Jackson R A, Hawa M I, Roshania R D, Sim B M, DiSilvio L, Jaspan J B
Cobbold Laboratories, Middlesex Hospital, London, United Kingdom.
Diabetes. 1988 Jan;37(1):119-29. doi: 10.2337/diab.37.1.119.
Mechanisms of glucose intolerance with aging were studied by comparing the metabolic response to glucose ingestion in 10 young (20-23 yr) and 10 elderly (73-80 yr) normal men with the simultaneous application of the forearm and double-isotope techniques. The latter technique consisted of a primed-constant infusion of [3-3H]glucose followed by the administration of an oral glucose load (mean +/- SE, 90.7 +/- 0.7 g) containing [1-14C]glucose. Fasting plasma glucose and insulin concentrations were similar in young and elderly subjects, but in the elderly, glucose tolerance was markedly impaired. Although in the elderly the initial rise in insulin levels (delta, i.e., the incremental area under the curve) from 0 to 30 min was delayed (P less than .02), the response from 0 to 45 min, 0 to 60 min, and thereafter equaled that in the young group, and from 90 to 240 min insulin concentrations in the elderly exceeded those in young subjects. Basal hepatic glucose output (HGO) was similar in young and elderly men (2.13 +/- 0.10 and 1.97 +/- 0.14 mg.kg-1.min-1, respectively). Similar proportional reductions in HGO from 0 to 270 min after glucose loading occurred in young (59.7 +/- 10.3%) and elderly (50.3 +/- 4.9%) subjects but was delayed in the elderly. Suppression of HGO was observed in the young 30 min after glucose ingestion (P less than .02), but not before 60 min in the elderly subjects (P less than .05). The systemic appearance of ingested glucose (0-270 min) was slowed with age (80.7 +/- 3.1 and 66.9 +/- 4.3% of the oral load in the young and elderly groups, respectively; P less than .02). Initial increments in both total glucose disappearance (Rd) and forearm glucose uptake (FGU) from 0 to 60 min after glucose loading were decreased in the elderly (Rd, 4.1 +/- 0.7 vs. 11.5 +/- 1.3 g, P less than .001; FGU, 17.2 +/- 1.4 vs. 24.6 +/- 2.5 md/dl forearm, P less than .02). The overall increment (delta, 0-270 min) in Rd was reduced with age (47.2 +/- 2.9 and 34.5 +/- 3.6 g, P less than .02 in the young and elderly, respectively), but the corresponding data for FGU were similar in the two groups.(ABSTRACT TRUNCATED AT 400 WORDS)
通过同时应用前臂和双同位素技术，比较了10名年轻（20 - 23岁）和10名老年（73 - 80岁）正常男性摄入葡萄糖后的代谢反应，以此研究衰老过程中葡萄糖不耐受的机制。后一种技术包括先静脉注射一定剂量的[3 - 3H]葡萄糖，然后口服含有[1 - 14C]葡萄糖的葡萄糖负荷（平均±标准误，90.7±0.7 g）。年轻和老年受试者的空腹血糖和胰岛素浓度相似，但老年人的葡萄糖耐量明显受损。尽管老年人从0到30分钟胰岛素水平的初始上升（δ，即曲线下增量面积）延迟（P＜0.02），但0到45分钟、0到60分钟以及之后的反应与年轻组相当，且从90到240分钟老年人的胰岛素浓度超过年轻受试者。年轻和老年男性的基础肝葡萄糖输出（HGO）相似（分别为2.13±0.10和1.97±0.14 mg·kg-1·min-1）。葡萄糖负荷后0到270分钟，年轻（59.7±10.3%）和老年（50.3±4.9%）受试者的HGO均有相似比例的下降，但老年人下降延迟。年轻受试者在摄入葡萄糖30分钟后观察到HGO受到抑制（P＜0.02），而老年受试者在60分钟之前未观察到（P＜0.05）。随着年龄增长，摄入葡萄糖的全身出现速率（0 - 270分钟）减慢（年轻组和老年组分别为口服负荷的80.7±3.1%和66.9±4.3%；P＜0.02）。葡萄糖负荷后0到60分钟，老年人的总葡萄糖消失率（Rd）和前臂葡萄糖摄取量（FGU）的初始增量均降低（Rd，4.1±0.7 vs. 11.5±1.3 g，P＜0.001；FGU，17.2±1.4 vs. 24.6±2.5 md/dl前臂，P＜0.02）。Rd的总体增量（δ，0 - 270分钟）随年龄增长而降低（年轻组和老年组分别为47.2±2.9和34.5±3.6 g，P＜0.02），但两组FGU的相应数据相似。（摘要截断于400字）
