File:Schematic description of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) function in various organs.jpg

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English: Schematic description of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) function in various organs. Traditionally, in brown adipocytes (BAT) and white adipocytes (WAT), mitochondrial biogenesis and BAT gene expression are regulated by PGC-1α. Adrenergic stimulation and lower temperature trigger signaling cascades, including the upregulation of UCP-1 level, thereby resulting in body thermogenesis. In skeletal muscle and WAT, the transcriptional activity of PGC-1α is responsible for the expression of gene networks that control glucose uptake, glycolysis, fatty acid (FA) oxidation, tricarboxylic acid cycle, oxidative phosphorylation (OXPHOS), mitochondrial biogenesis, and protein uncoupling. Therefore, increasing exercise will increase mitochondrial gene biogenesis and secretion of myokines (such as irisin), which results in WAT browning and liver gluconeogenesis to prevent obesity and insulin resistance. In epicardial adipose tissue (EAT), increased heme oxygenase 1 (HO-1) expression depends on the PGC-1α–UCP-1 axis activity, which then decreases free radicals and reactive oxygen species (ROS) production, thus reducing cardiomyopathy. However, whether increased expression of cytokines such as TNF-α, IL-6, or adipokines by the PGC-1α–UCP-1 axis can reduce cardiomyopathy or not is still unclear.
Español: Descripción esquemática de la función del coactivador gamma-1α (PGC-1α) del receptor activado por proliferador de peroxisomas en varios órganos. Tradicionalmente, en los adipocitos marrones (BAT) y los adipocitos blancos (WAT), la biogénesis mitocondrial y la expresión del gen BAT están reguladas por PGC-1α. La estimulación adrenérgica y la temperatura más baja desencadenan cascadas de señalización, incluida la regulación positiva del nivel de UCP-1, lo que resulta en la termogénesis corporal. En el músculo esquelético y WAT, la actividad transcripcional de PGC-1α es responsable de la expresión de redes genéticas que controlan la captación de glucosa, la glucólisis, la oxidación de los ácidos grasos (FA), el ciclo de los ácidos tricarboxílicos, la fosforilación oxidativa (OXPHOS), la biogénesis mitocondrial y la proteína. desacoplamiento. Por lo tanto, aumentar el ejercicio aumentará la biogénesis de los genes mitocondriales y la secreción de mioquinas (como la irisina), lo que da como resultado el pardeamiento del WAT y la gluconeogénesis hepática para prevenir la obesidad y la resistencia a la insulina. En el tejido adiposo epicárdico (EAT), el aumento de la expresión de hemo oxigenasa 1 (HO-1) depende de la actividad del eje PGC-1α-UCP-1, que luego disminuye la producción de radicales libres y especies reactivas de oxígeno (ROS), reduciendo así la miocardiopatía. Sin embargo, aún no está claro si el aumento de la expresión de citocinas como TNF-α, IL-6 o adipocinas por el eje PGC-1α-UCP-1 puede reducir la miocardiopatía o no.
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Source https://www.mdpi.com/1422-0067/19/11/3447
Author MDPI

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