Herz Carsten T, Brix Johanna M, Ludvik Bernhard, Schernthaner Guntram, Schernthaner Gerit-Holger
Division of Endocrinology and Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Department of Medicine I, Klinik Landstraße, Vienna, Austria.
Obes Surg. 2021 Jun;31(6):2545-2550. doi: 10.1007/s11695-020-05200-0. Epub 2021 Feb 4.
Dipeptidyl peptidase 4 (DPP4) is expressed and secreted by adipocytes. DPP4 induces insulin resistance independently of its effect on glucagon-like peptide 1, thus it is conceivable that DPP4 directly contributes to metabolic dysfunction in patients with morbid obesity. The aim of this study was to investigate the impact of weight loss induced by bariatric surgery on DPP4 activity, and whether these changes are associated with improvements in markers of metabolic dysfunction and fatty liver disease.
We included 68 non-diabetic patients who underwent bariatric surgery. Serum DPP4 activity was measured using a fluorogenic substrate before and after surgery.
Results: After a median follow-up period of 12 (IQR 11-17) months, median serum DPP4 activity decreased from 230 (IQR: 194-273) to 193 (164-252) pmol/min (p=0.012). The decrease in DPP4 activity was significantly correlated with decreases in BMI, improved cholesterol levels, reduced hepatic injury markers as well as improved post-prandial insulin sensitivity. After multivariable adjustment, ΔDPP4 activity remained significantly associated with Δcholesterol (beta=0.341, p=0.025), ΔLDL cholesterol (beta=0.350, p=0.019), Δgamma-glutamyltransferase (beta=0.323, p=0.040) and ΔMatsuda index (beta=-0.386, p=0.045).
We demonstrated that weight loss induced by bariatric surgery results in decreased circulating DPP4 activity beyond the initial phase of weight loss. The associations between decreased DPP4 activity and improved cholesterol levels as well as hepatic injury markers point towards pleiotropic effects of DPP4 beyond glucose metabolism which warrant further investigation.
二肽基肽酶4（DPP4）由脂肪细胞表达和分泌。DPP4可独立于其对胰高血糖素样肽1的作用诱导胰岛素抵抗，因此可以想象DPP4直接导致病态肥胖患者的代谢功能障碍。本研究的目的是调查减肥手术引起的体重减轻对DPP4活性的影响，以及这些变化是否与代谢功能障碍和脂肪性肝病标志物的改善有关。
我们纳入了68例接受减肥手术的非糖尿病患者。术前和术后使用荧光底物测量血清DPP4活性。
在中位随访期12（四分位间距11 - 17）个月后，血清DPP4活性中位数从230（四分位间距：194 - 273）降至193（164 - 252）pmol/分钟（p = 0.012）。DPP4活性的降低与BMI的降低、胆固醇水平的改善、肝损伤标志物的降低以及餐后胰岛素敏感性的改善显著相关。多变量调整后，ΔDPP4活性仍与Δ胆固醇（β = 0.341，p = 0.025）、Δ低密度脂蛋白胆固醇（β = 0.350，p = 0.019）、Δγ-谷氨酰转移酶（β = 0.323，p = 0.040）和Δ松田指数（β = -0.386，p = 0.045）显著相关。
我们证明减肥手术引起的体重减轻导致循环DPP4活性在体重减轻的初始阶段之后降低。DPP4活性降低与胆固醇水平改善以及肝损伤标志物之间的关联表明DPP4在葡萄糖代谢之外具有多效性作用，值得进一步研究。
