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Biofactors ; 42(6): 638-646, 2016 Nov 12.
Artículo en Inglés | MEDLINE | ID: mdl-27248050

RESUMEN

Prevention of ischemia-reperfusion liver injury is achieved by a combined omega-3 and thyroid hormone (T3 ) protocol, which may involve peroxisome-proliferator activated receptor-α (PPAR-α)-fibroblast growth factor 21 (FGF21) signaling supporting energy requirements. Combined docosahexaenoic acid (DHA; daily doses of 300 mg/kg for 3 days) plus 0.05 mg T3 /kg given to fed rats elicited higher hepatic DHA contents and serum T3 levels, increased PPAR-α mRNA and its DNA binding, with higher mRNA expression of the PPAR-α target genes for carnitine-palmitoyl transferase 1α, acyl-CoA oxidase, and 3-hydroxyl-3-methylglutaryl-CoA synthase 2, effects that were mimicked by 0.1 mg T3 /kg given alone or by the PPAR-α agonist WY-14632. Under these conditions, the mRNA expression of retinoic X receptor-α (RXR-α) is also increased, with concomitant elevation of the hepatic mRNA and protein FGF21 levels and those of serum FGF21. It is concluded that PPAR-α-FGF21 induction by DHA combined with T3 may involve ligand activation of PPAR-α by DHA and enhanced expression of PPAR-α by T3 , with consequent upregulation of the FGF21 that is controlled by PPAR-α. Considering the beneficial effects of PPAR-α-FGF21 signaling on carbohydrate and lipid metabolism, further investigations are required to clarify its potential therapeutic applications in human metabolic disorders. © 2016 BioFactors, 42(6):638-646, 2016.


Asunto(s)
Ácidos Docosahexaenoicos/farmacología , Factores de Crecimiento de Fibroblastos/metabolismo , Hígado/metabolismo , PPAR alfa/metabolismo , Daño por Reperfusión/prevención & control , Triyodotironina/farmacología , Animales , Ácidos Docosahexaenoicos/farmacocinética , Ácidos Docosahexaenoicos/uso terapéutico , Evaluación Preclínica de Medicamentos , Quimioterapia Combinada , Factores de Crecimiento de Fibroblastos/genética , Expresión Génica/efectos de los fármacos , Hígado/efectos de los fármacos , Masculino , PPAR alfa/genética , Ratas Sprague-Dawley , Receptor alfa X Retinoide/genética , Receptor alfa X Retinoide/metabolismo , Transducción de Señal , Activación Transcripcional , Triyodotironina/farmacocinética , Triyodotironina/uso terapéutico , Regulación hacia Arriba
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