ArticleDiabetologia2015
Deletion of the gene for adiponectin accelerates diabetic nephropathy in the Ins2 (+/C96Y) mouse.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- A Systematic Review and Meta-Analysis of the Association Between Obesity and Albuminuria in Asian People.International journal of hypertension · 2026Review
- Waist-to-height ratio and the incidence of rapid kidney function decline and chronic kidney disease: insights from the China health and retirement longitudinal study.BMC nephrology · 2025Article
- Obesity-Related Kidney Disease: A Growing Threat to Renal Health.International journal of molecular sciences · 2025Review
- Integrin Trafficking, Fibronectin Architecture, and Glomerular Injury upon Adiponectin Receptor 1 Depletion.Journal of the American Society of Nephrology : JASN · 2025Article
- Adiponectin-to-leptin ratio and incident chronic kidney disease: Sex and body composition-dependent association.Journal of cachexia, sarcopenia and muscle · 2024Article
- Obesity and the kidney: mechanistic links and therapeutic advances.Nature reviews. Endocrinology · 2024Review
- Recent Advances in the Emerging Therapeutic Strategies for Diabetic Kidney Diseases.International journal of molecular sciences · 2022Review
- Sanziguben polysaccharides inhibit diabetic nephropathy through NF-κB-mediated anti-inflammation.Nutrition & metabolism · 2021Article
- Adiponectin receptor agonist AdipoRon ameliorates renal inflammation in diet-induced obese mice and endotoxin-treated human glomeruli ex vivo.Diabetologia · 2021Article
- Adiponectin in Chronic Kidney Disease.International journal of molecular sciences · 2020Review
- Adiponectin in renal fibrosis.Aging · 2020Review
- Chronic kidney disease attenuates the impact of obesity on quality of life.Scientific reports · 2020Article
- Recombinant adiponectin peptide promotes neuronal survival after intracerebral haemorrhage by suppressing mitochondrial and ATF4-CHOP apoptosis pathways in diabetic mice via Smad3 signalling inhibition.Cell proliferation · 2020Article
- Epidermal Growth Factor Receptor: A Potential Therapeutic Target for Diabetic Kidney Disease.Frontiers in pharmacology · 2020Review
- Adiponectin for the treatment of diabetic nephropathy.The Korean journal of internal medicine · 2019Review
- The Susceptibility Genes in Diabetic Nephropathy.Kidney diseases (Basel, Switzerland) · 2018Review
- Article
- Sex dimorphism in ANGII-mediated crosstalk between ACE2 and ACE in diabetic nephropathy.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- β-Carotene Inhibits Activation of NF-κB, Activator Protein-1, and STAT3 and Regulates Abnormal Expression of Some Adipokines in 3T3-L1 Adipocytes.Journal of cancer prevention · 2018Article
- Uric acid upregulates the adiponectin‑adiponectin receptor 1 pathway in renal proximal tubule epithelial cells.Molecular medicine reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
aims/hypothesisDiabetic nephropathy is one of the most common forms of chronic kidney disease. The role of adiponectin in the development of diabetic nephropathy has not been elucidated, and the aim of the present study was to investigate the hypothesis that deletion of the gene for adiponectin would accelerate diabetic nephropathy in the Akita mouse.
methodsWe followed four groups of mice from 4 weeks to 16 weeks of age (n ≥ 10 in each group): wild-type (WT) (Ins2 (+/+) Adipoq(+/+)) mice; APN(-/-) (Ins2(+/+) Adipoq(-/-)) mice; Akita (Ins2(+/C96Y) Adipoq(+/+)) mice and Akita/APN(-/-) (Ins2(+/C96Y) Adipoq(-/-)) mice. The mice were then killed and diabetic kidney injury was assessed. In vitro experiments were performed in primary mesangial cells.
resultsMice from both diabetic groups exhibited increased glomerular adiponectin receptor 1 (adipoR1) expression, kidney hypertrophy, glomerular enlargement, increased albuminuria and tissue oxidative stress compared with the WT control. Deletion of the adiponectin gene had no effect on glycaemia. However, Akita/APN(-/-) mice exhibited a greater extent of renal hypertrophy. In vitro, adiponectin attenuated high-glucose-induced phosphorylation of mammalian target of rapamycin (mTOR) and ribosomal protein S6 kinase (S6K). A higher level of fibrosis was observed in the tubulointerstitial and glomerular compartments of the Akita/APN(-/-) mice and adiponectin was found to inhibit TGFβ-induced Smad2 and Smad3 phosphorylation in vitro. There was an exaggerated inflammatory response in the Akita/APN(-/-) mice. Adiponectin also inhibited high-glucose-induced activation of nuclear factor κB (NFκB) in mesangial cells. CONCLUSIONS/
interpretationOur data suggest that adiponectin is an important determinant of the kidney response to high glucose in vivo and in vitro.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.