最近,上海生科院营养科学研究所研究组揭示了亮氨酸缺乏时中枢神经系统调节外周脂质代谢的机制。该研究组前期研究表明:亮氨酸缺乏能够引起机体外周组织的广泛代谢变化,包括肝脏脂肪酸合成抑制、胰岛素敏感性增强,腹部脂肪快速丢失以及褐色脂肪组织产热增加等;研究还发现亮氨酸缺乏能够引起下丘脑内多个信号通路发生变化,提示下丘脑能够感应亮氨酸缺乏这一营养状态,并经过系列信号整合后进一步调控外周脂质代谢,但具体机制不清。进一步研究中发现,用亮氨酸缺乏饲料喂养的小鼠经侧脑室注射亮氨酸后,能够很快恢复下丘脑内的亮氨酸水平;并能够阻止亮氨酸缺乏导致的白色脂肪丢失和褐色脂肪产热增加的表型变化。研究表明,中枢注射亮氨酸能够改变白色脂肪组织激素敏感脂肪酶(HSL)的磷酸化水平和褐色脂肪组织解耦联蛋白1 Recently, the Shanghai Institutes for Biological Sciences, Institute of Nutritional Sciences revealed the mechanism of central nervous system regulation of peripheral lipid metabolism during leucine deficiency. The research group’s previous studies showed that: leucine deficiency can cause a wide range of metabolic changes in peripheral tissues, including inhibition of fatty acid synthesis in the liver, increased insulin sensitivity, rapid loss of abdominal fat and increased production of brown adipose tissue; study also found that bright ammonia Acid deficiency can cause multiple signal pathways in the hypothalamus to change, suggesting that the hypothalamus can sense the nutritional status of leucine deficiency, and after a series of signal integration and further regulation of peripheral lipid metabolism, but the specific mechanism is unclear. Further studies found that leucine-deficient mice fed leucine injected into the lateral ventricle quickly recovered leucine levels in the hypothalamus and prevented white fat loss due to leucine deficiency Phenotypic changes with increased production of brown fat. Studies have shown that central injection of leucine alters the phosphorylation of white adipose tissue-hormone-sensitive lipase (HSL) and brown adipose tissue-uncoupling protein 1