Ross S A, Morrison D, McArthur R G
Pediatrics. 1981 Feb;67(2):252-4.
Failure of secretion of an insulinotropic enteric hormone has been postulated as a cause for the impaired insulin secretion observed following a glycemic stimulus in children with cystic fibrosis (CF). Gastric inhibitory polypeptide (GIP), a hormone located primarily in the duodenum, is the main hormonal stimulus to insulin release from the gastrointestinal tract. To determine whether hyposecretion of GIP was present in CF subjects, GIP secretion was measured in 15 control children and ten children with CF, following a standard oral glucose tolerance test. None of the subjects was diabetic but the CF children demonstrated significant insulinopenia compared to the normal control subjects. GIP secretion in the CF children was significantly greater than in the normal control subjects (normal, 38.8 +/- 4.6 ng/ml . min; CF, 54.9 +/- 6.1 ng/ml . min, P less than .01). These findings indicate that there is increased production of GIP in CF children rather than impaired secretion as had been postulated. The demonstration of hypersecretion of GIP in nondiabetic insulinopenic individuals adds further support to the hypothesis that insulin exerts feedback control on GIP secretion.
胰岛素促分泌性肠激素分泌不足被认为是囊性纤维化（CF）患儿在血糖刺激后胰岛素分泌受损的一个原因。胃抑制性多肽（GIP）是一种主要位于十二指肠的激素，是胃肠道刺激胰岛素释放的主要激素。为了确定CF患者是否存在GIP分泌不足，在15名对照儿童和10名CF儿童中进行了标准口服葡萄糖耐量试验后测量了GIP分泌。所有受试者均无糖尿病，但与正常对照受试者相比，CF儿童表现出明显的胰岛素缺乏。CF儿童的GIP分泌明显高于正常对照受试者（正常，38.8±4.6 ng/ml·min；CF，54.9±6.1 ng/ml·min，P＜0.01）。这些发现表明，CF儿童中GIP的产生增加，而不是如之前所假设的那样分泌受损。在非糖尿病性胰岛素缺乏个体中GIP分泌过多的证明进一步支持了胰岛素对GIP分泌施加反馈控制的假说。
