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正常胰腺和糖尿病大鼠进食后的胰岛素与饱腹感

Insulin and satiety from feeding in pancreatic-normal and diabetic rats.

作者信息

Vanderweele D A

机构信息

Department of Psychology, Occidental College, Los Angeles, CA 90041.

出版信息

Physiol Behav. 1993 Sep;54(3):477-85. doi: 10.1016/0031-9384(93)90239-c.

DOI:10.1016/0031-9384(93)90239-c
PMID:8415941
Abstract

Insulin's role in food ingestion and satiety was investigated in streptozotocin-diabetic and pancreatic-normal rats. Markedly diabetic rats (60-65 mg/kg b.wt. streptozotocin with mean glycemia of 380 mg/dl) were observed for daily food/water intake and body weight changes and meal pattern in a standard operant chamber. Diabetic animals showed an immediate hypophagia (days 1-4) by decreasing meal size (MS). As animals lost weight, a significant hyperphagia appeared, accomplished by an elevation in MS. Treatment with insulin infused via osmotic minipump at a stable rate (6.0 U/24 h) reduced polyuria and glycemia, eliminated glycosuria, and restored weight gain. MS did not, however, return to baseline immediately. In a second experiment with milder diabetes (20-22 mg/rat streptozotocin, which produced glycemia ranging from 148 to 304 mg/dl), significant hyperphagia appeared, again attributable to an increase in MS. Minipumps infusing 2.4-4.0 U insulin/24 h reversed this hyperphagia. In pancreatic-normal rats, pumps infusing insulin at 1.2 or 2.4 U/24 h produced a modest hypophagia accomplished by a primary decrease in nocturnal intake (11% suppression in dark feeding). Subdiaphragmatically vagotomized rats showed an attenuation of this suppression (no significant effects on food or water intake produced by insulin infused). Insulin appears to participate in satiety by limiting MS, without significantly shortening latency to take the next meal.

摘要

在链脲佐菌素诱导的糖尿病大鼠和胰腺正常的大鼠中研究了胰岛素在食物摄取和饱腹感中的作用。观察明显糖尿病大鼠(给予60 - 65毫克/千克体重的链脲佐菌素,平均血糖为380毫克/分升)在标准操作箱中的每日食物/水摄入量、体重变化和进食模式。糖尿病动物通过减小餐量(MS)立即出现摄食减少(第1 - 4天)。随着动物体重减轻,出现显著的摄食亢进,这是由餐量增加所致。通过渗透微型泵以稳定速率(6.0单位/24小时)输注胰岛素进行治疗可减少多尿和血糖,消除糖尿,并恢复体重增加。然而,餐量并没有立即恢复到基线水平。在第二个实验中,使用病情较轻的糖尿病大鼠(每只大鼠给予20 - 22毫克链脲佐菌素,血糖范围为148至304毫克/分升),再次出现显著的摄食亢进,同样归因于餐量增加。输注2.4 - 4.0单位胰岛素/24小时的微型泵可逆转这种摄食亢进。在胰腺正常的大鼠中,以1.2或2.4单位/24小时输注胰岛素的微型泵会导致适度的摄食减少,这主要是由夜间摄入量的降低引起的(黑暗进食时抑制11%)。膈下迷走神经切断的大鼠显示这种抑制作用减弱(输注胰岛素对食物或水的摄入量没有显著影响)。胰岛素似乎通过限制餐量参与饱腹感调节,而不会显著缩短吃下一顿饭的延迟时间。

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