Diabetes & Metabolism Journal糖尿病与代谢杂志
Diabetes & Metabolism Journal(英文缩写 DIABETES METAB J),ISSN 2233-6079,eISSN 2233-6087,中文译名:糖尿病与代谢杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 5.893 | Q2 |
| 2022 | 5.900 | Q1 |
| 2023 | 6.800 | Q1 |
| 2024 | 8.500 | Q1 |
| 2025 | 8.200 | Q1 |
Diabetes & Metabolism Journal 最新收录文献
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1. Prognostic Impact of Sodium-Glucose Cotransporter 2 Inhibitors in Patients with Type 2 Diabetes Mellitus and Coronary Ischemia: A Retrospective Cohort Study.
1. 钠-葡萄糖协同转运蛋白2抑制剂对2型糖尿病合并冠状动脉缺血患者的预后影响：一项回顾性队列研究PMID:日期:2026-09-30该文献暂无摘要。
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2. Differential Associations of Social Determinants of Health with Diabetic Kidney Disease and Treatment Targets in Korean Adults with Diabetes.
PMID:日期:2026-09-30Social determinants of health (SDOH) are linked to adverse diabetes outcomes internationally, but it remains unclear whether these associations are uniform or concentrated across major treatment targets in Korea's universal-coverage setting. We analyzed two Korea National Health and Nutrition Examination Survey cohorts (2021??024, n=3,129; 2011??014, n=2,602). A 4-item SDOH composite was derived from 14 candidate items; because the cohort×SDOH interaction was nonsignificant (P=0.36), the cohorts were pooled (n=5,731). Outcomes included diabetic kidney disease (DKD)-related laboratory abnormalities, defined using Kidney Disease: Improving Global Outcomes (KDIGO)-consistent single-measurement thresholds, severe hyperglycemia (glycosylated hemoglobin [HbA1c] ≥8%), uncontrolled blood pressure (≥140/85 mm Hg), and elevated low-density lipoprotein cholesterol (LDL-C; ≥100 mg/dL). Associations were analyzed using survey-weighted logistic regression adjusted for age, sex, body mass index, and cohort. The composite showed a dose-response association with DKD-related laboratory abnormalities (15.9% [score 0] to 34.2% [score ??]; odds ratio [OR] per +1 item, 1.23; 95% confidence interval [CI], 1.14 to 1.33; P<0.001). It was associated with severe hyperglycemia (OR, 1.13; 95% CI, 1.03 to 1.23), but not uncontrolled blood pressure (OR, 0.95; 95% CI, 0.88 to 1.02) or elevated LDL-C (OR, 1.00; 95% CI, 0.94 to 1.08). The HbA1c association was threshold-dependent, emerging only at severe-hyperglycemia levels. This pattern persisted among actively treated patients. Sequential adjustment for HbA1c ≥8% and blood pressure attenuated the SDOH-DKD association by less than 1%. Cumulative social disadvantage was associated with DKD-related laboratory abnormalities and severe hyperglycemia, but not failure to meet blood pressure or lipid targets. These exploratory findings may inform future SDOH assessment in Korean diabetes care. Longitudinal registry-linked studies are needed to confirm chronicity and temporality.
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3. Association between Changes in Status Based on Multiple Metabolic Syndrome Criteria and Cardiovascular Disease Risk (Diabetes Metab J 2026;dmj.2025.0197).
3. 基于多种代谢综合征标准的状态变化与心血管疾病风险之间的关联（Diabetes Metab J 2026;dmjPMID:日期:2026-09-29该文献暂无摘要。
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5. Basal Metabolic Rate, Genetic Susceptibility, and Type 2 Diabetes Mellitus Events in Adults.
PMID:日期:2026-09-01该文献暂无摘要。
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6. Sodium-Glucose Cotransporter-2 Inhibitor-Metformin Therapy in South Asians: From Guideline Adoption to Context-Specific Safety Gaps.
6. 南亚人群中的钠-葡萄糖协同转运蛋白-2抑制剂-二甲双胍治疗：从指南采纳到特定情境下的安全性差距PMID:日期:2026-09-01该文献暂无摘要。
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8. Hypothalamic Inflammaging: A Central Driver of Type 2 Diabetes Mellitus and Metabolic Disease in Aging.
8. 下丘脑炎性衰老：衰老过程中2型糖尿病和代谢疾病的中心驱动因素PMID:日期:2026-09-01Aging is a major risk factor for type 2 diabetes mellitus (T2DM) and is accompanied by chronic, low-grade inflammation known as inflammaging. Emerging evidence indicates that the hypothalamus, a central regulator of energy and glucose homeostasis, undergoes age-associated inflammatory remodeling that contributes to metabolic dysfunction. In particular, glial cells, including microglia, astrocytes, tanycytes, and neural stem cells, acquire senescence-associated phenotypes characterized by impaired homeostatic functions and increased secretion of pro-inflammatory mediators. These changes disrupt hypothalamic neuronal circuits involved in glucose sensing, energy balance, and insulin responsiveness, thereby potentially promoting systemic insulin resistance and T2DM progression. In this review, we summarize current evidence on the cellular and molecular mechanisms of hypothalamic glial inflammaging and discuss how age-related glial dysfunction may contribute to metabolic abnormalities. We also highlight emerging therapeutic strategies targeting neuroinflammation and glial senescence for the prevention and treatment of age-associated T2DM.
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9. Beyond Fat Loss: Addressing the Sarcopenia Challenge of Incretin-Based Therapies.
9. 超越减脂：应对基于肠促胰素的疗法所面临的肌少症挑战PMID:日期:2026-09-01Incretin-based therapies have transformed the treatment of type 2 diabetes mellitus and obesity by producing a weight-loss magnitude that was previously achievable only through intensive caloric restriction or bariatric surgery. This therapeutic shift has moved the clinical focus from the quantity of weight loss to the quality of weight loss. Lean mass reduction is frequently observed during weight loss induced by glucagon-like peptide-1 receptor agonists (GLP-1RAs), dual glucose-dependent insulinotropic polypeptide/GLP-1RAs, or emerging multi-agonists. However, loss of lean body mass does not necessarily indicate equivalent loss of contractile skeletal muscle or sarcopenia. Incretin-based therapy is generally associated with preferential fat mass reduction, relative preservation of lean mass, and potential improvement in muscle quality through reduced myosteatosis. Thus, the clinically relevant question is whether incretin-associated body-composition changes lead to deterioration in muscle strength or physical performance, an increased risk of falls or fractures, or impaired quality of life. Available evidence does not show obvious functional harm; however, long-term data remain limited, especially in people with reduced muscle reserve. A muscle-conscious approach that integrates body-composition assessment, functional monitoring, resistance training, nutritional optimization, and emerging pharmacologic muscle-preserving strategies is needed to achieve high-quality weight loss.
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10. Mitochondrial Proteostasis Links Diabetes and Sarcopenia: Cross-Scale Convergence from Experimental Models to Human Multi-Omics.
10. 线粒体蛋白质稳态关联糖尿病与肌少症：从实验模型到人类多组学的跨尺度汇聚PMID:日期:2026-09-01Sarcopenia in type 2 diabetes mellitus is increasingly recognized as a mechanistic consequence of chronic metabolic stress rather than mere age-related comorbidity. This review synthesizes evidence demonstrating how insulin resistance, hyperglycemia, lipotoxicity, and inflammation converge on skeletal muscle mitochondrial proteostasis to drive progressive decline. We evaluate seven pathway modules-mitochondrial dynamics, mitophagy, biogenesis, oxidative phosphorylation, nicotinamide adenine dinucleotide (NAD+)/sirtuin (SIRT)-linked regulation, protein import, and the mitochondrial unfolded protein response (UPRmt)-across an evidence map encompassing basic, clinical, and multi-omics studies. Dynamics and mitophagy represent mechanistically central quality-control nodes; their impairment permits dysfunctional organelle accumulation and promotes atrophic cascades. Direct evidence density, however, remains weighted toward oxidative phosphorylation and mitochondrial biogenesis. NAD+/SIRT-linked regulation, protein import fidelity, and UPRmt represent mechanistically upstream but comparatively underinvestigated signals. We propose a diabetes-centered framework where mitochondrial proteostasis failure mediates atrophy and reinforces insulin resistance via a self-amplifying feed-forward loop, supported by pathway responsiveness to coherent interventions. Human multi-omics data highlight network-level dysregulation rather than isolated defects, underscoring module-based biomarker strategies. Translationally, exercise remains the mechanistic cornerstone, while pathway-directed adjuncts-NAD+ precursor repletion, mitophagy modulators, and emerging pharmacotherapeutics-are warranted for patients with identifiable module-specific failure patterns.