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Berberine remodels adipose tissue to attenuate metabolic disorders by activating sirtuin 3

  
@article{APS10566,
	author = {Dan Li and Chao Yang and Jian-zhong Zhu and Eduardo Lopez and Tian Zhang and Qiang Tong and Cheng Peng and Li-gen Lin},
	title = {Berberine remodels adipose tissue to attenuate metabolic disorders by activating sirtuin 3},
	journal = {Acta Pharmacologica Sinica},
	volume = {43},
	number = {5},
	year = {2022},
	keywords = {},
	abstract = {Adipose tissue remodelling is considered a critical pathophysiological hallmark of obesity and related metabolic diseases. Berberine (BBR), a natural isoquinoline alkaloid, has potent anti-hyperlipidaemic and anti-hyperglycaemic effects. This study aimed to explore the role of BBR in modulating adipose tissue remodelling and the underlying mechanisms. BBR protected high fat diet (HFD)-fed mice against adiposity, insulin resistance and hyperlipidemia. BBR alleviated adipose tissue inflammation and fibrosis by inhibiting macrophage infiltration, pro-inflammatory macrophage polarization and the abnormal deposition of extracellular matrix, and the effect was mediated by BBR directly binding and activating the deacetylase Sirtuin 3 (SIRT3) and suppressing the activation of the mitogen-activated protein kinases and nuclear factor-κB signalling pathways. Furthermore, BBR decreased microRNA-155-5p secretion by macrophages, which in turn ameliorated liver injury. Moreover, BBR mitigated inflammatory responses in both LPS-stimulated macrophages and TNF-α-treated adipocytes and suppressed macrophage migration towards adipocytes by activating SIRT3. Collectively, this study revealed that BBR improved adipose tissue remodelling, and subsequently inhibited the secretion of microRNA-155-5p by macrophages, which alleviated adiposity, insulin resistance and liver injury in obese mice. The modulation of adipose tissue remodelling by activating SIRT3 could contribute to the anti-hyperlipidemic and anti-hyperglycemic effects of BBR.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/10566}
}