Ji Hae Kim, Nami Kim, Ga Young You, Ji Wook Moon, Jie Sha, Su Jin Kim, Yong Woo Lee, Ho Jin Kang, Sun-Hwa Park, Hyeon Soo Kim

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Coenzyme Q10(CoQ10) is a known anti-adipogenic factor. However, the mechanism by which CoQ10 acts is unclear. In this study, we found that CoQ10 increased the phosphorylation of AMP-activated protein kinase (AMPK) in 3T3-L1preadipocytes. CoQ10 induced an increase in cytoplasmic calcium concentrations, which is reflected by increased Fluo-3 intensity under confocal microscopy recording. Either inhibition of Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) or knock-down CaMKK blocked CoQ10-induced AMPK phosphorylation, suggesting the involvement of calcium in CoQ10-mediated AMPK signaling. CoQ10 also increased the expression of peroxisome proliferator-activated receptor alpha (PPARα) at both the mRNA and protein levels. Knock down of AMPK with siRNA or inhibition of AMPK using an AMPK inhibitor compound C blocked CoQ10-induced expression of PPARα, indicating that AMPK plays a critical role in PPARα induction. In addition, CoQ10 increased fatty acid oxidation in 3T3-L1preadipocytes. The promoter activity of PPARα was increased by CoQ10 in an AMPK-dependent fashion. Moreover, the induction of acyl-CoA oxidase (ACO), a target gene of PPARα, was blocked under the PPARα knock down condition. Furthermore, treatment with CoQ10 blocked differentiation-induced adipogenesis. This blockade was not observed under the PPARα knock-down condition. Collectively, these results demonstrate that CoQ10 induces PPARα expression via the calcium-mediated AMPK signal pathway and suppresses differentiation-induced adipogenesis.

Original languageEnglish
Pages (from-to)2329-2336
Number of pages8
JournalCellular Signalling
Volume24
Issue number12
DOIs
Publication statusPublished - 2012 Dec 1

Fingerprint

coenzyme Q10
PPAR alpha
AMP-Activated Protein Kinases
Fatty Acids
Adipogenesis
Calcium-Calmodulin-Dependent Protein Kinases
Calcium
Phosphotransferases
Phosphorylation

Keywords

  • Adipogenesis
  • AMPK
  • Coenzyme Q10
  • Fatty acid oxidation
  • PPARα

ASJC Scopus subject areas

  • Cell Biology

Cite this

Coenzyme Q10 increases the fatty acid oxidation through AMPK-mediated PPARα induction in 3T3-L1 preadipocytes. / Lee, Soo Kyung; Lee, Jung Ok; Kim, Ji Hae; Kim, Nami; You, Ga Young; Moon, Ji Wook; Sha, Jie; Kim, Su Jin; Lee, Yong Woo; Kang, Ho Jin; Park, Sun-Hwa; Kim, Hyeon Soo.

In: Cellular Signalling, Vol. 24, No. 12, 01.12.2012, p. 2329-2336.

Research output: Contribution to journalArticle

Lee, SK, Lee, JO, Kim, JH, Kim, N, You, GY, Moon, JW, Sha, J, Kim, SJ, Lee, YW, Kang, HJ, Park, S-H & Kim, HS 2012, 'Coenzyme Q10 increases the fatty acid oxidation through AMPK-mediated PPARα induction in 3T3-L1 preadipocytes', Cellular Signalling, vol. 24, no. 12, pp. 2329-2336. https://doi.org/10.1016/j.cellsig.2012.07.022
Lee, Soo Kyung ; Lee, Jung Ok ; Kim, Ji Hae ; Kim, Nami ; You, Ga Young ; Moon, Ji Wook ; Sha, Jie ; Kim, Su Jin ; Lee, Yong Woo ; Kang, Ho Jin ; Park, Sun-Hwa ; Kim, Hyeon Soo. / Coenzyme Q10 increases the fatty acid oxidation through AMPK-mediated PPARα induction in 3T3-L1 preadipocytes. In: Cellular Signalling. 2012 ; Vol. 24, No. 12. pp. 2329-2336.
@article{27e15d24985e46d3975844023ea809d1,
title = "Coenzyme Q10 increases the fatty acid oxidation through AMPK-mediated PPARα induction in 3T3-L1 preadipocytes",
abstract = "Coenzyme Q10(CoQ10) is a known anti-adipogenic factor. However, the mechanism by which CoQ10 acts is unclear. In this study, we found that CoQ10 increased the phosphorylation of AMP-activated protein kinase (AMPK) in 3T3-L1preadipocytes. CoQ10 induced an increase in cytoplasmic calcium concentrations, which is reflected by increased Fluo-3 intensity under confocal microscopy recording. Either inhibition of Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) or knock-down CaMKK blocked CoQ10-induced AMPK phosphorylation, suggesting the involvement of calcium in CoQ10-mediated AMPK signaling. CoQ10 also increased the expression of peroxisome proliferator-activated receptor alpha (PPARα) at both the mRNA and protein levels. Knock down of AMPK with siRNA or inhibition of AMPK using an AMPK inhibitor compound C blocked CoQ10-induced expression of PPARα, indicating that AMPK plays a critical role in PPARα induction. In addition, CoQ10 increased fatty acid oxidation in 3T3-L1preadipocytes. The promoter activity of PPARα was increased by CoQ10 in an AMPK-dependent fashion. Moreover, the induction of acyl-CoA oxidase (ACO), a target gene of PPARα, was blocked under the PPARα knock down condition. Furthermore, treatment with CoQ10 blocked differentiation-induced adipogenesis. This blockade was not observed under the PPARα knock-down condition. Collectively, these results demonstrate that CoQ10 induces PPARα expression via the calcium-mediated AMPK signal pathway and suppresses differentiation-induced adipogenesis.",
keywords = "Adipogenesis, AMPK, Coenzyme Q10, Fatty acid oxidation, PPARα",
author = "Lee, {Soo Kyung} and Lee, {Jung Ok} and Kim, {Ji Hae} and Nami Kim and You, {Ga Young} and Moon, {Ji Wook} and Jie Sha and Kim, {Su Jin} and Lee, {Yong Woo} and Kang, {Ho Jin} and Sun-Hwa Park and Kim, {Hyeon Soo}",
year = "2012",
month = "12",
day = "1",
doi = "10.1016/j.cellsig.2012.07.022",
language = "English",
volume = "24",
pages = "2329--2336",
journal = "Cellular Signalling",
issn = "0898-6568",
publisher = "Elsevier Inc.",
number = "12",

}

TY - JOUR

T1 - Coenzyme Q10 increases the fatty acid oxidation through AMPK-mediated PPARα induction in 3T3-L1 preadipocytes

AU - Lee, Soo Kyung

AU - Lee, Jung Ok

AU - Kim, Ji Hae

AU - Kim, Nami

AU - You, Ga Young

AU - Moon, Ji Wook

AU - Sha, Jie

AU - Kim, Su Jin

AU - Lee, Yong Woo

AU - Kang, Ho Jin

AU - Park, Sun-Hwa

AU - Kim, Hyeon Soo

PY - 2012/12/1

Y1 - 2012/12/1

N2 - Coenzyme Q10(CoQ10) is a known anti-adipogenic factor. However, the mechanism by which CoQ10 acts is unclear. In this study, we found that CoQ10 increased the phosphorylation of AMP-activated protein kinase (AMPK) in 3T3-L1preadipocytes. CoQ10 induced an increase in cytoplasmic calcium concentrations, which is reflected by increased Fluo-3 intensity under confocal microscopy recording. Either inhibition of Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) or knock-down CaMKK blocked CoQ10-induced AMPK phosphorylation, suggesting the involvement of calcium in CoQ10-mediated AMPK signaling. CoQ10 also increased the expression of peroxisome proliferator-activated receptor alpha (PPARα) at both the mRNA and protein levels. Knock down of AMPK with siRNA or inhibition of AMPK using an AMPK inhibitor compound C blocked CoQ10-induced expression of PPARα, indicating that AMPK plays a critical role in PPARα induction. In addition, CoQ10 increased fatty acid oxidation in 3T3-L1preadipocytes. The promoter activity of PPARα was increased by CoQ10 in an AMPK-dependent fashion. Moreover, the induction of acyl-CoA oxidase (ACO), a target gene of PPARα, was blocked under the PPARα knock down condition. Furthermore, treatment with CoQ10 blocked differentiation-induced adipogenesis. This blockade was not observed under the PPARα knock-down condition. Collectively, these results demonstrate that CoQ10 induces PPARα expression via the calcium-mediated AMPK signal pathway and suppresses differentiation-induced adipogenesis.

AB - Coenzyme Q10(CoQ10) is a known anti-adipogenic factor. However, the mechanism by which CoQ10 acts is unclear. In this study, we found that CoQ10 increased the phosphorylation of AMP-activated protein kinase (AMPK) in 3T3-L1preadipocytes. CoQ10 induced an increase in cytoplasmic calcium concentrations, which is reflected by increased Fluo-3 intensity under confocal microscopy recording. Either inhibition of Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) or knock-down CaMKK blocked CoQ10-induced AMPK phosphorylation, suggesting the involvement of calcium in CoQ10-mediated AMPK signaling. CoQ10 also increased the expression of peroxisome proliferator-activated receptor alpha (PPARα) at both the mRNA and protein levels. Knock down of AMPK with siRNA or inhibition of AMPK using an AMPK inhibitor compound C blocked CoQ10-induced expression of PPARα, indicating that AMPK plays a critical role in PPARα induction. In addition, CoQ10 increased fatty acid oxidation in 3T3-L1preadipocytes. The promoter activity of PPARα was increased by CoQ10 in an AMPK-dependent fashion. Moreover, the induction of acyl-CoA oxidase (ACO), a target gene of PPARα, was blocked under the PPARα knock down condition. Furthermore, treatment with CoQ10 blocked differentiation-induced adipogenesis. This blockade was not observed under the PPARα knock-down condition. Collectively, these results demonstrate that CoQ10 induces PPARα expression via the calcium-mediated AMPK signal pathway and suppresses differentiation-induced adipogenesis.

KW - Adipogenesis

KW - AMPK

KW - Coenzyme Q10

KW - Fatty acid oxidation

KW - PPARα

UR - http://www.scopus.com/inward/record.url?scp=84865625922&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84865625922&partnerID=8YFLogxK

U2 - 10.1016/j.cellsig.2012.07.022

DO - 10.1016/j.cellsig.2012.07.022

M3 - Article

VL - 24

SP - 2329

EP - 2336

JO - Cellular Signalling

JF - Cellular Signalling

SN - 0898-6568

IS - 12

ER -