Lipid transport in cholecystokinin knockout mice.
Lipid transport in cholecystokinin knockout mice.
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DOI：
10.1016/j.physbeh.2015.07.009
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发表时间：
2015-11-01
影响因子：
2.9
通讯作者：
Lo CC
中科院分区：
文献类型：
--
作者：
King A;Yang Q;Huesman S;Rider T;Lo CC
胆囊收缩素（CCK）是响应于脂肪喂养而释放的，并调节对营养吸收至关重要的胰腺消化酶。我们以前的报告表明，胆囊收缩素敲除（CCK-KO）小鼠喂养10周的HFD减少了体脂量，但白色脂肪组织和骨骼肌的葡萄糖摄取相当。我们假设CCK参与能量稳态和脂质从小肠转运到组织，以响应饮食脂质的急性治疗。具有可比脂肪吸收的CCK-KO小鼠具有增加的能量消耗，并且对HFD诱导的肥胖具有抗性。通过十二指肠内输注黄油脂肪和静脉输注Liposyn III，我们确定了CCK-KO小鼠中脂质从小肠转运到淋巴和脂肪细胞中沉积的机制。CCK-KO小鼠对绒毛膜内脂质的急性处理有延迟的Apo B48-乳糜微粒分泌，脂质转运至淋巴系统，以及附睾脂肪对甘油三酯（TG）衍生的脂肪酸的摄取。相比之下，CCK-KO小鼠对乳糜微粒样乳剂中的TG有相当的TG清除率和白色脂肪细胞的脂质摄取。因此，我们得出结论，CCK是重要的脂质运输和能量消耗，以控制体重，以响应饮食脂肪喂养。
Cholecystokinin (CCK) is released in response to lipid feeding and regulates pancreatic digestive enzymes vital to the absorption of nutrients. Our previous reports demonstrated that cholecystokinin knockout (CCK-KO) mice fed a 10 weeks of HFD had reduced body fat mass, but comparable glucose uptake by white adipose tissues and skeletal muscles. We hypothesized that CCK is involved in energy homeostasis and lipid transport from small intestine to tissues in response to acute treatment with dietary lipids. CCK-KO mice with comparable fat absorption had increased energy expenditure and were resistant to HFD-induced obesity. Using intraduodenal infusion of butter fat and intravenous infusion using Liposyn III, we determined the mechanism of lipid transport from small intestine to deposition in lymph and adipocytes in CCK-KO mice. CCK-KO mice had delayed secretion of Apo B48-chylomicrons, lipid transport to the lymphatic system, and triglyceride (TG)-derived fatty acid uptake by epididymal fat in response to acute treatment of introdudenal lipids. In contrast, CCK-KO mice had comparable TG clearance and lipid uptake by white adipocytes in response to TG in chylomicron-like emulsion. Thus, we concluded that CCK is important for lipid transport and energy expenditure to control body weight in response to dietary lipid feeding.