| First Author | Schiazza AR | Year | 2021 |
| Journal | Physiol Rep | Volume | 9 |
| Issue | 23 | Pages | e15007 |
| PubMed ID | 34877823 | Mgi Jnum | J:317732 |
| Mgi Id | MGI:6842182 | Doi | 10.14814/phy2.15007 |
| Citation | Schiazza AR, et al. (2021) Loss of renal olfactory receptor 1393 leads to improved glucose homeostasis in a type 1 diabetic mouse model. Physiol Rep 9(23):e15007 |
| abstractText | Renal olfactory receptor 1393 (Olfr1393) is an understudied sensory receptor that contributes to glucose handling in the proximal tubule. Our previous studies have indicated that this receptor may serve as a regulator of the sodium glucose co-transporters (SGLTs) and contributes to the development of glucose intolerance and hyperfiltration in the setting of diet-induced obesity. We hypothesized that Olfr1393 may have a similar function in Type 1 Diabetes. Using Olfr1393 wildtype (WT) and knockout (KO) mice along with streptozotocin (STZ) to induce pancreatic beta-cell depletion, we tracked the development and progression of diabetes over 12 weeks. Here we report that diabetic male Olfr1393 KO mice have a significant improvement in hyperglycemia and glucose tolerance, despite remaining susceptible to STZ. We also confirm that Olfr1393 localizes to the renal proximal tubule, and have uncovered additional expression within the glomerulus. Collectively, these data indicate that loss of renal Olfr1393 affords protection from STZ-induced type 1 diabetes and may be a general regulator of glucose handling in both health and disease. |
