Exposure to a static magnetic field attenuates hepatic damage and function abnormality in obese and diabetic mice

Static magnetic fields (SMFs) exhibit significant effect on health care. However, the effect of SMF on hepatic metabolism and function in obesity and diabetes are still unknown. Liver is not only the main site for glucolipid metabolism but also the core part for iron metabolism regulation. Dysregula...

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Veröffentlicht in:Biochimica et biophysica acta. Molecular basis of disease 2023-08, Vol.1869 (6), p.166719-166719, Article 166719
Hauptverfasser: Lv, Huanhuan, Wang, Yijia, Liu, Junyu, Zhen, Chenxiao, Zhang, Xinyi, Liu, Yuetong, Lou, Chenge, Guo, Huijie, Wei, Yunpeng
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Sprache:eng
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Zusammenfassung:Static magnetic fields (SMFs) exhibit significant effect on health care. However, the effect of SMF on hepatic metabolism and function in obesity and diabetes are still unknown. Liver is not only the main site for glucolipid metabolism but also the core part for iron metabolism regulation. Dysregulations of iron metabolism and redox status are risk factors for the development of hepatic injury and affect glucolipid metabolism in obesity and diabetes. Mice of HFD-induced obesity and HFD/streptozocin-induced diabetes were exposed to a moderate-intensity SMF (0.4–0.7 T, direction: upward, 4 h/day, 8 weeks). Results showed that SMF attenuated hepatic damage by decreasing inflammation and fibrosis in obese and diabetic mice. SMF had no effects on improving glucose/insulin tolerance but regulated proteins (GLUT1 and GLUT4) and genes (G6pc, Pdk4, Gys2 and Pkl) participating in glucose metabolism with phosphorylation of Akt/AMPK/GSK3β. SMF also reduced lipid droplets accumulation through decreasing Plin2 and Plin5 and regulated lipid metabolism with elevated hepatic expressions of PPARγ and C/EBPα in obese mice. In addition, SMF decreased hepatic iron deposition with lower FTH1 expression and modulated systematic iron homeostasis via BMP6-mediated regulation of hepcidin. Moreover, SMF balanced hepatic redox status with regulation on mitochondrial function and MAPKs/Nrf2/HO-1 pathway. Finally, we found that SMF activated hepatic autophagy and enhanced lipophagy by upregulating PNPLA2 expression in obese and diabetic mice. Our results demonstrated that SMF significantly ameliorated the development of hepatic injury in obese and diabetic mice by inhibiting inflammatory level, improving glycolipid metabolism, regulating iron metabolism, balancing redox level and activating autophagy. [Display omitted] •SMF attenuated hepatic damage, regulated glucose metabolism and reduced lipid droplets in obese and diabetic mice.•SMF decreased hepatic iron deposition and modulated systemic iron metabolism through BMP6–mediated regulation of hepcidin in obese and diabetic mice.•SMF decreased hepatic oxidative level, increased antioxidant defense and improved mitochondrial function with activation of MAPKs/Nrf2 /HO-1 antioxidant pathway in obese and diabetic mice.•SMF activated hepatic autophagy to promote lipophagy in obese and diabetic mice.
ISSN:0925-4439
1879-260X
DOI:10.1016/j.bbadis.2023.166719