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Thermogenesis induced by osmotic stimulation of the intestines in the rat

机译:渗透性刺激大鼠肠道引起的生热

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摘要

class="enumerated" style="list-style-type:decimal">Infusion of 5-20 % glucose, 1.8-3.6 % NaCl, 20 % methylglucose, 20 % fructose, or 5-10 % solutions of various amino acids (10 ml kg−1) into the duodenum induced dose-dependent thermogenesis in urethane-anaesthetized rats. In contrast, infusion of 0.9 % NaCl, distilled water, or safflower oil had no effect on the metabolic rate. Infusion of 7.2 % urea induced a small and transient increase in the metabolic rate. These results suggested that the thermogenesis was caused mainly by changes in osmolality rather than by a specific action of the different solute molecules.The respiratory exchange ratio increased after the infusion of glucose, fructose, glycine, or serine, did not change after the infusion of NaCl, methylglucose, safflower oil, or distilled water, and decreased after infusion of arginine. Therefore, there was no relationship between substrate utilization and the occurrence of thermogenesis.Intestinal infusion of 3.6 % NaCl elevated the plasma osmolality, with a plateau increase of ≈20 mosmol kg−1. However, intravenous infusion of the same amount of NaCl induced a significantly smaller thermogenic response, although it elevated the plasma osmolality with a time course and magnitude similar to those obtained after the intestinal infusion. Infusion of NaCl into the hepatic portal vein or the peritoneal cavity also produced a significantly small thermogenic response. These results suggested an intestinal or mesenteric location for osmoreceptors.To test for possible stimulation of intestinal osmoreceptors after intake of a normal meal, we measured the osmolality of the intestinal contents. The osmolality of the duodeno-jejunal contents was 600-800 mosmol kg−1, whereas the plasma osmolality was 306 ± 1 mosmol kg−1, which suggests that the intestinal osmoreceptors are stimulated after meals and are involved in diet-induced thermogenesis.
机译:class =“ enumerated” style =“ list-style-type:decimal”> <!-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 将5-20%的葡萄糖,1.8-3.6%的NaCl,20%的甲基葡萄糖,20%的果糖或5-10%的各种氨基酸溶液(10 ml kg -1 )注入十二指肠氨基甲酸乙酯麻醉大鼠的剂量依赖性生热作用。相反,输注0.9%NaCl,蒸馏水或红花油对代谢率没有影响。输注7.2%的尿素会引起代谢率的短暂而短暂的增加。这些结果表明,热生成主要是由重量克分子渗透压浓度的变化引起的,而不是由不同溶质分子的特定作用引起的。 输注葡萄糖,果糖,甘氨酸或丝氨酸后呼吸交换率增加,输注氯化钠,甲基葡萄糖,红花油或蒸馏水后无变化,而输注精氨酸后无变化。因此,底物利用率与生热的发生之间没有关系。 肠内注入3.6%NaCl会增加血浆渗透压,使平台渗透压升高约20 mosmol kg −1 。但是,静脉输注相同量的NaCl会引起显着较小的产热反应,尽管其血浆渗透压升高的时间和幅度与肠输注后的相似。将NaCl注入肝门静脉或腹膜腔也产生显着较小的产热反应。这些结果暗示了渗透压感受器的肠道或肠系膜位置。 为了测试正常进餐后肠道渗透压感受器的可能刺激,我们测量了肠道内容物的渗透压。十二指肠空肠内容物的重量克分子渗透压浓度为600-800 mosmol kg -1 ,而血浆重量克分子渗透压浓度为306±1 mosmol kg -1 ,这表明肠道渗透压感受器饭后会受到刺激,并参与饮食引起的生热。

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