Voyles N R, Bhathena S J, Kennedy B, Wilkins S D, Michaelis O E, Zalenski C M, Timmers K I, Recant L
Proc Soc Exp Biol Med. 1987 May;185(1):49-54. doi: 10.3181/00379727-185-42515.
A potential role for somatostatin (SRIF) in the pathogenesis of the hyperinsulinemia of obese rats was considered. SRIF like immunoreactivity (ng/mg protein) was therefore measured in hot 2 N acetic acid extracts of pancreas, stomach, pituitary, and hypothalamus in tissues obtained from three models of genetic obesity in rats. These models included the obese and lean controls of LA/N-cp, SHR/N-cp, and Zucker rats. To assess the effects of diet on SRIF levels, mixed diets were provided ad lib which contained a carbohydrate as either sucrose or starch. Some groups were fed chow diets. No significant dietary effects on tissue levels of SRIF were obtained. However, two of the three models (Zucker and SHR/N-cp) showed phenotypic effects on SRIF levels in pancreas; namely, obese rats showed a significantly greater concentration of SRIF (P less than 0.0005 and less than 0.0002, respectively) than did the lean littermates. These findings were confirmed by measurement of total pancreas SRIF content. Gastric levels were significantly altered only in the obese Zucker rats (P less than 0.005) where obese tissues had lower concentrations than those of lean animals. However similar directional changes in pancreas and stomach were observed in all models. It is concluded that the hyperinsulinemia of the obese animals studied is not due to absolute deficiency in pancreatic SRIF content. It is postulated however that decreased pancreatic SRIF secretion (paracrine or otherwise) relative to pancreatic insulin content could still play a role.
人们认为生长抑素（SRIF）在肥胖大鼠高胰岛素血症的发病机制中可能发挥作用。因此，在从三种大鼠遗传性肥胖模型获取的组织中，测量了胰腺、胃、垂体和下丘脑在热2N乙酸提取物中的SRIF样免疫反应性（纳克/毫克蛋白质）。这些模型包括LA/N-cp、SHR/N-cp和Zucker大鼠的肥胖和瘦对照。为了评估饮食对SRIF水平的影响，随意提供了含有蔗糖或淀粉作为碳水化合物的混合饮食。一些组喂食普通饮食。未获得饮食对组织SRIF水平的显著影响。然而，三个模型中的两个（Zucker和SHR/N-cp）对胰腺中的SRIF水平表现出表型效应；也就是说，肥胖大鼠的SRIF浓度（分别P小于0.0005和小于0.0002）显著高于瘦同窝仔鼠。通过测量胰腺总SRIF含量证实了这些发现。仅在肥胖的Zucker大鼠中胃水平有显著改变（P小于0.005），其中肥胖组织的浓度低于瘦动物。然而，在所有模型中胰腺和胃中观察到类似的方向变化。结论是，所研究的肥胖动物的高胰岛素血症不是由于胰腺SRIF含量的绝对缺乏。然而据推测，相对于胰腺胰岛素含量，胰腺SRIF分泌减少（旁分泌或其他方式）仍可能起作用。
