ArticleMetabolic brain disease2015
Sitagliptin protects proliferation of neural progenitor cells in diabetic mice.
Article in Metabolic brain disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Sitagliptin as a therapeutic approach for social anxiety disorder: the role of DPP4 and NPY in modulating social fear and comorbid depressive-like behavior in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Sitagliptin Attenuates the Cognitive Deficits in L-Methionine-Induced Vascular Dementia in Rats.BioMed research international · 2022Article
- Sitagliptin Reduces Endothelial Dysfunction and Apoptosis Induced by High-Fat Diet and Palmitate in Thoracic Aortas and Endothelial Cells via ROS-ER Stress-CHOP Pathway.Frontiers in pharmacology · 2021Article
- Sitagliptin improves functional recovery via GLP-1R-induced anti-apoptosis and facilitation of axonal regeneration after spinal cord injury.Journal of cellular and molecular medicine · 2020Article
- Dipeptidyl Peptidase-4 Inhibitors for the Potential Treatment of Brain Disorders; A Mini-Review With Special Focus on Linagliptin and Stroke.Frontiers in neurology · 2019Review
- Sitagliptin ameliorates diabetic nephropathy by blocking TGF-β1/Smad signaling pathway.International journal of molecular medicine · 2018Article
- Sitagliptin ameliorates high glucose-induced cell proliferation and expression of the extracellular matrix in glomerular mesangial cells.Experimental and therapeutic medicine · 2017Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sitagliptin (SIT) is a dipeptidyl peptidase-4 (DPP-4) inhibitor that enhances the effects of incretin hormones, such as Glucose-dependent Insulinotropic Peptide (also known as Gastric Inhibitory Polypeptide, GIP) and Glucagon-Like Peptide 1 (GLP-1). We have now evaluated the effect of SIT on proliferation of neural progenitors in diabetic mice. A condition resembling the non-obese type 2 diabetes mellitus (D2) was achieved by a combination of streptozotocin and nicotinamide (NA-STZ), whereas a type 1-like disease (D1) was provoked by STZ without NA. Non-diabetic mice received vehicle injections. Cell proliferation was estimated by bromodeoxyuridine (BrdU) incorporation in two different regions of the subventricular zone (SVZ), the largest reserve of neural stem cells in the adult brain. SIT treatment did not modify the high fasting blood glucose (BG) levels and intraperitoneal glucose tolerance test (IPGTT) of D1 mice. By contrast, in D2 mice, SIT treatment significantly reduced BG and IPGTT. Both D1 and D2 mice showed a substantial reduction of BrdU labeling in the SVZ. Remarkably, SIT treatment improved BrdU labeling in both conditions. Our findings suggest that SIT would protect proliferation of neural progenitor cells even in the presence of non-controlled diabetic alterations.
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