Senthilkumar Gandhipuram Periyasamy, Anithalekshmi Melepallappil Sabeenakumari, Yasir Md, Parameswaran Sreejith, Packirisamy Rajaa Muthu, Bobby Zachariah
Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry-605006, India.
Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry-605006, India.
Diabetes Metab Syndr. 2018 Jan-Mar;12(1):23-26. doi: 10.1016/j.dsx.2017.08.005. Epub 2017 Aug 24.
Diabetic nephropathy (DN) is one of the major chronic vascular complication of T2DM and leading cause of end-stage renal disease. Inflammation is one of the proposed pathway which explains microvascular complications in T2DM but exact mechanism is still unclear. Omentin-1 is an anti-inflammatory adipokine which promotes insulin signaling. IL-6 is a multifunctional cytokine having role in immune and inflammatory responses. The present study was conducted to elucidate the role of omentin-1 and IL-6 in the pathogenesis of DN and its association with insulin resistance. We aimed to assess and compare the serum levels of omentin-1 and IL-6 in T2DM patients with and without DN.
MATERIALS & METHODS: Our study comprised of 2 groups of 41 each. Group A (controls) included T2DM without nephropathy patients and group B (cases) included T2DM nephropathy patients. Parameters studied were serum omentin-1, insulin, IL-6, fasting blood glucose, urea, creatinine, lipid profile, HOMA-IR, eGFR and BMI.
RESULTS & CONCLUSION: Omentin-1 (p=0.03) was significantly decreased; concomitantly, significant increase in levels of insulin (p=0.004), IL-6 (p=0.023) and HOMA-IR (p=0.0004) were found in cases compared to controls. Bivariate analysis showed eGFR correlating positively with omentin-1 and negatively with insulin in the study population. Our study results, based on serum omentin-1 and IL-6 data suggest important role played by inflammatory mechanism and insulin resistance in the pathogenesis of diabetic nephropathy in type 2 diabetes mellitus patients.
糖尿病肾病（DN）是2型糖尿病主要的慢性血管并发症之一，也是终末期肾病的主要病因。炎症是解释2型糖尿病微血管并发症的一种推测途径，但确切机制仍不清楚。网膜素-1是一种抗炎脂肪因子，可促进胰岛素信号传导。白细胞介素-6是一种多功能细胞因子，在免疫和炎症反应中起作用。本研究旨在阐明网膜素-1和白细胞介素-6在糖尿病肾病发病机制中的作用及其与胰岛素抵抗的关系。我们旨在评估和比较有和没有糖尿病肾病的2型糖尿病患者血清网膜素-1和白细胞介素-6水平。
我们的研究包括两组，每组41人。A组（对照组）包括无肾病的2型糖尿病患者，B组（病例组）包括糖尿病肾病患者。研究的参数包括血清网膜素-1、胰岛素、白细胞介素-6、空腹血糖、尿素、肌酐、血脂谱、稳态模型评估的胰岛素抵抗指数（HOMA-IR）、估算肾小球滤过率（eGFR）和体重指数（BMI）。
与对照组相比，病例组的网膜素-1显著降低（p = 0.03）；同时，胰岛素（p = 0.004）、白细胞介素-6（p = 0.023）和HOMA-IR（p = 0.0004）水平显著升高。双变量分析显示，在研究人群中，eGFR与网膜素-1呈正相关，与胰岛素呈负相关。基于血清网膜素-1和白细胞介素-6数据的研究结果表明，炎症机制和胰岛素抵抗在2型糖尿病患者糖尿病肾病发病机制中起重要作用。
