PRDM16
内科学
内分泌学
褐色脂肪组织
磷酸果糖激酶
产热素
脂肪组织
代谢综合征
苯丁酸酯
糖酵解
肥胖
化学
生物
医学
新陈代谢
作者
Byong-Keol Min,Hyeon‐Ji Kang,Byung-Soo Choi,Yong Hyun Jeon,Je‐Yoel Cho,Inkyu Lee,Dong Wook Kim
标识
DOI:10.20944/preprints201901.0073.v1
摘要
Obesity, which is characterized by an excessive accumulation of body fat, is one of the critical factors causing metabolic syndrome. Many studies have been performed to identify appropriate agents to control obesity, but toxicity remains a problem. Herein, we identified that phenylbutyrate (PBA), which has been used to treat urea cycle disorder with very low toxicity for a long time, efficiently inhibited high fat-induced body weight gain in a diet-induced obesity mouse model (DIO model). PBA treatment decreased body fat mass and increased lean composition. Moreover, PBA increased brown adipose tissue (BAT) activity by increasing glucose uptake, thereby improving glucose tolerance and insulin tolerance. Interestingly, PBA could induce the expression of phosphofructokinase (PFKL), a key enzyme in the glycolytic pathway, and knocking down PFKL dramatically repressed the expression level of Ucp1 as well as those of Prdm16, Cidea, Pgc1α, and Pparγ, which are marker genes for BAT activation. These results strongly suggested that PBA could increase energy expenditure by increasing BAT activity via the induction of PFKL. Taken together, PBA could be used as a therapeutic agent for people with obesity to prevent the development of metabolic syndrome.
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