Snorgaard O, Lassen L H, Binder C
Steno Memorial and Hvidøre Hospital, Gentofte, Denmark.
Diabetes Care. 1992 Aug;15(8):1009-13. doi: 10.2337/diacare.15.8.1009.
To study the natural history of beta-cell function from onset of IDDM to expected deterioration of insulin (C-peptide) secretion and to identify different patterns of decline, if any.
A cohort of 204 consecutive newly diagnosed IDDM (clinical criteria) patients were followed prospectively for 7.4 yr (range 6-9 yr), measuring fasting C-peptide at onset, 1, 3, 6, 9, 12, and then every 6 mo until 106 wk (range 104-135 wk). Then, postprandial C-peptide was measured.
Fasting C-peptide was 0.17 nM (range 0.11-0.25 nM) at onset followed by an annual increase rate of 0.16 nM/yr (range 0.06-0.48 nM/yr) to a peak of 0.28 nM (range 0.23-0.34 nM/yr) after 25 wk (range 12-39 wk). The subsequent annual decline rate of fasting C-peptide was 0.08 (0.05-0.12) and of postprandial C-peptide 0.03 nM/yr (range 0.02-0.06 nM/yr). None of these parameters showed bimodality in their distribution. However, some parameters were important. In men, fasting C-peptide at onset was lower, but the initial C-peptide increase rate was more pronounced compared to women. Furthermore, insulin-free remission was related to higher C-peptide levels throughout the study. C-peptide was higher during the 1st yr of diabetes in subjects greater than 30 yr of age at onset compared with younger diabetic patients. Stepwise multiple regression analysis showed that age, male sex, and fasting C-peptide at onset were of some predictive value for the C-peptide levels at 5 yr. However, simple group comparisons revealed no significant differences.
No major heterogeneity exists in the pattern of decline of beta-cell function in IDDM, although small differences in pattern could be identified in both sexes, in different age-groups, and in relation to achieving insulin-free remission.
研究从胰岛素依赖型糖尿病（IDDM）发病到胰岛素（C肽）分泌预期恶化期间β细胞功能的自然病程，并确定是否存在不同的下降模式。
对204例连续新诊断的IDDM（临床标准）患者进行前瞻性随访7.4年（范围6 - 9年），在发病时、1、3、6、9、12个月时测量空腹C肽，然后每6个月测量一次，直至106周（范围104 - 135周）。之后，测量餐后C肽。
发病时空腹C肽为0.17 nM（范围0.11 - 0.25 nM），随后以每年0.16 nM/年的速率增加（范围0.06 - 0.48 nM/年），在25周（范围12 - 39周）后达到峰值0.28 nM（范围0.23 - 0.34 nM/年）。随后空腹C肽的年下降速率为0.08（0.05 - 0.12），餐后C肽为0.03 nM/年（范围0.02 - 0.06 nM/年）。这些参数在其分布中均未显示出双峰性。然而，一些参数很重要。男性发病时的空腹C肽较低，但与女性相比，初始C肽增加速率更明显。此外，在整个研究过程中，无胰岛素缓解与较高的C肽水平相关。发病时年龄大于30岁的糖尿病患者在糖尿病第1年的C肽水平高于年轻糖尿病患者。逐步多元回归分析表明，年龄、男性性别和发病时的空腹C肽对5年时的C肽水平有一定的预测价值。然而，简单的组间比较未发现显著差异。
IDDM中β细胞功能下降模式不存在主要异质性，尽管在性别、不同年龄组以及与无胰岛素缓解相关方面可发现模式上的小差异。
