The accumulation of advanced glycation end products (AGEs) plays critical roles in exacerbating obesity, arteriosclerosis, cardiovascular disease, diabetes, and their associated complications. Glycolaldehyde (GA) is the metabolic precursor of several AGEs, and its effects vary based on food and cooking methods. Here, 3T3-L1 adipocytes were used to examine the effects of GA on obesity and insulin resistance. We found that GA treatment did not increase lipid accumulation but increased the distribution of adipocyte differentiation. We also investigated the production of receptor for AGEs (RAGE) and reactive oxygen species (ROS) upon GA treatment, as well as the expression levels of peroxisome proliferator-activated receptors γ (PPARγ), CCAAT enhancer binding protein α (c/EBPα), and CCAAT enhancer binding protein β (c/EBPβ), which are transcription factors for adipogenesis, were significantly increased upon GA treatment in a concentration-dependent manner. GA arrested the cell cycle at the G0/G1 stage during the early phase of adipogenesis and suppressed the expression of p21 and p27. GA increased the expression of CDK2, phosphorylation of mitogen-activated protein kinases, and secretion of pro-inflammatory cytokines. Overall, these results suggest that GA can stimulate lipid metabolism, hence, we suggest that the stimulation of adipogenesis and insulin resistance by GA may be associated with the interaction between RAGE and adipogenic factors in adipocytes.

中文翻译：

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乙醇醛通过脂肪生成破坏胰岛素信号和葡萄糖摄取

晚期糖基化终产物 (AGEs) 的积累在加重肥胖、动脉硬化、心血管疾病、糖尿病及其相关并发症方面起着关键作用。乙醇醛 (GA) 是多种 AGE 的代谢前体，其作用因食物和烹饪方法而异。在这里，3T3-L1 脂肪细胞用于检查 GA 对肥胖和胰岛素抵抗的影响。我们发现 GA 处理不会增加脂质积累，但会增加脂肪细胞分化的分布。我们还研究了 GA 处理后 AGEs (RAGE) 和活性氧 (ROS) 受体的产生，以及过氧化物酶体增殖物激活受体 γ (PPARγ)、CCAAT 增强子结合蛋白 α (c/EBPα) 的表达水平和 CCAAT 增强子结合蛋白 β (c/EBPβ)，作为脂肪生成的转录因子，GA 处理后以浓度依赖性方式显着增加。GA 在脂肪生成的早期阶段在 G0/G1 阶段阻止细胞周期并抑制 p21 和 p27 的表达。GA 增加 CDK2 的表达、丝裂原活化蛋白激酶的磷酸化和促炎细胞因子的分泌。总的来说，这些结果表明 GA 可以刺激脂质代谢，因此，我们认为 GA 对脂肪生成和胰岛素抵抗的刺激可能与 RAGE 和脂肪细胞中脂肪生成因子之间的相互作用有关。GA 在脂肪生成的早期阶段在 G0/G1 阶段阻止细胞周期并抑制 p21 和 p27 的表达。GA 增加 CDK2 的表达、丝裂原活化蛋白激酶的磷酸化和促炎细胞因子的分泌。总的来说，这些结果表明 GA 可以刺激脂质代谢，因此，我们认为 GA 对脂肪生成和胰岛素抵抗的刺激可能与 RAGE 和脂肪细胞中脂肪生成因子之间的相互作用有关。GA 在脂肪生成的早期阶段在 G0/G1 阶段阻止细胞周期并抑制 p21 和 p27 的表达。GA 增加 CDK2 的表达、丝裂原活化蛋白激酶的磷酸化和促炎细胞因子的分泌。总的来说，这些结果表明 GA 可以刺激脂质代谢，因此，我们认为 GA 对脂肪生成和胰岛素抵抗的刺激可能与 RAGE 和脂肪细胞中脂肪生成因子之间的相互作用有关。