Please use this identifier to cite or link to this item: http://hdl.handle.net/10637/14504

Increased inflammation, oxidative stress and mitochondrial respiration in brown adipose tissue from obese mice

Title: Increased inflammation, oxidative stress and mitochondrial respiration in brown adipose tissue from obese mice
Authors : Alcalá Díaz-Mor, Martín
Calderón Domínguez, María
Bustos, Eduviges
Ramos, Dolores
Viana Arribas, Marta
Herrero, Laura
Keywords: ObesityMetabolic diseases
Publisher: Nature
Citation: Alcalá M, Calderon-Dominguez M, Bustos E, Ramos P, Casals N, Serra D, Viana M, Herrero L. Increased inflammation, oxidative stress and mitochondrial respiration in brown adipose tissue from obese mice. Sci Rep. 2017 Nov 22;7(1):16082. doi: 10.1038/s41598-017-16463-6.
Abstract: Obesity is associated with severe metabolic diseases such as type 2 diabetes, insulin resistance, cardiovascular disease and some forms of cancer. The pathophysiology of obesity-induced metabolic diseases has been strongly related to white adipose tissue (WAT) dysfunction through several mechanisms such as fibrosis, apoptosis, inflammation, ER and oxidative stress. However, little is known of whether these processes are also present in brown adipose tissue (BAT) during obesity, and the potential consequences on mitochondrial activity. Here we characterized the BAT of obese and hyperglycemic mice treated with a high-fat diet (HFD) for 20 weeks. The hypertrophic BAT from obese mice showed no signs of fibrosis nor apoptosis, but higher levels of inflammation, ER stress, ROS generation and antioxidant enzyme activity than the lean counterparts. The response was attenuated compared with obesity-induced WAT derangements, which suggests that BAT is more resistant to the obesity-induced insult. In fact, mitochondrial respiration in BAT from obese mice was enhanced, with a 2-fold increase in basal oxygen consumption, through the upregulation of complex III of the electron transport chain and UCP1. Altogether, our results show that obesity is accompanied by an increase in BAT mitochondrial activity, inflammation and oxidative damage.
URI: http://hdl.handle.net/10637/14504
Rights : http://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
openAccess
Issue Date: 22-Nov-2017
Center : Universidad San Pablo-CEU
Appears in Collections:Facultad de Farmacia





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