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Genistein stimulates fatty acid oxidation in a leptin receptor-independent manner through the JAK2-mediated phosphorylation and activation of AMPK in skeletal muscle.
Biochim Biophys Acta 2014; 1841(1):132-40BB

Abstract

Obesity is a public health problem that contributes to the development of insulin resistance, which is associated with an excessive accumulation of lipids in skeletal muscle tissue. There is evidence that soy protein can decrease the ectopic accumulation of lipids and improves insulin sensitivity; however, it is unknown whether soy isoflavones, particularly genistein, can stimulate fatty acid oxidation in the skeletal muscle. Thus, we studied the mechanism by which genistein stimulates fatty acid oxidation in the skeletal muscle. We showed that genistein induced the expression of genes of fatty acid oxidation in the skeletal muscle of Zucker fa/fa rats and in leptin receptor (ObR)-silenced C2C12 myotubes through AMPK phosphorylation. Furthermore, the genistein-mediated AMPK phosphorylation occurred via JAK2, which was possibly activated through a mechanism that involved cAMP. Additionally, the genistein-mediated induction of fatty acid oxidation genes involved PGC1α and PPARδ. As a result, we observed that genistein increased fatty acid oxidation in both the control and silenced C2C12 myotubes, as well as a decrease in the RER in mice, suggesting that genistein can be used in strategies to decrease lipid accumulation in the skeletal muscle.

Authors+Show Affiliations

Posgrado Ciencias Bioquímicas, Facultad de Química, UNAM, México, D.F. 04510, Mexico; Departamento de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México, D.F. 14000, Mexico.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24013029

Citation

Palacios-González, Berenice, et al. "Genistein Stimulates Fatty Acid Oxidation in a Leptin Receptor-independent Manner Through the JAK2-mediated Phosphorylation and Activation of AMPK in Skeletal Muscle." Biochimica Et Biophysica Acta, vol. 1841, no. 1, 2014, pp. 132-40.
Palacios-González B, Zarain-Herzberg A, Flores-Galicia I, et al. Genistein stimulates fatty acid oxidation in a leptin receptor-independent manner through the JAK2-mediated phosphorylation and activation of AMPK in skeletal muscle. Biochim Biophys Acta. 2014;1841(1):132-40.
Palacios-González, B., Zarain-Herzberg, A., Flores-Galicia, I., Noriega, L. G., Alemán-Escondrillas, G., Zariñan, T., ... Tovar, A. R. (2014). Genistein stimulates fatty acid oxidation in a leptin receptor-independent manner through the JAK2-mediated phosphorylation and activation of AMPK in skeletal muscle. Biochimica Et Biophysica Acta, 1841(1), pp. 132-40. doi:10.1016/j.bbalip.2013.08.018.
Palacios-González B, et al. Genistein Stimulates Fatty Acid Oxidation in a Leptin Receptor-independent Manner Through the JAK2-mediated Phosphorylation and Activation of AMPK in Skeletal Muscle. Biochim Biophys Acta. 2014;1841(1):132-40. PubMed PMID: 24013029.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Genistein stimulates fatty acid oxidation in a leptin receptor-independent manner through the JAK2-mediated phosphorylation and activation of AMPK in skeletal muscle. AU - Palacios-González,Berenice, AU - Zarain-Herzberg,Angel, AU - Flores-Galicia,Isabel, AU - Noriega,Lilia G, AU - Alemán-Escondrillas,Gabriela, AU - Zariñan,Teresa, AU - Ulloa-Aguirre,Alfredo, AU - Torres,Nimbe, AU - Tovar,Armando R, Y1 - 2013/09/05/ PY - 2013/05/22/received PY - 2013/08/02/revised PY - 2013/08/27/accepted PY - 2013/9/10/entrez PY - 2013/9/10/pubmed PY - 2014/2/22/medline KW - 007 KW - 5-amino 4-imidazolecarboxamide ribose KW - 5′-adenosine monophosphate-activated protein kinase KW - 8-(4-chlorophenylthio)-2-Omethyladenosine-3,5-cAMP KW - ACC KW - AICAR KW - AMPK KW - CAMKKβ KW - CPT1 KW - Ca(2+)/calmodulin-dependent protein kinase kinase β KW - Epac1 KW - FAO KW - FFA KW - Fatty acid oxidation KW - Genistein KW - HF KW - JAK2 KW - Janus kinase 2 KW - LEPR KW - ObR KW - PDE4 KW - PLC KW - PPARα KW - PPARδ KW - SCD KW - SIRT1 KW - SP KW - SREBP1c KW - Skeletal muscle KW - Soy protein KW - UCP3 KW - acetyl CoA carboxylase KW - cAMP-regulated guanine nucleotide exchange factor KW - carnitine palmitoyl transferase-1 KW - fatty acid oxidation KW - free fatty acids KW - high fat KW - leptin receptor KW - peroxisome proliferator activated receptor-δ PGC-1α, PPAR-γ coactivator-1α KW - peroxisome proliferator-activated receptor-α KW - phosphodiesterases KW - phospholipase C KW - sirtuin 1 KW - soy protein KW - stearoyl-CoA desaturase-1 KW - sterol regulatory element binding protein-1c KW - uncoupling carrier protein 3 SP - 132 EP - 40 JF - Biochimica et biophysica acta JO - Biochim. Biophys. Acta VL - 1841 IS - 1 N2 - Obesity is a public health problem that contributes to the development of insulin resistance, which is associated with an excessive accumulation of lipids in skeletal muscle tissue. There is evidence that soy protein can decrease the ectopic accumulation of lipids and improves insulin sensitivity; however, it is unknown whether soy isoflavones, particularly genistein, can stimulate fatty acid oxidation in the skeletal muscle. Thus, we studied the mechanism by which genistein stimulates fatty acid oxidation in the skeletal muscle. We showed that genistein induced the expression of genes of fatty acid oxidation in the skeletal muscle of Zucker fa/fa rats and in leptin receptor (ObR)-silenced C2C12 myotubes through AMPK phosphorylation. Furthermore, the genistein-mediated AMPK phosphorylation occurred via JAK2, which was possibly activated through a mechanism that involved cAMP. Additionally, the genistein-mediated induction of fatty acid oxidation genes involved PGC1α and PPARδ. As a result, we observed that genistein increased fatty acid oxidation in both the control and silenced C2C12 myotubes, as well as a decrease in the RER in mice, suggesting that genistein can be used in strategies to decrease lipid accumulation in the skeletal muscle. SN - 0006-3002 UR - https://www.unboundmedicine.com/medline/citation/24013029/Genistein_stimulates_fatty_acid_oxidation_in_a_leptin_receptor_independent_manner_through_the_JAK2_mediated_phosphorylation_and_activation_of_AMPK_in_skeletal_muscle_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1388-1981(13)00189-3 DB - PRIME DP - Unbound Medicine ER -