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Effects of Intraportal Glucagon Administration Concurrent to Feeding on Meal Pattern and Hepatic Glycogen Content in the Rat

生糖素於進餐之同時由門脈給予對白鼠餐型及肝醣含量之影響

摘要


當大白鼠進食之際,由門靜脈同時灌注生糖素溶液,觀察對餐型之影響,並以肝醣含量之變化作參考。動物經手術後,置於測驗箱內,任自由飲食,每在食槽內移去一顆飼粒(Noyes,45 mg)時,便激發送食器補充一粒,同時又啓動灌注幫浦,將液體以0.35 ml/min之速率由門靜脈灌注30秒。每晝夜有23小時容許自我灌注,留1小時作為人工調整之用,按下列順序連續15天:5天(1-5)生理鹽水,7天(6-12)生糖素生理鹽水,及3天(13-15)生理鹽水。在實驗過程中,有每組5隻之7組動物在不同時間予以犧牲,以測定肝醣含量及門靜脈與肝靜脈之血糖濃度。10隻白鼠接受12天之灌注,其中5隻又完成15天之全程灌注,其數據用作餐型分析。結果顯示,在生糖素溶液灌注期間,食量呈均勻之抑制,而此抑制全由每餐提前結束所致,進餐次數則維持不變。肝醣對生糖素之反應則為起初消竭繼之回升,但肝靜脈血糖濃度仍保持高位。結論為生糖素係一強有力之飽足因子,但此效果似非全賴因肝醣分解而起之單純性血糖升高。

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並列摘要


Yin, T.H. and P.C. Yu: Effect of intraportal glucagon administration concurrent to feeding on meal pattern and hepatic glycogen content in the rat. Chinese J. Physiol., 29(2): 71-78, 1986: Effects of intraportal influsion of glucagon in vehicle concurrent to feeding on meal pattern were studied in rats with reference to the changes of glycogen content in the liver. The feeding of the animal was monitored by an eatometer in the test chamber. The removal of a Noyes peller, 45 mg, in the food trough activated both a food dispensor to deliver another one and an infusion pump to infuse fluid into the hepatoportal vein at a rate of 0.35ml/min for 30 sec. The infusion pump was on active state 23 hr/day for consecutive 15 days with a sequence: saline from 1st to 5th day, glucagons in saline (3 μg/ml) from 6th to 12th day, and again saline from 13th to 15th day. During the experiment, 7 groups of 5 rats in each were sacrificed at different times for determination of the glycogen content of the liver and the glucose level in the hepatic and hepatoportal veins. The data of 10 rats that proceeded up to the 12th day of infusion and those of 5 that continued to complete the whole course of 15 days infusion were used for analysis of meal pattern. The results revealed that the food intake was uniformly depressed during the period of glucagon administration and that the reduced food intake was totally accounted for by the premature termination of meals. The hepatic glycogen was depleted with glucagon initially but tended to come back with time. However, hepatic hyperglycemia was maintained without abating. Because of its specific effect on the meal length in spite of sustained hyperglycemia, it was concluded that glucagon is a potent satiety factor but its effect may not entirely depend upon glycogenolysis.

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