Bin Rihong, Zheng Xinsheng, Luo Ju, Liu Zhijie, Zhong Haiyan, Yang Feike
Department of First-Aid Center, Zhuzhou Central Hospital, Zhuzhou, Hunan, 412000, People's Republic of China.
Department of Geriatric Medicine, Changsha Central Hospital, Changsha, Hunan, 410000, People's Republic of China.
Int J Gen Med. 2025 Aug 12;18:4369-4378. doi: 10.2147/IJGM.S516414. eCollection 2025.
To identify the hub genes involved in sarcopenia and analyze their correlation with lipid metabolism.
Differentially expressed genes (DEGs) from sarcopenia/non-sarcopenia cohorts in and datasets were cross-analyzed with diabetes-related genes (GeneCards). Key genes underwent functional enrichment and protein-protein interaction (PPI) network analysis. The expression and receiver operating characteristic (ROC) curve of the hub gene was analyzed in both datasets. Enzyme-linked immunosorbent assay (ELISA) was utilized to quantify hub gene levels in sarcopenia, type 2 diabetes (T2DM), and healthy samples.
Twenty key genes were identified through differential expression and diabetes-related gene screening. Functional enrichment analysis revealed their involvement in external stimulus response, inflammatory regulation, extracellular processes, adenosine monophosphate-activated protein kinase (AMPK) signaling pathway, and insulin signaling pathways (p<0.05). Adiponectin () emerged as the hub gene via PPI network analysis, showing significant overexpression in sarcopenia (GSE111006: p<0.01; GSE111010: p<0.05) with diagnostic AUCs of 0.944 (0.869-1.000) and 0.696 (0.471-0.920) respectively. Ultimately, 60 sarcopenia, 10 type 2 diabetes, 10 healthy samples were collected. Seventy percent of the samples exhibited abnormal lipid metabolism. Adiponectin and AMPK were overexpressed in sarcopenia samples ( < 0.01). However, and AMPK were no difference in the expression levels between individuals with T2DM and healthy individuals (>0.05). This study identified a significant correlation between , AMPK, and blood lipids in sarcopenia ( vs AMPK, < 0.0001, = 0.736; vs HDL-C, = 0.0003, = -0.448; AMPK vs HDL-C, = 0.001, = -0.415).
The present study confirms that glycolipid metabolism is a risk factor for sarcopenia. Both ADIPOQ and AMPK are overexpressed in sarcopenia and demonstrate a significant positive correlation. This study hypothesizes that may regulate AMPK activity, affect lipid metabolism, and accelerate the occurrence and development of sarcopenia.
鉴定与肌肉减少症相关的枢纽基因，并分析它们与脂质代谢的相关性。
将来自肌肉减少症/非肌肉减少症队列在[具体数据集1]和[具体数据集2]中的差异表达基因（DEGs）与糖尿病相关基因（基因卡片）进行交叉分析。对关键基因进行功能富集和蛋白质-蛋白质相互作用（PPI）网络分析。在两个数据集中分析枢纽基因的表达及受试者工作特征（ROC）曲线。采用酶联免疫吸附测定（ELISA）法对肌肉减少症、2型糖尿病（T2DM）和健康样本中的枢纽基因水平进行定量。
通过差异表达和糖尿病相关基因筛选鉴定出20个关键基因。功能富集分析显示它们参与外部刺激反应、炎症调节、细胞外过程、腺苷单磷酸激活蛋白激酶（AMPK）信号通路和胰岛素信号通路（p<0.05）。通过PPI网络分析，脂联素（Adiponectin）成为枢纽基因，在肌肉减少症中显著过表达（GSE111006：p<0.01；GSE111010：p<0.05），诊断AUC分别为0.944（0.869 - 1.000）和0.696（0.471 - 0.920）。最终，收集了60例肌肉减少症、10例2型糖尿病、10例健康样本。70%的样本存在脂质代谢异常。脂联素和AMPK在肌肉减少症样本中过表达（p<0.01）。然而，脂联素和AMPK在T2DM患者与健康个体之间的表达水平无差异（p>0.05）。本研究确定了肌肉减少症中脂联素、AMPK与血脂之间存在显著相关性（脂联素与AMPK，p<0.0001，r = 0.736；脂联素与高密度脂蛋白胆固醇（HDL-C），p = 0.0003，r = -0.448；AMPK与HDL-C，p = 0.001，r = -0.415）。
本研究证实糖脂代谢是肌肉减少症的一个危险因素。ADIPOQ和AMPK在肌肉减少症中均过表达，并表现出显著正相关。本研究推测脂联素可能调节AMPK活性，影响脂质代谢，并加速肌肉减少症的发生和发展。
