Strbák V, Ouafik L H, Resetková E, Oliver C, Giraud P, Dutour A, Salers P, Randusková A
Institute of Experimental Endocrinology, CPS Slovak Academy of Sciences, Bratislava, Czechoslovakia.
Life Sci. 1989;44(12):779-87. doi: 10.1016/0024-3205(89)90375-5.
The effect of maternal diabetes (induced by i.p. injections of 40-50 mg/kg BW Streptozotocin on the day of mating) on TRH in the pancreas of newborn rats was studied. Determination of peptide alpha amidation activity and TRH precursor level on the day of birth revealed decreased biosynthesis of TRH resulting in profoundly (10 times) lower pancreatic TRH and TRH-OH concentrations in pups of diabetic rats. Pancreatic His-Pro-diketopiperazine (His-Pro-DKP) remained unaffected by maternal diabetes. The depression of pancreatic TRH was less profound 24 h later, and even elevated TRH was measured in the pancreas of pups of diabetic mothers on postnatal day 5. Short term postnatal starvation or nursing of intact pups by the diabetic foster mother did not affect pancreatic TRH. It could be postulated that postnatal TRH development in the rat pancreas is retarded by maternal diabetes, while His-Pro-DKP remains unaltered.
研究了母体糖尿病(在交配当天腹腔注射40 - 50 mg/kg体重链脲佐菌素诱导)对新生大鼠胰腺中促甲状腺激素释放激素(TRH)的影响。出生当天对肽α酰胺化活性和TRH前体水平的测定显示,TRH的生物合成减少,导致糖尿病大鼠幼崽的胰腺TRH和TRH - OH浓度大幅降低(降低10倍)。胰腺组氨酸 - 脯氨酸二酮哌嗪(His - Pro - DKP)不受母体糖尿病的影响。24小时后胰腺TRH的降低程度较小,甚至在出生后第5天糖尿病母亲的幼崽胰腺中检测到TRH升高。新生后短期饥饿或由糖尿病代孕母亲哺育完整的幼崽不会影响胰腺TRH。可以推测,母体糖尿病会阻碍大鼠胰腺中出生后TRH的发育,而His - Pro - DKP则保持不变。