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Given that dipeptidyl peptidase\u20104 (DPP4) is upregulated in stressed adipose and vascular tissues and modulates intracellular signaling pathways related to glucagon\u2010like peptide\u20101 (GLP\u20101) metabolism, we investigated the role of the DPP4\/GLP\u20101 axis by examining adipose inflammation and dysfunction in mice subjected to chronic stress. Eight\u2010week\u2010old male wild\u2010type mice (DPP4\n                    <jats:sup>+\/+<\/jats:sup>\n                    ) and DPP4\u2010knockout (DPP4\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) mice were randomly assigned to non\u2010stress or 2\u2010week immobilization stress groups for morphological and biochemical analyses. On Day 14 post\u2010stress, the stressed mice had reduced subcutaneous adipose tissue (SWAT) weights and detrimental changes in the protein and\/or mRNA levels of phospho\u2010phosphatidylinositol 3\u2010kinase, phospho\u2010protein kinase B, oxidative stress (gp91\n                    <jats:sup>phox<\/jats:sup>\n                    )\u2010, apoptosis (cytochrome\n                    <jats:italic>c<\/jats:italic>\n                    , caspase\u20108, B\u2010cell lymphoma 2 and Bcl2\u2010associated X protein)\u2010, monocyte chemoattractant protein\u20101, interleukin\u20106, tumor\u2010necrosis factor\u2010\u03b1, and inducible nitric oxide synthase\u2010related molecules, plus increased F4\/80\n                    <jats:sup>+<\/jats:sup>\n                    macrophage infiltration; these changes were reversed by DPP4 deficiency. The GLP\u20101 receptor agonist exenatide mimicked the adipose benefits of DPP4 deletion. In\u00a0vitro, exenatide reduced the production of reactive oxygen species and the apoptosis induced by stressed serum, and it altered the levels of p\u2010AKT protein. DPP4 deletion also reduced these changes. These findings suggest that DPP4 functions as an important mediator of chronic stress\u2010stimulated adipose inflammation and dysfunction via the modulation of adipocyte oxidative stress production and apoptosis that is mediated by the GLP\u20101\/PI3K\u2010AKT axis, indicating that DPP4 inhibition and\/or GLP\u20101R stimulation may have applications for treating metabolic disorders of patients under chronic stress conditions.\n                  <\/jats:p>","DOI":"10.1096\/fj.202502147r","type":"journal-article","created":{"date-parts":[[2025,7,31]],"date-time":"2025-07-31T14:09:26Z","timestamp":1753970966000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Increased Dipeptidyl Peptidase\u20104 Promotes Adipose Inflammation and Dysfunction in Mice Under Chronic Stress"],"prefix":"10.1096","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-4517-7420","authenticated-orcid":false,"given":"Meiping","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Cardiology and Hypertension Jilin Provincial Key Laboratory of Stress and Cardiovascular Disease, Yanbian University Hospital  Yanji Jilin P.R. 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