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- Brunetta 2020 J Physiol + (Evidence has accumulated to indicate that … Evidence has accumulated to indicate that dietary nitrate alters energy expenditure and the metabolic derangements associated with a high-fat diet, however, the mechanism(s) of action remain incompletely elucidated. Therefore, we aimed to determine if dietary nitrate (4 mm sodium nitrate via drinking water) could prevent high-fat diet (HFD) mediated glucose intolerance in association with improved mitochondrial bioenergetics within both white (WAT) and brown (BAT) adipose tissue. HFD-feeding caused glucose intolerance (P < 0.05) and increased body weight. As a result of higher body weight, energy expenditure increased proportionally. HFD-fed mice displayed greater mitochondrial uncoupling and a 2-fold increase in UCP-1 content within BAT. Within epididymal adipose tissue (eWAT), HFD increased cell size (i.e. hypertrophy), mitochondrial H<sub>2</sub>O<sub>2</sub> emission, oxidative stress, JNK phosphorylation, leucocyte infiltration, and induced insulin resistance. Remarkably, dietary nitrate consumption attenuated and/or mitigated all these responses, including rendering mitochondria more coupled within BAT, and normalizing mitochondrial H<sub>2</sub>O<sub>2</sub> emission and insulin-mediated Akt-Thr308 phosphorylation within eWAT. Intriguingly, the positive effects of dietary nitrate appear to be independent of eWAT mitochondrial respiratory capacity and content. Altogether, these data suggest that dietary nitrate attenuates the development of HFD-induced insulin resistance in association with attenuating WAT inflammation and redox balance, independent of changes within either WAT or BAT mitochondrial respiratory capacity/content. This article is protected by copyright. All rights reserved.al respiratory capacity/content. This article is protected by copyright. All rights reserved.)
