期刊
CLINICAL NUTRITION
卷 39, 期 1, 页码 49-56出版社
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.clnu.2019.01.006
关键词
Type 1 diabetes; Diabetic nephropathy; Vitamin B complex; Homocysteine; Cystatin C
Background: Homocysteine levels are elevated in patients with type 1 diabetes mellitus (T1DM) and could induce renal injury. B vitamins have an important role in preventing microvascular complications of diabetes. Aim: We performed a randomized-controlled trial of oral supplementation with vitamin B complex as an adjuvant therapy for nephropathy in pediatric T1DM patients and assessed its relation to homocysteine and cystatin C as a marker of nephropathy. Methods: This trial included 80 T1 DM patients with microalbuminuria, despite oral angiotensin-converting enzyme inhibitors, aged 12-18 years with at least 5 years disease duration and HbA1c <= 8.5%. Patients were randomly assigned into two groups: intervention group which received oral vitamin B complex (B1, B6 and B12) once daily and placebo group. Both groups were followed-up for 12 weeks with assessment of plasma homocysteine, HbA1c, urinary albumin excretion (UAE) and cystatin C. Results: Both groups were well-matched in baseline clinical and laboratory parameters. Baseline homocysteine levels were elevated in both groups compared with reference control values. After 12 weeks, supplementation with vitamin B complex for the intervention group resulted in a significant decrease of homocysteine, fasting blood glucose. HbA1c, triglycerides, total cholesterol, UAE and cystatin C compared with baseline levels (p < 0.001) and with placebo group (p < 0.001). No adverse reactions were reported. Baseline cystatin C was negatively correlated to vitamin 1312 (r = -0.77, p = 0.001). Conclusions: Vitamin B complex improved glycemic control and renal function through decreasing homocysteine and could be a safe and effective strategy for treatment of early stage nephropathy in pediatric T1DM. (C) 2019 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
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