Objective To compare the levels of apolipoprotein A5 (apoA5), insulin resistance (IR) and the secretion function of islet β-cells between subjects with impaired fasting glucose and impaired glucose tolerance, and to investigate the underlying pathogenesis. Methods Twenty-three patients with impaired fasting glucose (IFG group), 24 with impaired glucose tolerance (IGT group), and 30 individuals with normal glucose tolerance (NGT group, as control) were enrolled in present study. All subjects underwent intravenous glucose tolerance test (IVGTT). Fasting apoA5 was assayed by ELISA. Fasting free fatty acid and the free fatty acid at 120 min after glucose loading were measured by colorimetry. Triglyeride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), total cholesterol (TC), fasting plasma glucose (FPG) and plasma glucose at 2 hours after glucose loading (2hPG) were determined. Homeostasis model assessments for insulin resistance (HOMA-IR) and for β-cell function (HOMA-B) were calculated. The relationships between apoA5 and those indexes mentioned above were analyzed. Results The levels of apoA5, AIR0-10 , HOMA-B were significantly lower in IFG and IGT groups than in NGT group (P<0.05), the levels of TG, FFA, 2hFFA, HOMA-IR and FINS were significantly higher in IFG and IGT groups than in NGT group (P<0. 05). The levels of apoA5, AIR0-10, HOMA-B, FINS and 2hPG were significantly lower in IFG group than in IGT group (P<0. 05), the levels of TG, FFA, 2hFFA, HOMA-IR and FPG increased significantly in IFG group than in IGT group (P<0.05). ApoA5 was positively correlated with AIRo-io, HOMA-B and HDL-C, and negatively correlated with TG, FFA, 2hFFA, LDL-C, FPG, 2hPG, FINS, HOMA-IR, M and WHR Stepwise multiple regression analysis showed that AIR0-10, , TG, FFA and HOMA-IR were independent factors of apoA5. Conclusions The insulin resistance and impaired secretion function of islet β-cell are more severe in the subjects with IFG than those with IGT. It is conjectured that the subjects with IFG have lower level of plasma apo A5, thus by raising the level of plasma apoA5 might be a possible pathway to prevent and delay IFG to develop into diabetes mellitus.%目的 比较空腹血糖受损(IFG)与糖耐量减低(IGT)者的血浆载脂蛋白A5(apoA5)、甘油三酯(TG)、胰岛素抵抗(IR)及胰岛β细胞功能,初步探讨IFG与IGT发病机制中的差异.方法 选取23例空腹血糖受损者(IFG组)、24例糖耐量减低者(IGT组)及30例正常糖耐量者(NGT组),行静脉葡萄糖耐量试验(IVGTT),测0～10min胰岛素水平,计算急性胰岛素反应0-10(AIR0-10),并采用ELISA法测定空腹apoA5水平,比色法测定空腹游离脂肪酸(FFA)及糖负荷后120min FFA(2hFFA)水平,稳态模型评价胰岛素抵抗指数(HOMA-IR)及胰岛β细胞功能(HOMA-B),探讨apoA5与AIR0-10、TG、HOMA-B、HOMA-IR、FFA、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、总胆固醇(TC)、FPG及2hPG的关系.结果 IFG组和IGT组apoA5、AIR0-10、HOMA-B显著低于NGT组(P＜0.05),而TG、FFA、2hFFA、HOMA-IR、FINS明显高于NGT组(P＜0.05);IFG组apoA5、AIR0-10、HOMA-B、FINS、2hPG显著低于IGT组(P＜0.05),TG、FFA、2hFFA、HOMA-IR、FPG明显高于IGT组(P＜0.05).相关分析显示,apoA5与AIR0-10、HOMA-B、HDL-C呈正相关,而与TG、FFA、2hFFA、LDL-C、FPG、2hPG、FINS、HOMA-IR、BMI、WHR呈负相关;多元逐步回归分析显示,AIR0-10、TG、FFA、HOMA-IR是apoA5的独立影响因素.结论 IFG人群的IR和胰岛β细胞分泌功能受损较IGT人群更严重,其机制可能与IFG人群血浆中apoA5水平更低有关,提示apoA5可能是预防及延缓IFG进展为糖尿病的新靶点之一.
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