Ziegler D, Langen K J, Herzog H, Kuwert T, Mühlen H, Feinendegen L E, Gries F A
Diabetes Research Institute, Heinrich-Heine-University, Düsseldorf, Germany.
Diabet Med. 1994 Mar;11(2):205-9. doi: 10.1111/j.1464-5491.1994.tb02021.x.
To evaluate whether cerebral glucose metabolism is impaired in diabetes the [18F]-2-deoxy-2-fluoro-D-glucose method and positron emission tomography were used to determine the regional cerebral metabolic rate of glucose in 12 healthy subjects, 8 newly diagnosed Type 1 diabetic patients 6 Type 1 diabetic subjects without peripheral neuropathy, and 7 Type 1 diabetic patients with symptomatic peripheral neuropathy, all of whom were men. In addition, multimodal evoked potentials were assessed. Cerebral glucose consumption was significantly reduced in the group with neuropathy as compared with the newly diagnosed diabetic patients and the healthy subjects (26.9 +/- 1.0 vs 33.9 +/- 1.9 and 32.5 +/- 1.1 mumol 100 g-1 min-1; p < 0.05), while in the patients without neuropathy it was 30.2 +/- 2.5 mumol 100 g-1 min-1 (NS vs the remaining groups). There were no significant differences between the groups regarding brainstem auditory and visual evoked potentials. No relationship was noted between cerebral glucose metabolism and P300 latency of event-related potentials as an index of cognitive function, but there was an inverse correlation with age (r = -0.42; p < 0.05) and duration of diabetes (r = -0.67; p < 0.05). These results suggest that cerebral glucose metabolism is normal at the time of diagnosis of Type 1 diabetes, but may become altered with both increasing duration of diabetes and age in the absence of central conduction deficits or cognitive dysfunction. Diabetic neuropathy may constitute a possible additional correlate of reduced cerebral glucose consumption.
为评估糖尿病患者脑葡萄糖代谢是否受损，采用[18F]-2-脱氧-2-氟-D-葡萄糖法和正电子发射断层扫描技术，测定了12名健康男性、8名新诊断的1型糖尿病患者、6名无周围神经病变的1型糖尿病患者以及7名有症状性周围神经病变的1型糖尿病患者的局部脑葡萄糖代谢率。此外，还评估了多模式诱发电位。与新诊断的糖尿病患者和健康受试者相比，神经病变组的脑葡萄糖消耗显著降低（分别为26.9±1.0、33.9±1.9和32.5±1.1 μmol 100 g-1 min-1；p<0.05），而无神经病变的患者为30.2±2.5 μmol 100 g-1 min-1（与其余组相比无显著差异）。各组之间的脑干听觉和视觉诱发电位无显著差异。脑葡萄糖代谢与作为认知功能指标的事件相关电位P300潜伏期之间未发现相关性，但与年龄（r = -0.42；p<0.05）和糖尿病病程（r = -0.67；p<0.05）呈负相关。这些结果表明，1型糖尿病诊断时脑葡萄糖代谢正常，但在无中枢传导缺陷或认知功能障碍的情况下，可能会随着糖尿病病程的延长和年龄的增长而发生改变。糖尿病性神经病变可能是脑葡萄糖消耗减少的一个可能的附加相关因素。
