ArticleScientific reports2015
Inhibition of dipeptidyl peptidase 8/9 impairs preadipocyte differentiation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- DPP8/9 processing of human AK2 unmasks an IAP binding motif.EMBO reports · 2025Article
- Targeting dipeptidyl peptidase-8/9 to combat inflammation-induced osteoclastogenesis in RAW264.7 macrophages and analysis of anti-osteoclastogenesis potential of chrysin.Iranian journal of basic medical sciences · 2025Article
- Beyond Small Molecules: Antibodies and Peptides for Fibroblast Activation Protein Targeting Radiopharmaceuticals.Pharmaceutics · 2024Review
- GWAS-significant loci and severe COVID-19: analysis of associations, link with thromboinflammation syndrome, gene-gene, and gene-environmental interactions.Frontiers in genetics · 2024Article
- Non-Specific Inhibition of Dipeptidyl Peptidases 8/9 by Dipeptidyl Peptidase 4 Inhibitors Negatively Affects Mesenchymal Stem Cell Differentiation.Journal of clinical medicine · 2023Article
- Chemoproteomics-Enabled Identification of 4-Oxo-β-Lactams as Inhibitors of Dipeptidyl Peptidases 8 and 9.Angewandte Chemie (International ed. in English) · 2022Article
- Oo-site: A dashboard to visualize gene expression during Drosophila oogenesis suggests meiotic entry is regulated post-transcriptionally.Biology open · 2022Article
- Role and mechanism(s) of incretin-dependent therapies for treating diabetes mellitus.Environmental science and pollution research international · 2022Review
- New insights into the role of dipeptidyl peptidase 8 and dipeptidyl peptidase 9 and their inhibitors.Frontiers in pharmacology · 2022Review
- Article
- A genome-wide association study identifies novel candidate genes for susceptibility to diabetes mellitus in non-obese cats.PloS one · 2021Article
- Predictors of the Efficacy of Dipeptidyl Peptidase-4 Inhibitors in Taiwanese Patients with Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
- Sex-specific epigenetic mediators between early life social disadvantage and adulthood BMI.Epigenomics · 2018Article
- Structures and mechanism of dipeptidyl peptidases 8 and 9, important players in cellular homeostasis and cancer.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The expression of proline-specific enzymes in the human lung.Annals of translational medicine · 2017Review
- Article
- Metabolic role of dipeptidyl peptidase 4 (DPP4) in primary human (pre)adipocytes.Scientific reports · 2016Article
- Prognostic and Therapeutic Significance of DPP4 in SMARCA4-Deficient Non-Small Cell Lung Cancer.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Adipocytes are the primary cells in adipose tissue, and adipocyte dysfunction causes lipodystrophy, obesity and diabetes. The dipeptidyl peptidase (DPP) 4 family includes four enzymes, DPP4, DPP8, DPP9 and fibroblast activation protein (FAP). DPP4 family inhibitors have been used for the treatment of type 2 diabetes patients, but their role in adipocyte formation are poorly understood. Here we demonstrate that the DPP8/9 selective inhibitor 1G244 blocks adipogenesis in preadipocyte 3T3-L1 and 3T3-F422A, while DPP4 and FAP inhibitors have no effect. In addition, knockdown of DPP8 or DPP9 significantly impairs adipocyte differentiation in preadipocytes. We further uncovered that blocking the expression or activities of DPP8 and DPP9 attenuates PPARγ2 induction during preadipocyte differentiation. Addition of PPARγ agonist thiazolidinediones (TZDs), or ectopic expression of PPARγ2, is able to rescue the adipogenic defect caused by DPP8/9 inhibition in preadipocytes. These results indicate the importance of DPP8 and DPP9 on adipogenesis.
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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.