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首页> 外文期刊>Physiology & behavior >Stress alters food intake and glucosensing response in hypothalamus, hindbrain, liver, and Brockmann bodies of rainbow trout.
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Stress alters food intake and glucosensing response in hypothalamus, hindbrain, liver, and Brockmann bodies of rainbow trout.

机译:压力会改变虹鳟鱼下丘脑,后脑,肝脏和布罗克曼氏体的食物摄入和葡萄糖代谢反应。

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摘要

In fish food intake is altered under stress conditions, and in a fish teleost model like rainbow trout food intake is associated with the activity of the glucosensor systems. Thus, we aimed to evaluate the possible interaction of stress with the response of glucosensor mechanisms in rainbow trout. Thus, we subjected rainbow trout (via intraperitoneal injections) to normoglycaemic (control), hypoglycaemic (4 mg.kg(-1) bovine insulin) or hyperglycaemic (500 mg.kg(-1) glucose body mass) conditions for 5 days under normal stocking density (NSD, 10 kg fish mass.m(-3)) or stress conditions induced by high stocking density (HSD, 70 kg fish mass.m(-3)). The experimental design was appropriate since hypoglycemia and hyperglycemia were observed in fish under NSD whereas in normoglycaemic fish HSD induced changes in stress-related parameters similar to those reported in fish literature, such as increased levels of cortisol and glucose in plasma and decreased levels of glycogen in liver. Food intake did not respond to changes in plasma glucose levels in fish under HSD conditions, in contrast with the decreased food intake observed when glucose levels increased in fish under NSD conditions. Moreover, the changes with the increase in plasma glucose levels in parameters involved in glucosensing in liver, Brockmann bodies (BB), hypothalamus, and hindbrain of fish in NSD either disappeared (DHAP and GAP levels, and GK, PK, and GPase activities in liver; glucose, DHAP and GAP levels in BB; glucose and DHAP levels, and GK and PK activities in hypothalamus; glycogen and DHAP levels, and GSase activity in hindbrain) or changed (cortisol levels in plasma; glycogen and GAP levels, and GSase and FBPase activities in liver; GK and PK activities in BB; GK and PK activities in hindbrain) in fish under HSD. Those changes suggest for the first time in fish the existence of an interaction between glucosensing capacity and stress. The readjustment in the activity of glucosensor systems is also associated with changes in food intake resulting in an inability of the fish to compensate with changes in food intake those of circulating glucose levels as observed in fish under non-stressed conditions.
机译:在鱼类中,食物的摄入量会在压力条件下发生变化,而在鱼类硬骨鱼模型中,例如虹鳟鱼的食物摄入量则与葡萄糖传感器系统的活性相关。因此,我们旨在评估虹鳟鱼中压力与葡萄糖传感器机制反应的可能相互作用。因此,我们将虹鳟鱼(通过腹膜内注射)在正常血糖(对照),低血糖(4 mg.kg(-1)牛胰岛素)或高血糖(500 mg.kg(-1)葡萄糖体重)的条件下进行了5天的测试正常放养密度(NSD,10千克鱼质量.m(-3))或高放养密度引起的胁迫条件(HSD,70千克鱼质量.m(-3))。实验设计是适当的,因为在NSD下观察到鱼的低血糖和高血糖,而在正常血糖的鱼中,HSD诱导的应激相关参数的变化与鱼类文献中报道的类似,例如血浆中皮质醇和葡萄糖水平的增加以及糖原水平的降低在肝脏中。在HSD条件下,食物摄入量对鱼类血浆葡萄糖水平的变化无反应,而在NSD条件下,鱼体内葡萄糖含量增加时,食物摄入量下降。而且,NSD中鱼类肝脏,Brockmann体(BB),下丘脑和后脑的葡萄糖代谢相关参数中血浆葡萄糖水平的变化都消失了(DHAP和GAP水平,GK,PK和GPase活性升高)。肝脏; BB中的葡萄糖,DHAP和GAP水平;下丘脑中的葡萄糖和DHAP水平以及GK和PK活性;后脑中的糖原和DHAP水平以及GSase活性)或已发生变化(血浆中的皮质醇水平;糖原和GAP的水平以及GSase HSD下鱼的肝脏FBPase活性; BB中GK和PK活性;后脑中GK和PK活性)。这些变化首次在鱼类中提示糖化能力与压力之间存在相互作用。葡萄糖传感器系统活动的重新调整还与食物摄入量的变化有关,导致鱼类无法补偿在无压力条件下在鱼类中观察到的循环葡萄糖水平的食物摄入量的变化。

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