ArticleScientific reports2016
Metabolic role of dipeptidyl peptidase 4 (DPP4) in primary human (pre)adipocytes.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 69 citations in OpenAlex.
- Article
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- Developmental origins of immunometabolic health.Immunometabolism (Cobham, Surrey) · 2026Review
- Dipeptidyl peptidase-4 inhibitors suppress myofibroblastic differentiation and hyaluronan synthesis in Graves' orbitopathy fibroblasts.Frontiers in endocrinology · 2026Article
- Sustained-Release Sitagliptin Microneedles for Scar Prevention via Fibroblast-to-Adipocyte Conversion.Small science · 2025Article
- Integrating network analysis and machine learning to elucidate chemical-induced pancreatic toxicity in zebrafish embryos.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- GLP-1 mimetics and diabetic ketoacidosis: possible interactions and clinical consequences.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Effect of broccoli extract supplement on carcass traits and lipid metabolism in Holstein steers.Frontiers in genetics · 2025Article
- In silico evaluation of berberine and silymarin against metabolic targets: a rationale for OMICS technology-based co-formulation.In silico pharmacology · 2025Article
- Adipose stem cells are sexually dimorphic cells with dual roles as preadipocytes and resident fibroblasts.Nature communications · 2024Article
- Screening of Genes Related to Fat Deposition of Pekin Ducks Based on Transcriptome Analysis.Animals : an open access journal from MDPI · 2024Article
- One for all-human kidney Caki-1 cells are highly susceptible to infection with corona- and other respiratory viruses.Journal of virology · 2023Article
- Whey protein hydrolysates improve high-fat-diet-induced obesity by modulating the brain-peripheral axis of GLP-1 through inhibition of DPP-4 function in mice.European journal of nutrition · 2023Article
- Soluble dipeptidyl peptidase-4 induces epithelial-mesenchymal transition through tumor growth factor-β receptor.Pharmacological reports : PR · 2023Article
- Non-Specific Inhibition of Dipeptidyl Peptidases 8/9 by Dipeptidyl Peptidase 4 Inhibitors Negatively Affects Mesenchymal Stem Cell Differentiation.Journal of clinical medicine · 2023Article
- Incretins-Based Therapies and Their Cardiovascular Effects: New Game-Changers for the Management of Patients with Diabetes and Cardiovascular Disease.Pharmaceutics · 2023Review
- Regulation of Adropin by Sitagliptin monotherapy in participants with newly diagnosed type 2 Diabetes.BMC endocrine disorders · 2022Article
- Article
- Dipeptidyl Peptidase 4 (DPP4) as A Novel Adipokine: Role in Metabolism and Fat Homeostasis.Biomedicines · 2022Review
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dipeptidyl peptidase 4 (DPP4) is the target of the gliptins, a recent class of oral antidiabetics. DPP4 (also called CD26) was previously characterized in immune cells but also has important metabolic functions which are not yet fully understood. Thus, we investigated the function of DPP4 in human white preadipocytes and adipocytes. We found that both cell types express DPP4 in high amounts; DPP4 release markedly increased during differentiation. In preadipocytes, lentiviral DPP4 knockdown caused significant changes in gene expression as determined by whole-genome DNA-array analysis. Metabolic genes were increased, e.g. PDK4 18-fold and PPARγC1α (=PGC1α) 6-fold, and proliferation-related genes were decreased (e.g. FGF7 5-fold). These effects, contributing to differentiation, were not inhibited by the PPARγ antagonist T0070907. Vice versa, the PPARγ agonist pioglitazone induced a different set of genes (mainly FABP4). DPP4 knockdown also affected growth factor signaling and, accordingly, retarded preadipocyte proliferation. In particular, basal and insulin-induced ERK activation (but not Akt activation) was markedly diminished (by around 60%). This indicates that DPP4 knockdown contributes to adipocyte maturation by mimicking growth factor withdrawal, an early step in fat cell differentiation. In mature adipocytes, DPP4 becomes liberated so that adipose tissue may constitute a relevant source of circulating DPP4.
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