作者: Claude K. Lardinois , Robert B. Richeson , Gale H. Starich , Diane Mazzu , Ernest L. Mazzaferri
DOI: 10.1016/0024-3205(90)90473-5
关键词: Islet 、 Internal medicine 、 Gastrointestinal hormone 、 Intracellular 、 Pancreatic hormone 、 Insulin 、 Gastric inhibitory polypeptide 、 Enzyme inhibitor 、 Biology 、 Phospholipase A2 、 Endocrinology
摘要: The cellular mechanisms whereby gastric inhibitory polypeptide (GIP) augments glucose-dependent insulin secretion remains poorly defined. Since is modulated by membrane associated phospholipase A2 (PLA2) and intracellular lipoxygenase (LPX) cyclooxygenase (CO) we hypothesize that GIP's augmentation of involves these enzyme systems. Neonatal rat pancreatic islet cell cultures were preincubated with 5.6mM glucose for 60 minutes. then stimulated minutes 16mM alone or GIP without the addition PLA2, LPX, CO inhibitors. Insulin significantly increased (P<0.05) when concentration was raised from 5.6 to this further augmented (P<0.05). PLA2 inhibitors (P<0.025) decreased but restored simultaneous GIP. LPX (P<0.01) decrease parsisted despite Simultaneous treatment yielded responses indistinguishable inhibition alone. These studies suggest exerts its influence in part modulating activity. Furthermore, formation products appears be a pivotal step insulinotrophic action