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Nephrol."],"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>This study assessed the efficacy of INV-202, a novel peripherally restricted cannabinoid type-1 receptor (CB1R) inverse agonist, in a streptozotocin-induced type-1 diabetes nephropathy mouse model.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Diabetes was induced in 8-week-old C57BL6\/J male mice <jats:italic>via<\/jats:italic> intraperitoneal injection of streptozotocin (45 mg\/kg\/day for 5 days); nondiabetic controls received citrate buffer. Diabetic mice were randomized to 3 groups based on blood glucose, polyuria, and albuminuria, and administered daily oral doses for 28-days of INV-202 at 0.3 or 3 mg\/kg or vehicle.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>INV-202 did not affect body weight but decreased kidney weight compared with the vehicle group. While polyuria was unaffected by INV-202 treatment, urinary urea (control 30.77 \u00b1 14.93; vehicle 189.81 \u00b1 31.49; INV-202 (0.3 mg\/kg) 127.76 \u00b1 20; INV-202 (3 mg\/kg) 93.70 \u00b1 24.97 mg\/24h) and albumin (control 3.06 \u00b1 0.38; vehicle 850.08 \u00b1 170.50; INV-202 (0.3 mg\/kg) 290.65 \u00b1 88.70; INV-202 (3 mg\/kg) 111.29 \u00b1 33.47 \u00b5g\/24h) excretion both decreased compared with vehicle-treated diabetic mice. Compared with the vehicle group, there was a significant improvement in the urinary albumin to creatinine ratio across INV-202 groups. Regardless of the dose, INV-202 significantly reduced angiotensin II excretion in diabetic mice. The treatment also decreased <jats:italic>Agtr1a<\/jats:italic> renal expression in a dose-dependent manner. Compared with nondiabetic controls, the glomerular filtration rate was increased in the vehicle group and significantly decreased by INV-202 at 3 mg\/kg. While the vehicle group showed a significant loss in the mean number of podocytes per glomerulus, INV-202 treatment limited podocyte loss in a dose-dependent manner. Moreover, in both INV-202 groups, expression of genes coding for podocyte structural proteins nephrin (<jats:italic>Nphs1<\/jats:italic>), podocin (<jats:italic>Nphs2<\/jats:italic>), and podocalyxin (<jats:italic>Pdxl<\/jats:italic>) were restored to levels similar to nondiabetic controls. INV-202 partially limited the proximal tubular epithelial cell (PTEC) hyperplasia and normalized genetic markers for PTEC lesions. INV-202 also reduced expression of genes contributing to oxidative stress (<jats:italic>Nox2<\/jats:italic>, <jats:italic>Nox4<\/jats:italic>, and <jats:italic>P47phox<\/jats:italic>) and inflammation (<jats:italic>Tnf<\/jats:italic>). In addition, diabetes-induced renal fibrosis was significantly reduced by INV-202.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>INV-202 reduced glomerular injury, preserved podocyte structure and function, reduced injury to PTECs, and ultimately reduced renal fibrosis in a streptozotocin-induced diabetic nephropathy mouse model. These results suggest that INV-202 may represent a new therapeutic option in the treatment of diabetic kidney disease.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fneph.2023.1138416","type":"journal-article","created":{"date-parts":[[2023,3,24]],"date-time":"2023-03-24T14:34:40Z","timestamp":1679668480000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":17,"title":["Therapeutic potential of a novel peripherally restricted CB1R inverse agonist on the progression of diabetic 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