Yang Licong, Zhao Yan, Pan Yongfang, Li Dongming, Zheng Guodong
Jiangxi Key Laboratory of Natural Product and Functional Food, College of Food Science and Engineering, Jiangxi Agricultural University, Nanchang, 330045 China.
Nutr Metab (Lond). 2019 Jan 21;16:6. doi: 10.1186/s12986-019-0333-z. eCollection 2019.
Obesity has become a public health concern worldwide because it is linked to numerous metabolic disorders, such as hyperlipidemia, hypertension and cardiovascular disease. Therefore, there is an urgent need to develop new therapeutic strategies that are efficacious and have minimal side effects in obesity treatment. This study examined the effect of dietary supplement of L. ethanol extract (SCLE) on high-fat diet (HFD) induced obesity.
Fifty ICR mice were fed a normal diet, high-fat diet (HFD) or HFD supplemented with 0.25, 0.5% or 1% SCLE for 8 weeks. Body weight, intraperitioneal adipose tissue (IPAT) weight, serum biochemical parameters, and liver lipids were measured. Activity, mRNA and protein expressions of lipid metabolism-related enzymes were analyzed.
Over 0.5% SCLE had reduced cholesterol biosynthesis by the activation of AMP-activated protein kinase (AMPK), which subsequently suppressed the mRNA expression of both sterol regulatory element binding protein-2 and 3-hydroxy-3-methyl-glutaryl-CoA reductase. Thus, the plasma and liver cholesterol concentrations in the HFD-fed mice were decreased. AMPK activation caused by SCLE also significantly upregulated lipolysis by enhancing adipose triglyceride lipase and hormone-sensitive lipase activities. This accelerated triglyceride hydrolysis and fatty acid release. Finally, SCLE increased carnitine palmitoyltransferase 1 and acyl-CoA oxidase activities, which further promoted fatty acid β-oxidation.
SCLE could lead to a decrease in body weight gain and fat mass by inhibiting the lipid synthesis and promoting lipolysis and β-oxidation in HFD fed mice. The underlying mechanism is probably associated with regulating AMPK pathway.
肥胖已成为全球公共卫生问题，因为它与多种代谢紊乱相关，如高脂血症、高血压和心血管疾病。因此，迫切需要开发在肥胖治疗中有效且副作用最小的新治疗策略。本研究考察了膳食补充朝鲜淫羊藿乙醇提取物（SCLE）对高脂饮食（HFD）诱导的肥胖的影响。
将50只ICR小鼠分为正常饮食组、高脂饮食组或补充0.25%、0.5%或1%SCLE的高脂饮食组，喂养8周。测量体重、腹膜内脂肪组织（IPAT）重量、血清生化参数和肝脏脂质。分析脂质代谢相关酶的活性、mRNA和蛋白表达。
超过0.5%的SCLE通过激活AMP激活的蛋白激酶（AMPK）降低胆固醇生物合成，随后抑制固醇调节元件结合蛋白-2和3-羟基-3-甲基戊二酰辅酶A还原酶的mRNA表达。因此，高脂饮食喂养小鼠的血浆和肝脏胆固醇浓度降低。SCLE引起的AMPK激活还通过增强脂肪甘油三酯脂肪酶和激素敏感性脂肪酶的活性显著上调脂肪分解。这加速了甘油三酯水解和脂肪酸释放。最后，SCLE增加了肉碱棕榈酰转移酶1和酰基辅酶A氧化酶的活性，进一步促进了脂肪酸β氧化。
SCLE可通过抑制高脂饮食喂养小鼠的脂质合成、促进脂肪分解和β氧化导致体重增加和脂肪量减少。其潜在机制可能与调节AMPK途径有关。
