Harmon J S, Sheridan M A
Department of Zoology, North Dakota State University, Fargo 58105.
Gen Comp Endocrinol. 1992 Aug;87(2):214-21. doi: 10.1016/0016-6480(92)90025-f.
The effects of nutritional state, insulin, and glucagon on lipid mobilization were determined in rainbow trout, Oncorhynchus mykiss. In nutritional state experiments, fish were either fed continuously (except 24 to 36 hr prior to experimentation) with commercial trout chow or fasted for 4 weeks. Lipase activity in liver tissue isolated from fasted fish and cultured for 5 hr was greater than that in tissue isolated from fed fish and cultured. The presence of glucose (5.55 mM) in the incubation medium accentuates lipolytic activity in both liver and adipose tissue. Hormone response was assessed both in vivo and in vitro. Salmon insulin was injected into anesthetized fish (fed continuously except 24 hr prior to injections) in 10 microliters of saline/g body weight; final hormone dose was 100 ng/g body weight. Tissue and plasma were sampled 1 and 3 hr after injection. Insulin resulted in depressed plasma FA concentration and reduced hepatic triacylglycerol lipase activity. In vitro effects of hormones were evaluated by incubating liver and adipose tissue pieces in Hanks-MEM. Glucagon (bovine/porcine) directly stimulated lipid breakdown in both liver and adipose tissue. These actions were manifested by enhanced FA and glycerol released into the culture medium and by elevated triacylglycerol lipase activity. Insulin (bovine) generally appeared antilipolytic as this agent inhibited glucagon-stimulated lipase activity and glucagon-stimulated FA release. Furthermore, insulin (in the presence of glucose) reduced net lipolysis, as indicated by glycerol release, compared to control cultures. These results indicate that nutritional state and glucose are important modulators of lipid mobilization and that glucagon and insulin act directly on lipid storage sites to coordinate lipolysis in rainbow trout.
研究了营养状态、胰岛素和胰高血糖素对虹鳟（Oncorhynchus mykiss）脂质动员的影响。在营养状态实验中，将虹鳟鱼分为两组，一组持续投喂商业鳟鱼饲料（实验前24至36小时除外），另一组禁食4周。从禁食4周的鱼体中分离肝脏组织，并培养5小时，其脂肪酶活性高于从投喂饲料的鱼体中分离并培养的肝脏组织。在孵育培养基中添加葡萄糖（5.55 mM）可增强肝脏和脂肪组织中的脂解活性。通过体内和体外实验评估激素反应。将鲑鱼胰岛素以10微升/克体重的生理盐水注射到麻醉的鱼体内（注射前24小时除外，持续投喂）；最终激素剂量为100纳克/克体重。注射后1小时和3小时采集组织和血浆样本。胰岛素导致血浆脂肪酸浓度降低，肝脏三酰甘油脂肪酶活性降低。通过将肝脏和脂肪组织块在Hanks-MEM中孵育来评估激素的体外作用。胰高血糖素（牛/猪）直接刺激肝脏和脂肪组织中的脂质分解。这些作用表现为释放到培养基中的脂肪酸和甘油增加，以及三酰甘油脂肪酶活性升高。胰岛素（牛）通常表现出抗脂解作用，因为该药物抑制胰高血糖素刺激的脂肪酶活性和胰高血糖素刺激的脂肪酸释放。此外，与对照培养相比，胰岛素（在有葡萄糖存在的情况下）降低了甘油释放所表明的净脂解作用。这些结果表明，营养状态和葡萄糖是脂质动员的重要调节因子，胰高血糖素和胰岛素直接作用于脂质储存部位，以协调虹鳟的脂解作用。
