时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
Type 2 diabetes mellitus (T2D) represents a worldwide health challenge, with its prevalence rising with the obesity epidemic and the increasing proportion of older adults in the global population [].；However, in the context of obesity- and age-induced inflammation, this regulatory feedback loop becomes dysregulated, perpetuating chronic inflammation, metabolic imbalance, and insulin resistance.；This study aimed to identify common molecular factors in pancreatic islets, AT, and the liver that might contribute to inflammatory processes leading to T2D.
方法
In contrast, for liver and AT, the limited number of available studies did not allow the application of the same criteria without substantially reducing the number of candidate genes.
核心结论
Pathways associated with apoptosis, cellular senescence, DNA damage response, and EGFR tyrosine kinase inhibitor resistance were also present in the analysis (Fig. ).；In AT, the analysis revealed significant alterations in multiple immune and metabolic pathways also present in pancreatic islets, including leptin signaling and several cytokine-mediated signaling pathways (TNF-α, IL-17, IL-4, IL-1).；In pancreatic islets, significant pathways included amino acid metabolism and biosynthesis, calcium signaling, ErbB signaling, fatty acid metabolism and degradation, focal adhesion–PI3K–Akt–mTOR signaling, Ras signaling, proteasome degradation, and regulation of the actin cytoskeleton. ‖ 结论：By unraveling these inflammatory signatures, this study offers insights for the identification of multi-dimensional biomarkers and the development of precision interventions tailored to the aged metabolic phenotype, with potential implications for mitigating inflammation-driven T2D.
局限
Preliminary evidence suggests regulation of MYD88, a key adaptor in TLR signaling, may be downstream of miR-3064 action.；This study has limitations that should be acknowledged.；The integration of multiple independent transcriptomic datasets, generated across different experimental platforms, methodologies, and study designs, may have influenced the identification of DEGs and enriched pathways, thereby limiting direct comparability across tissues.
对本项目的价值
★☆☆☆☆ 代谢轴既干预敏感性最高，也是老药新用供给最充足的来源。设计 multi-omics。
全文来源
PMC JATS 全文（正文 34,232 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Inflammatory networks between adipose tissue, liver and pancreatic islets in type 2 diabetes.
- 期刊与标识：Hum Genomics · PMID 42958439 · DOI 10.1186/s40246-026-01016-8
A 级证据分级：A 级（同行评议人体研究）
本文属人体研究证据，但需注意：观察性或小样本干预的结论不等于已证实临床获益；效应量与长期安全性仍需更大规模、更长随访的试验验证。
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