综述解读

老年肌少症-糖尿病共病的交互通路与治疗创新:通过整合照护打破负性自增强循环

来源:Diabetes, metabolic syndrome and obesity : targets and therapy · PMID 42974037 · DOI 10.2147/DMSO.S630510 · 来源:IMA 知识库《文献层·文献监控卡片》2026-11-05 期 · 全文级(file_id dAlZBwueyWSz,实际下载核验 1,395,640 B) · 全文已获取并通过三重归属校验

时间标签:数据日期 2026-11-05 · 生成时间 2026-11-05 05:30(Asia/Shanghai)| 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 | 情报发生日期 2026-11-05

研究问题

For patients with both chronic kidney disease and T2DM, it is currently unclear whether using DPP4is can prevent cardiovascular or renal complications.;Whether the weight loss derives predominantly from fat mass or also compromises skeletal muscle remains unresolved, and long-term safety data in older, sarcopenic, or prefrail populations are conspicuously absent.;Third, whether SGLT2is-induced fat reduction confers net benefit in patients with already diminished muscle mass has not been rigorously tested, and some authors have urged caution against uncritical use in this demographic.141 Collectively, these considerations suggest that the choice among DPP4is, SGLT2is, GLP-1 RAs, and dual agonists cannot be reduced to glycemic or cardiorenal metrics alone; it must explicitly incorporate muscle health as a therapeutic dimension.

方法

Linked by intricate pathophysiological pathways, these conditions establish a deleterious bidirectional relationship that significantly worsens health prognoses.2,3 Sarcopenia—defined as the progressive loss of skeletal muscle mass and function—not only disrupts glucose homeostasis, thereby increasing diabetes susceptibility, but also exacerbates metabolic instability in patients with established diabetes.;These caveats underscore the urgent need for longitudinal cohorts, subtype-stratified analyses, and mechanism-directed randomized trials.Inflammatory and Oxidative StressThe inherent low-grade inflammation of diabetes fosters IR via elevated secretion of cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α).;Reduced muscle mass compromises the primary site for glucose disposal, whereas excess fat, particularly visceral adiposity, promotes inflammation and lipotoxicity; these factors act synergistically to generate a destructive impact greater than the sum of their individual effects (“1+1>2”).36 Numerous studies derived from the Korean National Health Cohort, including follow-up analyses of cross-sectional data, report that among elderly or diabetic populations, the sarcopenic obesity group presents the highest homeostatic model assessment for IR indices.

核心结论

Temporal precedence between insulin resistance and muscle loss remains uncertain,17 and the independent contributions of US activation,18 AGE accumulation,19 microvascular disease, neuropathy, and renal impairment to sarcopenic progression have not been rigorously disentangled.20 Phenotyping tools (DXA/BIA) are confounded by hydration status and adiposity, while pooling type 1 and type 2 diabetes may obscure subtype-specific mechanisms.21 Crucially, no trial has yet demonstrated that targeting these pathways improves muscle mass or strength.;Providing pivotal early evidence of muscular metabolic dysfunction in diabetes, Petersen KF et al,27 used magnetic resonance spectroscopy to demonstrate, for the first time in humans, that skeletal muscle mitochondria in older adults have diminished oxidative phosphorylation capacity, a deficit directly correlating with IR severity.;Furthermore, Li H et al,28 identified NF-κB as the essential transcription factor linking inflammatory triggers, such as TNF-α, to the upregulation of genes driving skeletal muscle atrophy.Clinical EvidenceResearch indicates that the prevalence of sarcopenia is significantly elevated among individuals with T2DM.

局限

Specifically, advanced diabetic foot neuropathy correlates strongly with reduced fat-free mass indices.15 Moreover, inadequate glycemic control facilitates the accumulation of advanced glycation end products (AGEs) within muscle tissue, directly compromising fiber integrity and function.14,16 This coherent mechanistic framework, however, relies largely on cross-sectional correlations and animal-model extrapolations, with limited human longitudinal or interventional validation.;In contrast, pamiprevir exhibits a markedly lower propensity to induce muscle atrophy.106,107 A recent study reported an association between the use of second-generation sulfonylureas and a reduced risk of osteoporosis.108 However, these preliminary observations require validation through larger, well-designed prospective studies.Common Problems Among the Elderly Include Insufficient Protein Intake and Vitamin D DeficiencyVitamin D is a fat-soluble vitamin essential for the human body.;For patients with both chronic kidney disease and T2DM, it is currently unclear whether using DPP4is can prevent cardiovascular or renal complications.

对本项目的价值

中等价值:属「衰弱 / 肌少症功能结局」方向;肌肉骨骼 / 衰弱 / 肌少症栏目可用作本项目文献库与综述素材。 | 价值分 2.7/5(★★★☆☆)

全文来源

PubMed PMC JATS(正文 44,255 字符,题名指纹 0.72,已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验)

原文题录

  • 中文题名:老年肌少症-糖尿病共病的交互通路与治疗创新:通过整合照护打破负性自增强循环
  • 英文标题:Interactive Pathways and Therapeutic Innovations in Elderly Sarcopenia-Diabetes Comorbidity: Breaking the Negative Self-Reinforcing Loop Through Integrated Care.
  • 期刊与标识:Diabetes, metabolic syndrome and obesity : targets and therapy · PMID 42974037 · DOI 10.2147/DMSO.S630510 · PMC PMC13725092

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