Dietary Sinapic Acid Alleviates Adiposity and Inflammation in Diet-Induced Obese Mice.

IF 1.6 Q3 FOOD SCIENCE & TECHNOLOGY
Hye Jin Yoon, Dae Seong Yoon, Hea Ja Baek, Beodeul Kang, Un Ju Jung
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引用次数: 1

Abstract

Sinapic acid (SA), a hydroxycinnamic acid, is known to confer protection against oxidative stress, inflammation, diabetes, and liver disease. However, the effectiveness of SA in improving obesity remains obscure. Therefore, this study evaluated anti-obesity efficacy of SA and to elucidate its mechanism of action. Male mice were maintained for 16 weeks on high-fat diet (HFD) alone or with SA (0.004%, w/w) and bodyweight, fat mass, adipocyte size, food intake, and biochemical and molecular markers were evaluated. SA-supplemented mice demonstrated markedly decreased fat mass and adipocyte size compared to unsupplemented group, without any changes in bodyweight and food intake between the two groups. Plasma adipocytokines levels including leptin, resistin, monocyte chemoattractant protein (MCP)-1 and interleukin-6 were also markedly reduced by SA supplementation. SA tended to lower plasma insulin level and improved homeostatic index of insulin resistance and intraperitoneal glucose tolerance test in HFD-induced obese mice. The anti-adiposity effect of SA was maybe owing to down-regulation of the mRNA expression of lipogenic genes, including acetyl coenzyme A (CoA) carboxylase, fatty acid synthesis, stearoyl-CoA desaturase 1, and phosphatidate phosphatase, and peroxisome proliferator-activated receptor γ, a transcription factor responsible for governing lipid metabolism, in adipose tissues. SA significantly down-regulated pro-inflammatory nuclear factor kappa B, MCP-1, tumor necrosis factor-α, and Toll-like receptor 4 mRNA expression in adipose tissue. Thus, SA could be beneficial for the development of functional foods or herbal medications to combat obesity.

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膳食sinap酸减轻饮食性肥胖小鼠的肥胖和炎症。
Sinapic acid (SA)是一种羟基肉桂酸,具有抗氧化应激、炎症、糖尿病和肝脏疾病的作用。然而,SA在改善肥胖方面的有效性仍不清楚。因此,本研究评估SA的抗肥胖功效,并阐明其作用机制。雄性小鼠单独饲喂高脂饮食(HFD)或添加SA (0.004%, w/w)维持16周,观察体重、脂肪质量、脂肪细胞大小、食物摄入量以及生化和分子标志物。与未添加sa的小鼠相比,添加sa的小鼠的脂肪量和脂肪细胞大小明显减少,两组之间的体重和食物摄入量没有任何变化。血浆脂肪细胞因子水平包括瘦素、抵抗素、单核细胞趋化蛋白(MCP)-1和白细胞介素-6也显著降低。SA有降低hfd诱导肥胖小鼠血浆胰岛素水平、改善胰岛素抵抗和腹腔糖耐量试验等稳态指标的趋势。SA的抗肥胖作用可能是由于下调脂肪组织中脂肪生成基因的mRNA表达,包括乙酰辅酶A (CoA)羧化酶、脂肪酸合成、硬脂酰辅酶A去饱和酶1和磷脂酶,以及负责调节脂质代谢的转录因子过氧化物酶体增殖物激活受体γ。SA显著下调脂肪组织中促炎核因子κ B、MCP-1、肿瘤坏死因子-α和toll样受体4mrna的表达。因此,SA可能有利于开发功能性食品或草药来对抗肥胖。
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来源期刊
Preventive Nutrition and Food Science
Preventive Nutrition and Food Science Agricultural and Biological Sciences-Food Science
CiteScore
3.40
自引率
0.00%
发文量
35
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