Svensson A M, Hellerström C, Jansson L
Department of Medical Cell Biology, Uppsala University, Sweden.
J Endocrinol. 1996 Dec;151(3):507-11. doi: 10.1677/joe.0.1510507.
The aim of the present study was to evaluate the effects of diet-induced obesity on pancreatic islet blood perfusion in normal Wistar rats. Furthermore, we investigated to what extent any obesity-associated changes in islet blood flow could be reversed after reversion to a normal diet with normalization of body weight. Young adult female Wistar rats were offered a palatable mixed high-caloric diet (cafeteria diet) in addition to standard pelleted chow. Age-matched control rats received standard pelleted chow only. After 4 weeks the diet-treated rats had a body weight of approximately 15% more than that of the controls. All diet-treated rats had decreased glucose tolerance and increased serum insulin concentrations, but basal blood glucose concentrations were similar in anesthetized diet-treated and control rats. Whole pancreatic and islet blood flow rates were measured with a microsphere technique. The islet blood flow as well as fractional islet blood flow were increased (P < 0.01) in rats fed the cafeteria diet, while blood perfusion of the whole pancreas was similar to that of the control rats. In a second experiment, rats received the cafeteria diet for 4 weeks and were then fed standard pelleted food alone for another 3 weeks, while controls received standard diet for 7 weeks. After this period total body weight, retroperitoneal fat pad weight and glucose tolerance were similar to those of the controls. Whole pancreatic blood flow was unchanged as compared with that of control rats. However, both islet blood flow (P < 0.01) and fractional blood flow (P < 0.01) were increased. We conclude that diet-induced obesity in rats is associated with decreased glucose tolerance, hyperinsulinemia and a specific increase in absolute and fractional islet blood perfusion. This increase persists for at least 3 weeks after the diet is withdrawn despite normalization of body weight and glucose tolerance.
本研究的目的是评估饮食诱导的肥胖对正常Wistar大鼠胰岛血流灌注的影响。此外，我们还研究了在恢复正常饮食且体重恢复正常后，与肥胖相关的胰岛血流变化能在多大程度上得到逆转。除了标准颗粒饲料外，给年轻成年雌性Wistar大鼠提供美味的高热量混合饮食（自助餐厅饮食）。年龄匹配的对照大鼠仅接受标准颗粒饲料。4周后，饮食处理的大鼠体重比对照组大约高15%。所有饮食处理的大鼠葡萄糖耐量降低，血清胰岛素浓度升高，但麻醉状态下饮食处理的大鼠和对照大鼠的基础血糖浓度相似。用微球技术测量全胰腺和胰岛的血流速率。喂食自助餐厅饮食的大鼠，其胰岛血流以及胰岛血流分数均增加（P<0.01），而全胰腺的血流灌注与对照大鼠相似。在第二个实验中，大鼠接受4周的自助餐厅饮食，然后单独喂食标准颗粒饲料3周，而对照组接受7周的标准饮食。在此期间，总体重、腹膜后脂肪垫重量和葡萄糖耐量与对照组相似。与对照大鼠相比，全胰腺血流没有变化。然而，胰岛血流（P<0.01）和血流分数（P<0.01）均增加。我们得出结论，大鼠饮食诱导的肥胖与葡萄糖耐量降低、高胰岛素血症以及绝对和相对胰岛血流灌注的特定增加有关。尽管体重和葡萄糖耐量恢复正常，但在停止饮食后，这种增加至少持续3周。
