Ehrenreich H, Kolmar C, Pittius C, Goebel F D
Medizinische Poliklinik, Universität München.
Klin Wochenschr. 1988 Feb 15;66(4):175-80. doi: 10.1007/BF01727787.
Administration of synthetic human corticotropin-releasing factor (hCRF, 2 micrograms/kg body weight) during simultaneous application of the opioid antagonist naloxone (1.6 mg i.v. bolus, followed by an infusion at a rate of 1.2 mg/h) produced a significant increase in plasma C-peptide levels of six male Type 2 diabetic patients which even exceeded the postprandial values. This stimulatory effect of hCRF/naloxone on plasma C-peptide was less pronounced in six healthy men. hCRF alone did not provoke any reaction of plasma C-peptide in either group. The possibility of a paracrine, CRF-dependent mechanism in pancreatic islets which somehow involves inhibitory opioid receptors is preferentially discussed. Such a mechanism may underlie the stimulatory action of hCRF/naloxone on B cells and would explain the absent reaction of peripheral venous plasma C-peptide to hCRF alone as well as the amplifying effect of simultaneous opioid receptor blockade.
在同时应用阿片类拮抗剂纳洛酮(静脉推注1.6毫克,随后以1.2毫克/小时的速率输注)期间,对6名男性2型糖尿病患者给予合成人促肾上腺皮质激素释放因子(hCRF,2微克/千克体重),导致血浆C肽水平显著升高,甚至超过餐后值。hCRF/纳洛酮对血浆C肽的这种刺激作用在6名健康男性中不太明显。单独使用hCRF在两组中均未引起血浆C肽的任何反应。优先讨论了胰岛中一种旁分泌、CRF依赖性机制的可能性,该机制以某种方式涉及抑制性阿片受体。这种机制可能是hCRF/纳洛酮对B细胞刺激作用的基础,并可以解释外周静脉血浆C肽对单独hCRF无反应以及同时进行阿片受体阻断的放大作用。