This study investigated the effect of dietary sugars and advanced glycation end-products (AGE) on telomere dynamics in WIL2-NS cells. Dietary sugars [glucose (Glu) and fructose (Fru); 0.1 M each] were incubated with bovine serum albumin (BSA) (10 mg/ml) at 60 ± 1°C for 6 weeks to generate AGE-BSA. Liquid chromatography-mass spectrometry (LC-MS/MS) analysis showed total AGE levels as 87.74 ± 4.46 nmol/mg and 84.94 ± 4.28 nmol/mg respectively in Glu-BSA and Fru-BSA model. Cell treatment studies using WIL2-NS cells were based on either glucose, fructose (each 2.5–40 mM) or AGE-BSA (200–600 µg/ml) in a dose-dependent manner for 9 days. Telomere length (TL) was measured using qPCR. Nitric oxide (NO) production and tumour necrosis factor-α (TNF-α) levels were measured in WIL2-NS culture medium. An increasing trend for TNF-α and NO production was observed with higher concentration of glucose (R² = 0.358; P = 0.019; R² = 0.307; P = 0.027) and fructose (R² = 0.669; P = 0.001; R² = 0.339; P = 0.006). A decreasing trend for TL (R² = 0.828; P = 0.000), and an increasing trend for NO production (R² = 0.352; P = 0.031) were observed with increasing Glu-BSA concentrations. Fru-BSA treatment did not show significant trend on TL (R² = 0.135; P = 0.352) with increasing concentration, however, a significant reduction was observed at 600 µg/ml (P < 0.01) when compared to BSA treatment. No trends for TNF-α levels and a decreasing trend on NO production (R² = 0.5201; P = 0.019) was observed with increasing Fru-BSA treatment. In conclusion, this study demonstrates a potential relationship between dietary sugars, AGEs and telomere attrition. AGEs may also exert telomere shortening through the production of pro-inflammatory metabolites, which ultimately increase the risk of diabetes complications and age-related disease throughout lifespan.

中文翻译：

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先进的糖基化终产物可加速人WIL2-NS细胞中端粒的磨损并增加促炎介质。

这项研究调查了饮食糖和高级糖化终产物（AGE）对WIL2-NS细胞端粒动力学的影响。膳食糖[葡萄糖（Glu）和果糖（Fru）；将每个0.1 M]与牛血清白蛋白（BSA）（10 mg / ml）在60±1°C下孵育6周，以生成AGE-BSA。液相色谱-质谱（LC-MS / MS）分析显示，在Glu-BSA和Fru-BSA模型中，总AGE水平分别为87.74±4.46 nmol / mg和84.94±4.28 nmol / mg。使用WIL2-NS细胞进行的细胞治疗研究以葡萄糖，果糖（每个2.5–40 mM）或AGE-BSA（200–600 µg / ml）为基础，剂量依赖性地进行9天。使用qPCR测量端粒长度（TL）。在WIL2-NS培养基中测量一氧化氮（NO）的产生和肿瘤坏死因子-α（TNF-α）的水平。R ² = 0.358；P = 0.019；R ² = 0.307；P＝ 0.027）和果糖（R ²＝ 0.669；P＝ 0.001；R ²＝ 0.339；P＝ 0.006）。随着Glu-BSA浓度的增加，TL的下降趋势（R ² = 0.828；P = 0.000）和NO产生的趋势增加（R ² = 0.352；P = 0.031）。Fru-BSA治疗在TL上无明显趋势（R ² = 0.135; P= 0.352）随浓度增加而增加，但是与BSA处理相比，在600 µg / ml处观察到显着降低（P <0.01）。随着Fru-BSA处理的增加，未观察到TNF-α水平的趋势和NO产生的下降趋势（R ² = 0.5201；P = 0.019）。总之，这项研究证明了饮食糖，AGEs和端粒损耗之间的潜在关系。AGEs还可能通过促炎性代谢产物的产生而使端粒缩短，这最终会增加整个寿命期糖尿病并发症和与年龄有关的疾病的风险。