Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (798 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Conditions or pathological processes associated with the disease of diabetes mellitus. Due to the impaired control of blood glucose level in diabetic patients, pathological processes develop in numerous tissues and organs including the EYE, the kidney, the blood vessels, and the nerve tissue.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Diabetes Complication; Diabetic Complications; Diabetic Complication; Complications of Diabetes Mellitus; Diabetes Mellitus Complication; Diabetes Mellitus Complications; Diabetes-Related Complications; Diabetes-Related Complication.
Where it fits in the MeSH classification
- Broader topics
- Diabetes Mellitus
- Narrower topics
- Diabesity; Diabetic Angiopathies; Diabetic Cardiomyopathies; Diabetic Coma; Diabetic Ketoacidosis; Diabetic Nephropathies; Diabetic Neuropathies; Fetal Macrosomia
Related concepts
- Blood Glucose
- Kidney
- Blood Vessels
- Nerve Tissue
Research landscape
PubMed indexes 168,181 records tagged with the MeSH heading “Diabetes Complications” (counts retrieved 2026-11-04). 36,424 of them (21.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 50,102 records.
Reviews account for 29,802 records (17.7%) and meta-analyses for 2,594. Randomized controlled trials number 6,016 (3.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 50,102 |
| 2000-2009 | 34,686 |
| 2010-2019 | 46,969 |
| 2020 onward | 36,424 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 29,802 | 17.7% |
| Meta-analyses | 2,594 | 1.5% |
| Randomized controlled trials | 6,016 | 3.6% |
Method: PubMed query "Diabetes Complications"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in metabolism and endocrine disease
Studies of diabetes, obesity and hormone disorders often follow blood tests such as glucose, HbA1c or hormone levels, which are stand-ins for outcomes that matter more, such as complications. Lifestyle and diet research is largely observational, and weight and diabetes trials can differ in how long people were followed. Nothing on this page is advice about medicines, insulin or diet; talk to a qualified clinician about your own situation. Check whether the outcome was a lab value or a clinical event, and the type and duration of the condition studied.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Protein mediators of chronic kidney disease in Type 2 diabetes: A mendelian randomization study | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42726788 · DOI · PMC13568495 |
| CRISPR/Cas9-Driven Fndc5 Knockout Reveals Augmented Mitochondrial Structural and Dynamic Alterations in Diabetic Nephropathy | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42694879 · DOI · PMC13539912 |
| Blocking AGEs reduces airway epithelial viral susceptibility in diabetes-exacerbated COPD | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42608564 · DOI · PMC13562547 |
Protein mediators of chronic kidney disease in Type 2 diabetes: A mendelian randomization study [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundChronic kidney disease (CKD) occurs in 20-50% of the people living with Type 2 diabetes (T2D) and is the leading cause of kidney failure worldwide.
- Closing excerpt
- ConclusionsCollectively, these findings suggest that T2D influences the risk of CKD, in part, through increased circulating INHBC levels.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (336 words)
BackgroundChronic kidney disease (CKD) occurs in 20-50% of the people living with Type 2 diabetes (T2D) and is the leading cause of kidney failure worldwide. The cause of CKD is not fully understood, and few interventions prevent CKD in individuals living with diabetes. Here, we use large-scale proteomics data to identify circulating proteins that mediate the relationship between T2D and kidney disorders.Methods and findingsFirst, we used two-sample mendelian randomization (MR) and identified 71 circulating proteins whose levels were altered by genetic predisposition to T2D based on circulating proteomic GWAS from deCODE with 35,559 individuals and T2D GWAS with 80,154 cases. Then, we used cis-genetic variants to proxy the causal effect of some of these T2D-influenced circulating proteins and found that, collectively, five proteins (INHBC, GNPTG, LPO, AGRN, and CTSD) affected three kidney traits (blood urea nitrogen [BUN], estimated glomerular filtration rate [eGFR] and CKD risk) based on GWAS with up to 1,004,040 participants. Notably, we found that higher levels of circulating INHBC protein were estimated to lead to a lower eGFR and higher BUN based on MR analyses. We then replicated this MR analysis with proteomic GWAS from four additional cohorts, namely, UKB-PPP, Fenland, ARIC, and EPIC-Norfolk. We observed a consistent direction of effect across all four proteomic GWAS datasets, supporting the robustness of our results against platform and cohort variation. In observational analyses, increased circulating INHBC levels were associated with increased hazard for kidney disease diagnosis in 37,854 UK Biobank participants. We estimated that circulating INHBC levels mediate 1.3% (95% confidence interval [0.85%, 1.9%]) of the association between T2D and kidney disease diagnosis. There are important limitations in this study. Firstly, although we observed limited evidence for violations to the MR assumptions, some are untestable. Secondly, our study was not based on individuals with diabetic kidney diseases, but rather independent population-based studies assessing diabetes and kidney function separately. Therefore, additional functional analyses in disease specific cohort are needed.ConclusionsCollectively, these findings suggest that T2D influences the risk of CKD, in part, through increased circulating INHBC levels.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42726788 · DOI · PMC13568495
CRISPR/Cas9-Driven Fndc5 Knockout Reveals Augmented Mitochondrial Structural and Dynamic Alterations in Diabetic Nephropathy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- FNDC5 has been implicated in glucose homeostasis and is associated with mitochondrial function.
- Closing excerpt
- These findings underscore FNDC5's role in maintaining mitochondrial integrity and cellular health under diabetic conditions, positioning FNDC5 as a potential therapeutic target.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (287 words)
FNDC5 has been implicated in glucose homeostasis and is associated with mitochondrial function. Its role in diabetes and diabetic nephropathy (DN) remains unclear. This study hypothesizes that FNDC5 deficiency predisposes the kidney to accelerated mitochondrial dysfunction in diabetes and DN. Systemic Fndc5 knockout (KO) C57BL/6 mice were generated using CRISPR/Cas9. DN were induced in six-week-old Fndc5 wild-type (WT) and KO mice using high-fat diet combined with streptozotocin injection. Weekly blood and urine analyses assessed glucose, cholesterol, triglycerides, blood urea nitrogen, creatinine, and proteinuria. At 15 weeks, kidneys and metabolic tissues including pancreas, muscle and adipose were collected for histological and molecular analyses. Results showed that while both Fndc5 WT and KO mice were successfully induced with hyperglycemia, the Fndc5 KO DN group exhibited a slightly lower cumulative glycemic burden compared with the WT DN group. Despite this milder metabolic stress, proteinuria remained comparable between the two groups. Furthermore, histological analysis revealed that Fndc5 KO DN mice displayed more severe mesangial expansion, glomerular basement membrane thickening, and podocyte effacement compared with WT DN mice. The elevated lipid peroxidation, reduced PGC-1α expression, and increased DNA fragmentation were also evident in Fndc5 KO DN. More swollen mitochondria with a significantly higher percentage of disrupted cristae were observed in Fndc5 KO DN mice compared with WT DN mice. This was accompanied by the upregulation of mitochondrial fission-related genes (Dnm1l and Fis1), downregulation of the fusion-related gene (Mfn1), and reduced expression of ATP synthase subunits (ATP5A1 and ATP5B). Systemic analysis of other metabolic tissues, including the pancreas and muscle and adipose tissues, revealed increased lipid peroxidation and decreased PGC-1α expression. These findings underscore FNDC5's role in maintaining mitochondrial integrity and cellular health under diabetic conditions, positioning FNDC5 as a potential therapeutic target.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42694879 · DOI · PMC13539912
Blocking AGEs reduces airway epithelial viral susceptibility in diabetes-exacerbated COPD [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Although diabetic complications are well-established in multiple organs, their impact on the respiratory system remains unclear.
- Closing excerpt
- Our findings reveal a hyperglycemia-AGEs-RAGE/MD2 axis that increases viral susceptibility in COPD, highlighting AGEs targeting as a promising therapeutic strategy for COPD patients with diabetes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (175 words)
Although diabetic complications are well-established in multiple organs, their impact on the respiratory system remains unclear. Clinical evidence indicates accelerated chronic obstructive pulmonary disease (COPD) progression in individuals with diabetes, yet the underlying mechanisms are poorly defined. Using single-cell RNA sequencing of airway epithelium, we identified distinct transcriptional alterations in COPD patients with or without diabetes, particularly in host-defense pathways related to viral infection, which is a key driver of COPD exacerbations. Functionally, hyperglycemia enhanced influenza virus susceptibility in both COPD-derived epithelial cells and COPD mice with diabetes, indicating compromised airway defense. We further demonstrated that hyperglycemia promotes advanced glycation end products (AGEs) accumulation in airway epithelium, with AGEs levels correlating with infection severity. Pharmacological inhibition of AGEs formation with aminoguanidine significantly reduced viral load both in vitro and in vivo. Mechanistically, AGEs activate p38/ERK/IKK proinflammatory signaling via RAGE and MD2 receptors, leading to epithelial injury and heightened viral susceptibility. Our findings reveal a hyperglycemia-AGEs-RAGE/MD2 axis that increases viral susceptibility in COPD, highlighting AGEs targeting as a promising therapeutic strategy for COPD patients with diabetes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42608564 · DOI · PMC13562547
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The incidence of lower extremity amputation and its associated risk factors in patients with diabetic foot ulcers: A meta-analysis [4]
- Research article Ocular Adverse Events With Semaglutide: A Systematic Review and Meta-Analysis [5]
- Research article Anti-VEGF Injections vs. Panretinal Photocoagulation Laser Therapy for Proliferative Diabetic Retinopathy: A Systematic Review and Meta-Analysis [6]
- Research article Risk prediction models for diabetic nephropathy among type 2 diabetes patients in China: a systematic review and meta-analysis [7]
- Research article Incidence and risk factors for amputation in Chinese patients with diabetic foot ulcers: a systematic review and meta-analysis [8]
- Research article Prevalence and risk factors of painful diabetic neuropathy: A systematic review and meta-analysis [9]
References
- Liang KYH, Zheng TM, Tan D, Sasako T, Ilboudo Y, Chen Y, et al.. Protein mediators of chronic kidney disease in Type 2 diabetes: A mendelian randomization study. . 2026. PMID 42726788 · DOI · PMC13568495
- Huang CW, Chen HH, Jao TM, Li CJ, Sung JM, Tsai YS, et al.. CRISPR/Cas9-Driven Fndc5 Knockout Reveals Augmented Mitochondrial Structural and Dynamic Alterations in Diabetic Nephropathy. . 2026. PMID 42694879 · DOI · PMC13539912
- Chen Z, Qin Y, Lin B, Jiang L, Feng Z, Chen S, et al.. Blocking AGEs reduces airway epithelial viral susceptibility in diabetes-exacerbated COPD. . 2026. PMID 42608564 · DOI · PMC13562547
- Luo Y, Liu C, Li C, Jin M, Pi L, Jin Z. The incidence of lower extremity amputation and its associated risk factors in patients with diabetic foot ulcers: A meta-analysis. Int Wound J. 2024. PMID 38972836 · DOI · PMC11227953
- Natividade GR, Spiazzi BF, Baumgarten MW, Bassotto C, Pereira AA, Fraga BL, et al.. Ocular Adverse Events With Semaglutide: A Systematic Review and Meta-Analysis. JAMA Ophthalmol. 2025. PMID 40810985 · DOI · PMC12355393
- Macaron MM, Al Sabbakh N, Shami MZ, Akrobetu D, Bourdakos NE, Abdulsalam FAM, et al.. Anti-VEGF Injections vs. Panretinal Photocoagulation Laser Therapy for Proliferative Diabetic Retinopathy: A Systematic Review and Meta-Analysis. Ophthalmol Retina. 2025. PMID 39128789 · DOI
- Xu W, Zhou Y, Jiang Q, Fang Y, Yang Q. Risk prediction models for diabetic nephropathy among type 2 diabetes patients in China: a systematic review and meta-analysis. Front Endocrinol (Lausanne). 2024. PMID 39022345 · DOI · PMC11251916
- Zhang Y, Liu H, Yang Y, Feng C, Cui L. Incidence and risk factors for amputation in Chinese patients with diabetic foot ulcers: a systematic review and meta-analysis. Front Endocrinol (Lausanne). 2024. PMID 39280008 · DOI · PMC11393406
- Tao Y, Zhang HY, MacGilchrist C, Kirwan E, McIntosh C. Prevalence and risk factors of painful diabetic neuropathy: A systematic review and meta-analysis. Diabetes Res Clin Pract. 2025. PMID 40107621 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.