Endurance training enhances LXRα gene expression in Wistar male rats

Abstract

Liver X receptor α (LXRα) is a member of the ligand-activated transcription factor of nuclear hormonal receptor superfamily, whose activation leads to modulation in the expression of genes involved in cholesterol homeostasis including ATP-binding cassette transporter A1 (ABCA1), which plays a crucial role in plasma high-density lipoprotein cholesterol (HDL-C) remodeling. The purpose of this study was to investigate whether endurance training enhanced the expression level of liver LXRα gene. Twelve adult male Wistar rats (200-220 g) were divided into control and training groups. Training group received exercise on a motor-driven treadmill at 28 m/min (0 % grade) for 60 min/day, 5 days/week for 8 weeks. Twenty-four hours after the last exercise session, the rats were killed and blood was taken from the right ventricle of each rat. Plasma was collected for HDL-C, low-density lipoprotein cholesterol (LDL-C), TC and TG measurements. Furthermore, a portion of the liver of each rat was excised and washed in ice-cold saline and frozen in liquid nitrogen for assessment of LXRα and ABCA1 mRNA levels. Data indicated significant increase in both LXRα and ABCA1 mRNA levels in trained rats, compared to control rats. Plasma HDL-C concentration was significantly higher (P < 0.001) in trained rats at the end of treadmill exercise. However, there was a significant decrease in LDL-C (P < 0.003), TG, TC concentration, TC/HDL-C and LDL/HDL-C ratios in trained rats compared with those in the control group (P < 0.001). In conclusion, we found that endurance training induced significant elevation in LXRα gene expression, which correlated with enhanced levels of ABCA1 mRNA and plasma HDL-C concentration.

Previous physical exercise alters the hepatic profile of oxidative‐inflammatory status and limits the secondary brain damage induced by severe traumatic brain injury in rats

“…; Kazeminasab et al . ). Noteworthy, inflammatory modulation may differ among TBI acute and delayed phases (Ziebell & Morganti‐Kossmann, ).…”

“…Apart from being glucose sensors (Mitro et al 2007), LXRs also induce genes that inhibit the expression of inflammatory mediators, such as the ABCA1 (Spillmann et al 2014). Because glucose is an endogenous LXR ligand and ABCA1 inhibits the expression of inflammatory mediators (Spillmann et al 2014), it is plausible to propose that the anti-inflammatory effects elicited by exercise training involve hepatic glycogen metabolism (Hoene & Weigert, 2010) followed by LXR-α and ABCA1 mRNA increases (Ghanbari-Niaki et al 2007;Kazeminasab et al 2013). Noteworthy, inflammatory modulation may differ among TBI acute and delayed phases (Ziebell & Morganti-Kossmann, 2010).…”

Pengaruh Minyak Zaitun dan Olahraga Terhadap Kadar Trigliserida Tikus Wistar Diet Tinggi Lemak

“…Contoh olahraga aerobik termasuk bersepeda, menari, hiking, jogging, berenang, berjalan, dan yang semisalnya. Pada penelitian sebelumnya dilaporkan bahwa terdapat penurunan kadar trigliserida secara signifikan pada tikus terlatih setelah 8 minggu menjalankan program treadmill (10,11). (8,15).…”

Treinamento físico aeróbio altera seletivamente a concentração e o metabolismo arterial de óxidos de colesterol e reduz colesterol na aorta de camundongos dislipidêmicos

“…Corroborando o pensamento de que o exercício físico é um modulador positivo do transporte reverso de colesterol, outros autores ainda demonstram aumento da expressão gênica de Abca1, Abcg1 e Nr1h3 (LXRα) em diferentes tecidos (Butcher et al, 2008;Ghorbanian et al, 2013;Kazeminasab et al, 2013;Rocco et al, 2011).…”

“…Nesses dois modelos, o aumento no transporte reverso de colesterol pelo exercício regular foi atribuído a moduladores sistêmicos, como o aumento do HDL-c e maior expressão de receptores hepáticos para as lipoproteínas, como SR-BI e B-E. Corroborando o pensamento de que o exercício físico é um modulador positivo do transporte reverso de colesterol, outros autores ainda demonstram aumento da expressão gênica de Abca1, Abcg1 e Nr1h3 (LXRα) em diferentes tecidos (Butcher et al, 2008;Ghorbanian et al, 2013;Khabazian et al, 2009;Rocco et al, 2011;Kazeminasab et al, 2013).…”