补充12 个月海豹油可阻止已知的1 型糖尿病感觉运动多发性神经病变
摘要
目的：检验以下假设，即补充12 个月的海豹油omega-3 多不饱和脂肪酸（ω-3 PUFA）可以阻止已知的1 型糖尿病（T1DM）感觉运动多发性神经病变(DSP)的进展。
方法：招募符合多伦多临床神经病评分 ≥1 的1 型糖尿病（T1DM）患者，参与为期一年的海豹油ω-3 PUFA 补充剂（10 mL D-1；750 毫克二十碳五烯酸EPA，560 毫克二十二碳五烯酸DPA 和1,020 毫克二十二碳六烯酸DHA）的单臂开放标签性试验。主要结论是通过活体角膜共焦显微镜测量，显示角膜神经纤维长度（CNFL）一年变化，次要结论是感觉和神经传导的测试。
实验结果：四十名参与者（53％为女性），平均年龄48 ± 14，体重指数28.1 ± 5.8，糖尿病病程27 ± 18 年。23 名参与者具有临床DSP，17 名参与者无DSP。在补充实验12 个月后，基准CNFL 从8.3 ± 2.9 mm / mm2 增加到10.1 ± 3.7 mm / mm2（p = 0.002），增幅达29%。而神经传导或感觉功能没有改变。
结论：12 个月补充海豹油 与1 型糖尿病 的角膜神经纤维长度 CNFL 增加有关。
ABSTRACT
Objective: To test the hypothesis that 12 months of seal oil omega-3 polyunsaturated fatty acids (v-3 PUFA) supplementation will stop the known progression of diabetic sensorimotor polyneuropathy (DSP) in type 1 diabetes mellitus (T1DM).
Methods: Individuals with T1DM and evidence of DSP as determined by a Toronto Clinical Neuropathy Score $1 were recruited to participate in a single-arm, open-label trial of seal oil v-3 PUFA supplementation (10 mL.d21; 750 mg eicosapentaenoic acid, 560 mg docosapentaenoic acid, and 1,020 mg docosahexaenoic acid) for 1 year. The primary outcome was the 1-year change in corneal nerve fiber length (CNFL) measured by in vivo corneal confocal microscopy, with sensory and nerve conduction measures as secondary outcomes.
Results: Forty participants (53% female), aged 48 6 14 years, body mass index 28.1 6 5.8 with diabetes duration of 27 6 18 years, were enrolled. At baseline, 23 participants had clinical DSP and 17 did not. Baseline CNFL was 8.3 6 2.9 mm/mm2 and increased 29% to 10.1 6 3.7 mm/mm2 (p 5 0.002) after 12 months of supplementation. There was no change in nerve conduction or sensory function.
Conclusions: Twelve months of v-3 supplementation was associated with increase in CNFL in T1DM.
ClinicalTrials.govidentifier: NCT02034266.
Classification of evidence: This study provides Class IV evidence that for patients with T1DM and
evidence of DSP, 12 months of seal oil omega-3 supplementation increases CNFL. Neurology®
2017;88:2294–2301