Serum dipeptidyl peptidase-4 activity in insulin resistant patients with non-alcoholic fatty liver disease: a novel liver disease biomarker.
Serum dipeptidyl peptidase-4 activity in insulin resistant patients with non-alcoholic fatty liver disease: a novel liver disease biomarker.
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DOI：
10.1371/journal.pone.0012226
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发表时间：
2010-08-18
期刊：
影响因子：
3.7
通讯作者：
Somogyi A
中科院分区：
文献类型：
--
作者：
Firneisz G;Varga T;Lengyel G;Fehér J;Ghyczy D;Wichmann B;Selmeci L;Tulassay Z;Rácz K;Somogyi A
在一项横断面研究中，我们研究了未接受格列汀治疗的 2 型糖尿病患者、非酒精性脂肪性肝病 (NAFLD) 和健康对照 (CNTRL) 的空腹血清 DPP-4 酶活性 (sDPP-4) 和胰岛素抵抗指数 (HOMA2-IR)。 通过动力学测定，在 39 名 NAFLD（F/M：19/20，平均年龄：47.42 岁）和 82 名 2 型糖尿病（F/M：48/34，62.8 岁）患者和 26 名对照（F/M：14/12，35.3 岁）对照中测量了 sDPP-4。将 T2D 组定义为患有 2 型糖尿病但没有临床明显肝病的患者，创建了非重叠研究组。 NAFLD 的诊断基于超声检查并排除其他病因。 T2D 和 NAFLD 组的患者同样肥胖。 39 名 NAFLD 患者接受 75 g CH OGTT：24-NGT、4-IGT 或 IFG（“糖尿病前期”）、11 名 2 型糖尿病。 HOMA2-IR：CNTRL：1.44； T2D 组：2.62（p = 0.046 对比 CNTRL，参数测试）； NAFLD（仅限 NGT）：3.23（p = 0.0013 对比 CNTRL）； NAFLD（IFG/IGT/2 型糖尿病）：3.82（与 CNTRL 相比，p<0.001；与 2TD 组相比，p = 0.049）。 NAFLD 组（平均值：33.08U/L）和糖代谢异常（30.38U/L）的 sDPP-4 活性均高于 CNTRL 组（25.89U/L，p<0.001 和 p = 0.013）或 T2D 组（23.97U/L，p<0.001 和p = 0.004)。 sDPP-4 和 ALT 之间 NAFLD 的相关性：r = 0.4637，p = 0.0038 和 γGT：r = 0.4991，p = 0.0017 和 HOMA2-IR：r = 0.5295，p = 0.0026 HOMA2-IR和ALT之间：r = 0.4340，p = 0.0147和γGT：r = 0.4128，p = 0.0210。 如果有意排除肝病患者，则 T2D 患者的空腹血清 DPP-4 活性不会升高。 NAFLD 中的高血清 DPP-4 活性与肝脏测试相关，但与空腹血糖或 HbA1C 无关，这支持过量的 DPP-4 是肝脏来源的，并且可能会加速代谢恶化。 NAFLD 中 γGT、ALT 和血清 DPP-4 活性之间以及血清 DPP-4 活性与 HOMA2-IR 之间的相关性强烈表明，血清 DPP-4 活性应被视为一种新型肝病生物标志物。
In a cross-sectional study we studied the fasting serum DPP-4 enzymatic activity (sDPP-4) and the insulin resistance index (HOMA2-IR) in gliptin naïve patients with type 2 diabetes and in non-alcoholic fatty liver disease (NAFLD) and in healthy controls (CNTRL). sDPP-4 was measured by kinetic assay in 39 NAFLD (F/M:19/20, mean age: 47.42 yrs) and 82 type 2 diabetes (F/M:48/34, 62.8 yrs) patients and 26 (F/M:14/12, 35.3 yrs) controls. Definition of T2D group as patients with type 2 diabetes but without clinically obvious liver disease created non-overlapping study groups. Diagnosis of NAFLD was based on ultrasonography and the exclusion of other etiololgy. Patients in T2D and NAFLD groups were similarly obese. 75 g CH OGTT in 39 NAFLD patients: 24-NGT, 4-IGT or IFG (“prediabetes”), 11-type 2 diabetes. HOMA2-IR: CNTRL: 1.44; T2D-group: 2.62 (p = 0.046 vs CNTRL, parametric tests); NAFLD(NGTonly): 3.23 (p = 0.0013 vs CNTRL); NAFLD(IFG/IGT/type 2 diabetes): 3.82 (p<0.001 vs CNTRL, p = 0.049 vs 2TD group). sDPP-4 activity was higher in NAFLD both with NGT (mean:33.08U/L) and abnormal glucose metabolism (30.38U/L) than in CNTRL (25.89U/L, p<0.001 and p = 0.013) or in T2D groups (23.97U/L, p<0.001 and p = 0.004). Correlations in NAFLD among sDPP-4 and ALT: r = 0.4637,p = 0.0038 and γGT: r = 0.4991,p = 0.0017 and HOMA2-IR: r = 0.5295,p = 0.0026 and among HOMA2-IR and ALT: r = 0.4340,p = 0.0147 and γGT: r = 0.4128,p = 0.0210. The fasting serum DPP-4 activity was not increased in T2D provided that patients with liver disease were intentionally excluded. The high serum DPP-4 activities in NAFLD were correlated with liver tests but not with the fasting plasma glucose or HbA1C supporting that the excess is of hepatic origin and it might contribute to the speedup of metabolic deterioration. The correlation among γGT, ALT and serum DPP-4 activity and also between serum DPP-4 activity and HOMA2-IR in NAFLD strongly suggests that serum DPP-4 activity should be considered as a novel liver disease biomarker.
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