CAJ | 학술논문

目的：比较2型糖尿病（T2DM）合并非酒精性脂肪肝病（NAFLD）患者空腹和糖负荷后胰岛素敏感性的变化情况，并探讨其独立危险因素。方法选取2013~2014年住院的T2DM患者299例，据腹部超声结果分为2组，其中合并NAFLD组（T2DM＋NAFLD组）176例，单纯T2DM组123例。2组患者均测血脂，并行口服葡萄糖耐量（OGTT）和胰岛素释放试验，以胰岛素敏感指标（ISI）、定量检测胰岛素敏感性指数（QUICKI指数）、稳态模型评估的胰岛素抵抗指数（HOMA-IR）反映空腹胰岛素敏感性；稳态模型评估胰岛β细胞功能指数（HOMA-β）反映基础胰岛β细胞功能；Cederholm指数、Matsuda指数反映糖负荷后胰岛素敏感性；早期胰岛素分泌功能指数（ΔI30/ΔG30）、晚相胰岛素分泌功能指数（AUCI30-120/AUCG30-120）反映动态胰岛β细胞功能；以胰岛素抵抗指数（HIR）评估肝脏胰岛素抵抗程度。组间比较采用t检验或非参数检验，并行Logistic回归分析，筛查T2DM合并NAFLD患者的独立危险因素。结果与T2DM组相比，T2DM＋NAFLD组HOMA-IR、HIR升高（P均＜0.05），QUICKI指数、Matsuda指数、Cederholm指数、ISI降低（P均＜0.05），血脂、FPG、PPG、HOMA-β、早相和晚相胰岛素分泌功能指数差异无统计学意义（P均＞0.05）。Logistic回归结果显示Cederholm指数、Matsuda指数与T2DM伴NAFLD独立相关（OR值分别为0.956，0.840，P均＜0.05）。结论糖负荷后胰岛素敏感性下降在T2DM合并NAFLD患者发病机制中所占贡献更大；伴T2DM的NAFLD患者动态胰岛素分泌功能均下降，机体代偿分泌胰岛素能力减低。
목적：비교2형당뇨병（T2DM）합병비주정성지방간병（NAFLD）환자공복화당부하후이도소민감성적변화정황，병탐토기독립위험인소。방법선취2013~2014년주원적T2DM환자299례，거복부초성결과분위2조，기중합병NAFLD조（T2DM＋NAFLD조）176례，단순T2DM조123례。2조환자균측혈지，병행구복포도당내량（OGTT）화이도소석방시험，이이도소민감지표（ISI）、정량검측이도소민감성지수（QUICKI지수）、은태모형평고적이도소저항지수（HOMA-IR）반영공복이도소민감성；은태모형평고이도β세포공능지수（HOMA-β）반영기출이도β세포공능；Cederholm지수、Matsuda지수반영당부하후이도소민감성；조기이도소분비공능지수（ΔI30/ΔG30）、만상이도소분비공능지수（AUCI30-120/AUCG30-120）반영동태이도β세포공능；이이도소저항지수（HIR）평고간장이도소저항정도。조간비교채용t검험혹비삼수검험，병행Logistic회귀분석，사사T2DM합병NAFLD환자적독립위험인소。결과여T2DM조상비，T2DM＋NAFLD조HOMA-IR、HIR승고（P균＜0.05），QUICKI지수、Matsuda지수、Cederholm지수、ISI강저（P균＜0.05），혈지、FPG、PPG、HOMA-β、조상화만상이도소분비공능지수차이무통계학의의（P균＞0.05）。Logistic회귀결과현시Cederholm지수、Matsuda지수여T2DM반NAFLD독립상관（OR치분별위0.956，0.840，P균＜0.05）。결론당부하후이도소민감성하강재T2DM합병NAFLD환자발병궤제중소점공헌경대；반T2DM적NAFLD환자동태이도소분비공능균하강，궤체대상분비이도소능력감저。
Objective To compare the changing of fasting and sugar loading insulin sensitivity related to type 2 diabetes mellitus (T2DM) and the development of nonalcoholic fatty liver disease (NAFLD), and explore the independent risk factor.MethodsA total of 299 in-patients with T2DM were recruited in this study between 2013 and 2014. According to abdominal ultrasound results, they were divided into T2DM groups (T2DM group, 123 cases), T2DM with NAFLD (T2DM+NAFLD group, 176 cases), clinical data collected included plasma lipid levels, as well as results form oral glucose tolerance (OGTT) and insulin releasing test, insulin sensitivity index (ISI), quantitative insulin sensitivity index (QUICKI index), the steady-state model assessment of insulin resistance index (HOMA-IR) were used to estimate fasting insulin sensitivity; steady state model of the assessment islet beta cell function index (HOMA-beta) were used to estimate based islet beta cell function; Cederholm index, Matsuda index were used to estimate sugar loading insulin sensitivity; early insulin secretion index (delta I30/delta G30) and late phase insulin secretion index (AUCG30-120/AUCI30-120) were used to estimate dynamic islet beta cell function; hepatic insulin resistance index (HIR) was used to estimate hepatic insulin resistance. Thet-test and nonparametric test were used for statistical analyses, Logistic regression analysis was used to assess independent risk factors of T2DM with NAFLD.ResultsCompared with T2DM group, T2DM with NAFLD groups had higher HOMA-IR and HIR (P<0.05), QUICKI index, Matsuda index, Cederholm index and ISI were lower (P<0.05), plasma lipid levels, PPG, HOMA-β, early phase and late phase insulin secretion index had no statistically significant difference (P>0.05). Logistic regression analysis results showed Cederholm index and Matsuda index were independent related to T2DM with NAFLD (OR values were 0.956, 0.840,P<0.05).ConclusionThe decreasing of insulin sensitivity after sugar loading contributes more in T2DM patients with NAFLD; dynamic insulin secretion decreases in T2DM patients with NAFLD, the body compensatory ability to secrete insulin reduces.