Gentisic acid prevents diet-induced obesity in mice by accelerating the thermogenesis of brown adipose tissue.

Gentisic acid prevents diet-induced obesity in mice by accelerating the thermogenesis of brown adipose tissue.
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遗传酸通过加速棕色脂肪组织的产热来预防小鼠饮食引起的肥胖。

DOI:
10.1039/d0fo02474k
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发表时间:
2021-01
期刊:
影响因子:
6.1
通讯作者:
Xue Han;Jielong Guo;Yunxiao Gao;J. Zhan;Yilin You;Weidong Huang
Xue Han;Jielong Guo;Yunxiao Gao;J. Zhan;Yilin You;Weidong Huang
中科院分区:
农林科学1区
文献类型:
--
作者:
Xue Han;Jielong Guo;Yunxiao Gao;J. Zhan;Yilin You;Weidong Huang

文献摘要

相似文献

由于肥胖发生在能量摄入高于能量消耗时,因此增加能量消耗是预防或治疗肥胖的有效策略。棕色脂肪组织(BAT)是典型的能量消耗器官,其产热功能可被膳食成分激活。龙胆酸(2,5-二羟基苯甲酸,(DHB))广泛存在于食品中,具有许多生理功能,包括抗炎,抗菌,抗氧化和保肝特性。然而,其减肥效果和机制还有待研究。本研究从能量代谢的角度探讨DHB预防饮食诱导肥胖小鼠的作用及其机制。C57 BL/6小鼠分别饲喂正常饮食(ND)、高脂高果糖饮食(HFFD)或HFFD加2 mg mL-1 DHB(DHB + HFFD)12周。测量肥胖、脂代谢、能量代谢及BAT相关指标。此外,在体外以C3 H10 T1/2细胞为实验对象,观察DHB对棕色脂肪细胞的影响。结果表明,实验结束时,DHB + HFFD组小鼠的体重比HFFD组低14.97%。DHB降低了主要器官的重量,改善了胰岛素敏感性,并减少了全身脂质积累。此外,DHB管理显着增加能量代谢,这是(部分)由于激活BAT产热。此外,DHB的补充增强了脂肪酸氧化相关蛋白在BAT和棕色脂肪细胞中的表达,表明DHB增强了BAT对脂肪酸的利用,这是产热的主要物质。该研究表明,DHB给药通过(至少部分地)加速脂肪酸的氧化和刺激BAT的产热来防止HFFD诱导的小鼠肥胖。
Since obesity occurs when energy intake is higher than energy expenditure, increasing energy expenditure is an effective strategy to prevent or treat obesity. Brown adipose tissue (BAT) is a classic energy-consuming organ whose thermogenesis function can be activated by dietary components. Gentisic acid (2,5-dihydroxybenzoic acid, (DHB)) is widely found in food and exhibits many physiological functions, which include anti-inflammatory, antimicrobial, antioxidant, and hepatoprotective properties. However, its anti-obesity effect and mechanism have yet to be examined. This study investigated the effect and mechanism of DHB in preventing diet-induced obesity in mice from the perspective of energy metabolism. The C57BL/6 mice were fed a normal diet (ND), a high-fat and high-fructose diet (HFFD) or HFFD plus 2 mg mL-1 DHB (DHB + HFFD) for 12 weeks. Measuring obesity, lipid metabolism, energy metabolism and BAT related indicators. Moreover, the C3H10T1/2 cells were used to assess the effect of DHB on brown adipocytes in vitro. The results proved that, at the end of the experiment, the body weight of the mice in the DHB + HFFD group was 14.97% lower than in the HFFD group. DHB reduced the weight of the major organs, improved insulin sensitivity, and decreased systemic lipid accumulation. Moreover, DHB administration significantly increased energy metabolism, which was (partly) due to the activation of BAT thermogenesis. Furthermore, DHB supplementation enhanced the expression of the fatty acid oxidation related proteins in BAT and the brown adipocytes, indicating that DHB augmented the utilization of fatty acids by BAT, which is the primary substance of thermogenesis. This study reveals that DHB administration prevents HFFD induced obesity in mice by (at least partly) accelerating the oxidation of fatty acids and stimulating the thermogenesis of BAT.