Frier B M, Corrall R J, Ashby J P, Baird J D
Diabetologia. 1980 Apr;18(4):297-300. doi: 10.1007/BF00251009.
The plasma concentration of C-peptide, insulin (IRI) and glucose was measured in 9 healthy subjects during insulin-induced hypoglycaemia followed by a meal. Identical observations were made in the same subjects after an equivalent period of fasting without hypolycaemia (control study). Endogenous secretion of insulin was suppressed following administration of exogenous insulin and this persisted long after the blood glucose concentration had returned to normal. After the meal the mean blood glucose rose to a peak of 8.4 +/- 0.3 mmol/l (mean +/- SEM) at 60 min and was still raised at 7.5 +/- 0.3 mmol/l at 120 min, compared with a peak value of only 5.1 +/- 0.2 mmol/l at 30 min after the meal in the control study. Following hypoglycaemia the mean plasma IRI rose from 8.3 +/- 1.3 mU/l to a delayed peak of 81.6 +/- 12.7 mU/l at 60 min and was 123.5 +/- 14 mU/l at 120 min post-prandially, compared with a peak of 72.4 +/- 0.5 mU/l at 30 min after the meal in the control study. Acute hypoglycaemia may thus induce in abnormal pattern of insulin secretion in response to a meal, with impaired carbohydrate tolerance in normal subjects.
在9名健康受试者中,测定了胰岛素诱导低血糖后进食期间的C肽、胰岛素(IRI)和葡萄糖的血浆浓度。在相同受试者经过同等禁食期但无低血糖的情况下进行了相同观察(对照研究)。给予外源性胰岛素后,内源性胰岛素分泌受到抑制,且在血糖浓度恢复正常后仍持续很长时间。进食后,平均血糖在60分钟时升至峰值8.4±0.3毫摩尔/升(平均值±标准误),在120分钟时仍为7.5±0.3毫摩尔/升,而对照研究中进食后30分钟的峰值仅为5.1±0.2毫摩尔/升。低血糖后,平均血浆IRI从8.3±1.3毫国际单位/升在60分钟时升至延迟峰值81.6±12.7毫国际单位/升,餐后120分钟时为123.5±14毫国际单位/升,而对照研究中进食后30分钟的峰值为72.4±0.5毫国际单位/升。因此,急性低血糖可能会诱导正常受试者对进食产生异常的胰岛素分泌模式,并伴有碳水化合物耐量受损。