Liang Jia, Jia Ying, Yan Haijing, Shen Qingyu, Bian Weihua, Zhao Dongmei, Xu Yong, Jin Yongjun, Yang Meizi
Department of Pharmacology, Binzhou Medical University, Yantai, People's Republic of China.
Department of Cell Biology, Binzhou Medical University, Yantai, People's Republic of China.
Diabetes Metab Syndr Obes. 2021 Oct 27;14:4351-4360. doi: 10.2147/DMSO.S335526. eCollection 2021.
To investigate resistance to diet-induced obesity (DIO) and monosodium glutamate (MSG)-induced obesity as well as the underlying mechanisms.
Newborn mice were used to construct DIO and MSG-induced obesity models. Obesity indices, such as body weight, body length, Lee index, body temperature, food intake, fat weight, and leptin level, were examined. Mice that did not exhibit obesity were defined as the obesity-resistant group. The morphological changes of white adipose tissue were observed by hematoxylin and eosin staining, and expression levels of PR domain containing 16 (Prdm16) and uncoupling protein-1 (Ucp-1) in white adipose tissue were measured by Western blot.
Obesity-resistant mice fed a high-fat diet showed resistance beginning at week 5 along with lower weights and lengths than those in the obesity group from weeks 5 to 12. MSG-induced obesity-resistant mice showed features consistent with resistance to obesity from week 1 along with higher body lengths relative to the obesity group; however, the weight difference was not significant until week 10, when body weights decreased significantly in obesity-resistant mice. The Lee index was lower in obesity-resistant mice than in the obesity group and the normal group, further suggesting obesity resistance. Additionally, obesity-resistant mice showed higher levels of leptin, whereas obese mice induced by a high-fat diet showed leptin resistance. Furthermore, Prdm16 and Ucp-1 levels were both downregulated in the obesity group and upregulated in obesity-resistant mice, showing that white fat browning was highest in obesity-resistant mice.
The phenotypes of mice with DIO and MSG-induced obesity differed. Obesity resistance might be related to Prdm16 and Ucp-1-mediated white adipocyte browning.
研究饮食诱导肥胖（DIO）和味精（MSG）诱导肥胖的抗性及其潜在机制。
使用新生小鼠构建DIO和MSG诱导的肥胖模型。检测肥胖指标，如体重、体长、李氏指数、体温、食物摄入量、脂肪重量和瘦素水平。未表现出肥胖的小鼠被定义为肥胖抗性组。通过苏木精和伊红染色观察白色脂肪组织的形态变化，并通过蛋白质免疫印迹法检测白色脂肪组织中含PR结构域16（Prdm16）和解偶联蛋白-1（Ucp-1）的表达水平。
高脂饮食喂养的肥胖抗性小鼠从第5周开始表现出抗性，在第5至12周期间体重和体长均低于肥胖组。MSG诱导的肥胖抗性小鼠从第1周开始表现出与肥胖抗性一致的特征，相对于肥胖组体长更高；然而，直到第10周体重差异才显著，此时肥胖抗性小鼠体重显著下降。肥胖抗性小鼠的李氏指数低于肥胖组和正常组，进一步表明其具有肥胖抗性。此外，肥胖抗性小鼠的瘦素水平较高，而高脂饮食诱导的肥胖小鼠表现出瘦素抗性。此外，肥胖组中Prdm16和Ucp-1水平均下调，肥胖抗性小鼠中则上调，表明肥胖抗性小鼠的白色脂肪褐变程度最高。
DIO和MSG诱导肥胖的小鼠表型不同。肥胖抗性可能与Prdm16和Ucp-1介导的白色脂肪细胞褐变有关。
