胰岛素抵抗及其在肥胖青少年糖尿病前期发病机制中的作用

N.B. Minkova, Oleg Iu. Latyshev, G. Okminyan, Elena V. Kiseleva, Dar'ia S. Romaikina, Liubov N. Samsonova
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Materials and methods. The study involved 95 adolescents with obesity. Inclusion criteria: SDS BMI≥2.0, Tanner stage ≥II, age 18.0 years, exclusion criteria: diabetes mellitus. The sample was divided into prediabetics (n=40, mean age 14.0±1.53 years; SDS BMI 3.09±0.54, boys n=23) and non-prediabetics (n=55, mean age 14.6±1.67 years; SDS BMI 3.11±0.54; boys n=32). Both groups were matched on age, SDS BMI, sex (p=0.082, p=0.975, p=0.947, respectively). The research consisted of estimates of BMI, insulin, C-peptide, fasting venous blood glucose, HbA1c, cholesterol, low-density lipoprotein, high Density Lipoprotein, triglycerides, alanine aminotransferase, aspartat aminotransferase, HOMA-IR and TyG indices, results of oral glucose tolerance test at 0 and 2 hours after glucose load, ultrasound of the hepatobiliary system. Prediabetes in adolescents was diagnosed using American Diabetes Association criteria. Data was analyzed by using SPSS Statistics for Windows, Version 26.0. Results. Prediabetes was diagnosed in 42.1% (40/95) of cases. There were statistically significant differences between the indices of groups with prediabetes and normal glucose metabolism: fasting plasma glucose – FPG (mean 5.63±0.49; 95% confidence interval – CI 5.48–5.79 vs 5.03±0.42; 4.92–5.15 mmol/L; p0.001); 2hPG (mean 7.04±0.93; 95% CI 6.74–7.34 vs 6.23±0.82; 6.01–6.46 mmol/l; p0.001); HbA1c (mean 5.5±0.31; 95% CI 5.39–5.59% vs 5.2±0.25; 5.15–5.29%; p0.001); cholesterol (4.47±0.73; 95% CI 4.23–4.72 vs 3.96±0.92; 3.73–4.24 mmol/l; p=0.004), low-density lipoprotein (2.89±0.96, 95% CI 2.55–3.20 vs 2.46±0.89, 2.21–2.71 mmol/l; p=0.036). There were no significant differences in fasting insulin, C-peptide, triglycerides, high density lipoprotein, aspartat aminotransferase, alanine aminotransferase, HOMA-IR index and TyG, were also no significant differences in the frequency of hepatic steatosis (47.5% vs 52.7%; p=0.532). Conclusion. 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引用次数: 0

摘要

背景。在过去的三十年里,全球儿童肥胖症的发病率大幅上升,与肥胖症相关的疾病(包括碳水化合物代谢紊乱)的发病率也随之增加。胰岛素抵抗和胰岛素缺乏参与肥胖症前期糖尿病的发生已经得到证实。然而,每种病理机制在儿童和青少年糖尿病前期发展中的重要性尚未确定。因此,在儿童实践中,关于肥胖症糖尿病前期的预防和治疗方法还没有可靠的数据。 研究目的研究胰岛素抵抗在肥胖青少年糖尿病前期发展中的作用。 材料和方法。研究涉及 95 名肥胖青少年。纳入标准:SDS BMI≥2.0,Tanner 阶段≥II,年龄 18.0 岁,排除标准:糖尿病。样本分为糖尿病前期患者(n=40,平均年龄(14.0±1.53)岁;SDS BMI 3.09±0.54,男生 n=23)和非糖尿病患者(n=55,平均年龄(14.6±1.67)岁;SDS BMI 3.11±0.54,男生 n=32)。两组在年龄、SDS BMI、性别方面匹配(分别为 p=0.082、p=0.975、p=0.947)。研究内容包括 BMI、胰岛素、C 肽、空腹静脉血糖、HbA1c、胆固醇、低密度脂蛋白、高密度脂蛋白、甘油三酯、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、HOMA-IR 和 TyG 指数的估计值,葡萄糖负荷后 0 小时和 2 小时的口服葡萄糖耐量试验结果,肝胆系统超声波检查。青少年糖尿病前期的诊断采用美国糖尿病协会的标准。数据使用 SPSS Statistics for Windows 26.0 版进行分析。 结果42.1%的病例(40/95)被诊断为糖尿病前期。糖尿病前期组和糖代谢正常组之间的指标差异有统计学意义:空腹血浆葡萄糖 - FPG(平均值 5.63±0.49;95% 置信区间 - CI 5.48-5.79 vs 5.03±0.42;4.92-5.15 mmol/L;P0.001);2hPG(平均值 7.04±0.93;95% CI 6.74-7.34 vs 6.23±0.82;6.01-6.46 mmol/L;P0.001);HbA1c(平均5.5±0.31;95% CI 5.39-5.59% vs 5.2±0.25;5.15-5.29%;P0.001);胆固醇(4.47±0.73;95% CI 4.23-4.72 vs 3.96±0.92; 3.73-4.24 mmol/l;P=0.004)、低密度脂蛋白(2.89±0.96,95% CI 2.55-3.20 vs 2.46±0.89,2.21-2.71 mmol/l;P=0.036)。空腹胰岛素、C 肽、甘油三酯、高密度脂蛋白、天冬氨酸氨基转移酶、丙氨酸氨基转移酶、HOMA-IR 指数和 TyG 均无明显差异,肝脏脂肪变性的频率也无明显差异(47.5% vs 52.7%;P=0.532)。 结论患有肥胖症、糖尿病前期和没有碳水化合物代谢紊乱的青少年,其外周组织对胰岛素作用的敏感性水平相似。儿童肥胖症前期糖尿病的形成还有其他因素,有待今后的研究发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Insulin resistance and its role in the pathogenesis of pre-diabetes development in obese adolescents
Background. The prevalence of childhood obesity has increased significantly over the past three decades worldwide, and in this regard, the frequency of diseases associated with obesity, including disorders of carbohydrate metabolism, has increased. The involvement of insulin resistance and insulin deficiency in the development of prediabetes in obesity has been established. However, the significance of each pathological mechanism in the development of prediabetes in childhood and adolescence has not been established. In this regard, in children's practice, there is no reliable data on methods of prevention and treatment of prediabetes in obesity. Aim. To study the role of insulin resistance in the development of prediabetes in obese adolescents. Materials and methods. The study involved 95 adolescents with obesity. Inclusion criteria: SDS BMI≥2.0, Tanner stage ≥II, age 18.0 years, exclusion criteria: diabetes mellitus. The sample was divided into prediabetics (n=40, mean age 14.0±1.53 years; SDS BMI 3.09±0.54, boys n=23) and non-prediabetics (n=55, mean age 14.6±1.67 years; SDS BMI 3.11±0.54; boys n=32). Both groups were matched on age, SDS BMI, sex (p=0.082, p=0.975, p=0.947, respectively). The research consisted of estimates of BMI, insulin, C-peptide, fasting venous blood glucose, HbA1c, cholesterol, low-density lipoprotein, high Density Lipoprotein, triglycerides, alanine aminotransferase, aspartat aminotransferase, HOMA-IR and TyG indices, results of oral glucose tolerance test at 0 and 2 hours after glucose load, ultrasound of the hepatobiliary system. Prediabetes in adolescents was diagnosed using American Diabetes Association criteria. Data was analyzed by using SPSS Statistics for Windows, Version 26.0. Results. Prediabetes was diagnosed in 42.1% (40/95) of cases. There were statistically significant differences between the indices of groups with prediabetes and normal glucose metabolism: fasting plasma glucose – FPG (mean 5.63±0.49; 95% confidence interval – CI 5.48–5.79 vs 5.03±0.42; 4.92–5.15 mmol/L; p0.001); 2hPG (mean 7.04±0.93; 95% CI 6.74–7.34 vs 6.23±0.82; 6.01–6.46 mmol/l; p0.001); HbA1c (mean 5.5±0.31; 95% CI 5.39–5.59% vs 5.2±0.25; 5.15–5.29%; p0.001); cholesterol (4.47±0.73; 95% CI 4.23–4.72 vs 3.96±0.92; 3.73–4.24 mmol/l; p=0.004), low-density lipoprotein (2.89±0.96, 95% CI 2.55–3.20 vs 2.46±0.89, 2.21–2.71 mmol/l; p=0.036). There were no significant differences in fasting insulin, C-peptide, triglycerides, high density lipoprotein, aspartat aminotransferase, alanine aminotransferase, HOMA-IR index and TyG, were also no significant differences in the frequency of hepatic steatosis (47.5% vs 52.7%; p=0.532). Conclusion. Teenagers with obesity, with prediabetes, and without disorders of carbohydrate metabolism had a similar level of peripheral tissue sensitivity to the action of insulin. There are additional factors leading to the formation of prediabetes with obesity in the child population that have to be learned in future researches.
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