Diacylglycerol kinase works as a physiological regulator of plasma glucose level

二酰基甘油激酶epsilon敲除（DGKe-KO）小鼠饲喂高脂饲料（HFD） 40 d。这引起了体重和白色脂肪组织质量的急性增加，并导致肝脏中严重的脂质积累。由于肝脏脂质积累被认为是胰岛素抵抗的一种症状，我们进行了葡萄糖耐量试验。结果表明，HFD喂养的DGKe-KO小鼠高糖持续时间延长。免疫印迹分析显示，新型蛋白激酶C （nPKC）的磷酸化在白色脂肪组织中上调。已知它被二酰基甘油（DG）激活。据报道，HFD会增加组织或器官中的DG含量。由于DGKe-KO小鼠不能充分操纵增加的DG， nPKC激活加速。nPKC是诱导胰岛素抵抗的关键分子。目前的研究表明，在高脂饲料喂养的DGKe-KO小鼠中，胰岛素抵抗是通过加速nPKC在WAT中引起的。

Diacylglycerol kinase epsilon knock out (DGKe-KO) mouse was fed with high fat diet (HFD) for 40 days. This induced acute increase in body weight and white adipose tissue mass, and led to severe lipid accumulation in the liver. Since hepatic lipid accumulation is known as a symptom of insulin resistance, we performed glucose tolerance test. It revealed that HFD fed DGKe-KO mouse showed prolonged time of high glucose level. Immunoblot analysis showed that phosphorylation of novel class protein kinase C (nPKC) is upregulated in white adipose tissue. It is known to be activated by diacylglycerol (DG). HFD is reported to increase DG contents in tissues or organs. Since DGKe-KO mouse is not able to manipulate increased DG adequately, nPKC activation is accelerated. nPKC is key molecule which induces insulin resistance. Present study revealed that insulin resistance is invoked particularly in WAT via acceleration of nPKC in HFD fed DGKe-KO mouse.