Exposure to a static magnetic field attenuates hepatic damage and function abnormality in obese and diabetic mice
← Research streamIn obese and diabetic mouse models, exposure to a moderate-intensity static magnetic field (0.4–0.7 T, upward direction, 4 h/day for 8 weeks) decreased hepatic inflammation and fibrosis and reduced hepatic iron deposition, while modulating pathways related to…
Study snapshot
Abstract
Exposure to a static magnetic field attenuates hepatic damage and function abnormality in obese and diabetic mice Lv H, Wang Y, Liu J, Zhen C, Zhang X, Liu Y, Lou C, Guo H, Wei Y. Exposure to a static magnetic field attenuates hepatic damage and function abnormality in obese and diabetic mice. Biochim Biophys Acta Mol Basis Dis. 2023 Apr 26;1869(6):166719. doi: 10.1016/j.bbadis.2023.166719. Abstract 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. pubmed.ncbi.nlm.nih.gov
AI evidence extraction
Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.
Main findings
In obese and diabetic mouse models, exposure to a moderate-intensity static magnetic field (0.4–0.7 T, upward direction, 4 h/day for 8 weeks) decreased hepatic inflammation and fibrosis and reduced hepatic iron deposition, while modulating pathways related to redox balance and autophagy/lipophagy. The SMF did not improve glucose/insulin tolerance but was reported to regulate multiple glucose- and lipid-metabolism-related proteins/genes and signaling pathways.
Outcomes measured
- Hepatic damage (inflammation, fibrosis)
- Glucose/insulin tolerance
- Glucose metabolism markers (GLUT1, GLUT4; G6pc, Pdk4, Gys2, Pkl; Akt/AMPK/GSK3β phosphorylation)
- Hepatic lipid droplets accumulation; Plin2, Plin5; PPARγ, C/EBPα expression
- Hepatic iron deposition; FTH1 expression; systemic iron homeostasis (BMP6/hepcidin)
- Hepatic redox status; mitochondrial function; MAPKs/Nrf2/HO-1 pathway
- Hepatic autophagy/lipophagy; PNPLA2 expression
Limitations
- Sample size not reported in abstract
- Animal study; generalizability to humans not addressed in abstract
- Exposure source/context not specified beyond field strength, direction, and schedule
View raw extracted JSON
{
"study_type": "animal",
"exposure": {
"band": "static",
"source": null,
"frequency_mhz": null,
"sar_wkg": null,
"duration": "4 h/day for 8 weeks"
},
"population": "Mice with HFD-induced obesity and HFD/streptozocin-induced diabetes",
"sample_size": null,
"outcomes": [
"Hepatic damage (inflammation, fibrosis)",
"Glucose/insulin tolerance",
"Glucose metabolism markers (GLUT1, GLUT4; G6pc, Pdk4, Gys2, Pkl; Akt/AMPK/GSK3β phosphorylation)",
"Hepatic lipid droplets accumulation; Plin2, Plin5; PPARγ, C/EBPα expression",
"Hepatic iron deposition; FTH1 expression; systemic iron homeostasis (BMP6/hepcidin)",
"Hepatic redox status; mitochondrial function; MAPKs/Nrf2/HO-1 pathway",
"Hepatic autophagy/lipophagy; PNPLA2 expression"
],
"main_findings": "In obese and diabetic mouse models, exposure to a moderate-intensity static magnetic field (0.4–0.7 T, upward direction, 4 h/day for 8 weeks) decreased hepatic inflammation and fibrosis and reduced hepatic iron deposition, while modulating pathways related to redox balance and autophagy/lipophagy. The SMF did not improve glucose/insulin tolerance but was reported to regulate multiple glucose- and lipid-metabolism-related proteins/genes and signaling pathways.",
"effect_direction": "benefit",
"limitations": [
"Sample size not reported in abstract",
"Animal study; generalizability to humans not addressed in abstract",
"Exposure source/context not specified beyond field strength, direction, and schedule"
],
"evidence_strength": "low",
"confidence": 0.78,
"peer_reviewed_likely": "yes",
"keywords": [
"static magnetic field",
"SMF",
"0.4-0.7 T",
"obesity",
"diabetes",
"mouse",
"liver",
"hepatic injury",
"inflammation",
"fibrosis",
"iron metabolism",
"hepcidin",
"BMP6",
"oxidative stress",
"Nrf2",
"autophagy",
"lipophagy"
],
"suggested_hubs": [
{
"slug": "static-magnetic-fields",
"weight": 0.95,
"reason": "Study tests health effects of moderate-intensity static magnetic field exposure (0.4–0.7 T) in mice."
}
]
}AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.
Identifiers and source
DOI: 10.1016/j.bbadis.2023.166719
PubMed: 37116230
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