Richter G, Göke R, Göke B, Arnold R
Department of Internal Medicine, Philipps University of Marburg, Federal Republic of Germany.
J Endocrinol. 1990 Sep;126(3):445-50. doi: 10.1677/joe.0.1260445.
The effect of dexamethasone on binding of glucagon-like peptide-1(7-36)amide (GLP-1(7-36)amide) to rat insulinoma-derived cells (RINm5F) was investigated. Preincubation of RINm5F cells with dexamethasone (100 nmol/l) for 24 h resulted in a decrease of GLP-1(7-36)amide binding to 55.0 +/- 8.16% (mean +/- S.E.M.), incubation for 48 h to 39.1 +/- 1.76%, and for 72 h to 15.5 +/- 4.35% of maximal binding. The GLP-1(7-36)amide-induced stimulation of cyclic AMP (cAMP) production was significantly decreased to 61.03 +/- 7.4% of maximum production in cells pretreated with dexamethasone (100 nmol/l) for 48 h. The decreased binding was due to a reduction of the receptor number while the receptor affinity remained unchanged. These inhibitory effects on binding and cAMP formation induced by dexamethasone were completely abolished when the antiglucocorticoid RU 38486 (100 nmol/l) was added during preincubation with dexamethasone. RU 38486 alone had no effects. Our data suggest that the biological action of GLP-1(7-36)amide at the B-cell may be modified by glucocorticoids.
研究了地塞米松对胰高血糖素样肽-1(7-36)酰胺(GLP-1(7-36)酰胺)与大鼠胰岛素瘤来源细胞(RINm5F)结合的影响。将RINm5F细胞与地塞米松(100 nmol/l)预孵育24小时,导致GLP-1(7-36)酰胺结合减少至最大结合量的55.0±8.16%(平均值±标准误),孵育48小时减少至39.1±1.76%,孵育72小时减少至15.5±4.35%。在预孵育48小时的地塞米松(100 nmol/l)处理的细胞中,GLP-1(7-36)酰胺诱导的环磷酸腺苷(cAMP)生成刺激显著降低至最大生成量的61.03±7.4%。结合减少是由于受体数量减少,而受体亲和力保持不变。当在与地塞米松预孵育期间加入抗糖皮质激素RU 38486(100 nmol/l)时,地塞米松对结合和cAMP形成的这些抑制作用完全消除。单独使用RU 38486没有效果。我们的数据表明,糖皮质激素可能会改变GLP-1(7-36)酰胺在B细胞的生物学作用。