Zuo Jiacheng, Zhao Dandan, Yu Na, Fang Xin, Mu Qianqian, Ma Yue, Mo Fangfang, Wu Rui, Ma Rufeng, Wang Lili, Zhu Ruyuan, Liu Haixia, Zhang Dongwei, Gao Sihua
School of Preclinical Medicine, Beijing University of Chinese Medicine, Beijing, China.
Department of Endocrinology, Beijing University of Chinese Medicine, Third Affiliated Hospital, Beijing, China.
Cell Physiol Biochem. 2017;42(4):1514-1525. doi: 10.1159/000479268. Epub 2017 Jul 18.
BACKGROUND/AIMS: Obesity has become a major health concern with few effective medications. Cinnamaldehyde (CA) has been reported to exhibit anti-diabetic and anti-inflammatory properties. However, whether CA shows anti-obesity activity remains unknown. Therefore, the present study aimed to investigate the potential anti-obesity effects of CA on mice fed a high-fat diet (HFD) and to explore the possible mechanisms involved.
Male C57BL/6J mice fed an HFD for 12 weeks were supplemented with CA (40 mg/kg/day) via gavage for an additional 8 weeks. Mice fed a standard diet were used as normal controls.
The results revealed that CA treatment decreased body weight, fat mass, food intake, and serum lipid, free fatty acid and leptin levels. CA administration also improved insulin sensitivity in HFD-induced obese mice. Additionally, CA inhibited the hypertrophy of adipose tissue and induced browning of white adipose tissue. Uncoupling protein 1 (UCP1) was expressed in white adipose tissue after the oral administration of CA. Furthermore, CA enhanced the expression of the peroxisome proliferator-activated receptor γ (PPARγ), PR domain-containing 16 (PRDM16) and PPARγ coactivator 1α (PGC-1α) proteins in both brown and white adipose tissues.
The results suggest that CA exhibits therapeutic potency against obesity by inducing the browning of white adipose tissue in HFD-fed mice.
背景/目的:肥胖已成为一个主要的健康问题,且有效的药物很少。据报道,肉桂醛(CA)具有抗糖尿病和抗炎特性。然而,CA是否具有抗肥胖活性尚不清楚。因此,本研究旨在探讨CA对高脂饮食(HFD)喂养小鼠的潜在抗肥胖作用,并探索其可能的作用机制。
将雄性C57BL/6J小鼠喂养HFD 12周,然后通过灌胃补充CA(40毫克/千克/天),持续8周。喂养标准饮食的小鼠用作正常对照。
结果显示,CA治疗可降低体重、脂肪量、食物摄入量以及血清脂质、游离脂肪酸和瘦素水平。CA给药还改善了HFD诱导的肥胖小鼠的胰岛素敏感性。此外,CA抑制了脂肪组织的肥大,并诱导白色脂肪组织褐变。口服CA后,白色脂肪组织中表达了解偶联蛋白1(UCP1)。此外,CA增强了棕色和白色脂肪组织中过氧化物酶体增殖物激活受体γ(PPARγ)、含PR结构域16(PRDM16)和PPARγ共激活因子1α(PGC-1α)蛋白的表达。
结果表明,CA通过诱导HFD喂养小鼠白色脂肪组织褐变而表现出抗肥胖治疗潜力。