Sheriba Nermin A, Ahmed Iman Z, Abdelsalam Mona M, Eid Yara M, Mahdy Maram M, Mansour Hany K
Internal Medicine - Endocrinology and Metabolism unit, Ain-Shams University, Cairo, Egypt.
Curr Diabetes Rev. 2018;14(3):291-297. doi: 10.2174/1573399813666170112151108.
Insulin resistance may develop with Type 1 diabetes. Insulin resistance is currently recognized by the estimated glucose disposal rate. Serum fetuin has been accused as a risk factor for metabolic syndrome.
To determine the relationship between the serum fetuin and insulin resistance in Type 1 diabetes subjects and the effect of short-term Metformin therapy on this relationship.
40 T1DM male ≥ 18 years of age were screened for insulin resistance (defined using estimated glucose disposal rate). 20 subjects (Group I) were insulin resistant with a mean estimated glucose disposal rate of (7.15±0.37 mg/kg/min) while 20 subjects (Group II) were non-insulin resistant with a mean estimated glucose disposal rate of (9.08±0.42 mg/kg/min). Fasting blood sugar, 2 hours-post prandial blood sugar, HbA1c%, C-peptide, lipid profile, highly sensitive-C reactive protein, and serum fetuin were assessed. Group I were given 1gm Metformin twice daily for 3 months as an add-on to their insulin regimen. All anthropometric and laboratory parameters were reassessed at the end of the 3 months.
Group I had a higher age, BMI and waist/hip ratio, FBS, PPBS, HbA1c%, TC, LDL-C, TG, Hs-CRP and serum fetuin (ρ ≤ 0.001), and a lower C-peptide (ρ=0.001). Fetuin showed a positive correlation with age, FBS, HbA1c%, and Hs-CRP. After Metformin therapy, FBS, PPB and HbA1c%, Hs- CRP and fetuin decreased (ρ≤0.001) while eGDR and insulin dose in units/kg increased (ρ <0.001). Correlation after Metformin therapy within Group I showed that eGDR was inversely related with FBS and PPBS and fetuin showed a positive correlation with Hs-CRP.
Serum fetuin was elevated in insulin resistant T1DM, yet this was not associated with eGDR. Levels of fetuin-A and HsCRP decreased after Metformin therapy.
1型糖尿病患者可能会出现胰岛素抵抗。目前通过估计的葡萄糖处置率来识别胰岛素抵抗。血清胎球蛋白被认为是代谢综合征的一个风险因素。
确定1型糖尿病患者血清胎球蛋白与胰岛素抵抗之间的关系，以及短期二甲双胍治疗对这种关系的影响。
对40名年龄≥18岁的1型糖尿病男性患者进行胰岛素抵抗筛查（使用估计的葡萄糖处置率进行定义）。20名受试者（第一组）存在胰岛素抵抗，平均估计葡萄糖处置率为（7.15±0.37毫克/千克/分钟），而20名受试者（第二组）无胰岛素抵抗，平均估计葡萄糖处置率为（9.08±0.42毫克/千克/分钟）。评估空腹血糖、餐后2小时血糖、糖化血红蛋白（HbA1c）百分比、C肽、血脂谱、高敏C反应蛋白和血清胎球蛋白。第一组患者在胰岛素治疗方案基础上，每天两次服用1克二甲双胍，持续3个月。3个月末重新评估所有人体测量和实验室参数。
第一组患者年龄、体重指数、腰臀比、空腹血糖、餐后血糖、糖化血红蛋白百分比、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、甘油三酯（TG）、高敏C反应蛋白（Hs-CRP）和血清胎球蛋白更高（ρ≤0.001），而C肽更低（ρ = 0.001）。胎球蛋白与年龄、空腹血糖、糖化血红蛋白百分比和高敏C反应蛋白呈正相关。二甲双胍治疗后，空腹血糖、餐后血糖和糖化血红蛋白百分比、高敏C反应蛋白和胎球蛋白降低（ρ≤0.001），而估计的葡萄糖处置率（eGDR）和胰岛素剂量（单位/千克）增加（ρ <0.001）。第一组患者二甲双胍治疗后的相关性分析表明，估计的葡萄糖处置率与空腹血糖和餐后血糖呈负相关，胎球蛋白与高敏C反应蛋白呈正相关。
胰岛素抵抗的1型糖尿病患者血清胎球蛋白升高，但这与估计的葡萄糖处置率无关。二甲双胍治疗后胎球蛋白A和高敏C反应蛋白水平降低。
