Related Experiment Video
Updated: Oct 10, 2025
Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
Loss of renal olfactory receptor 1393 leads to improved glucose homeostasis in a type 1 diabetic mouse model
Alexis R Schiazza1, Elizabeth G Considine1, Madison Betcher1
1Department of Human Science, Georgetown University, Washington, District of Columbia, USA.
Abstract:
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 β-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.
Insights
Loss of renal olfactory receptor 1393 (Olfr1393) improves hyperglycemia and glucose tolerance in male mice with type 1 diabetes. This suggests Olfr1393 may be a therapeutic target for managing diabetes-related glucose dysregulation.
Area of Science:
- Nephrology
- Endocrinology
- Sensory Receptor Biology
Background:
- Renal olfactory receptor 1393 (Olfr1393) is implicated in glucose handling and sodium-glucose cotransporter (SGLT) regulation.
- Previous research linked Olfr1393 to glucose intolerance and hyperfiltration in diet-induced obesity.
Purpose of the Study:
- To investigate the role of Olfr1393 in the context of Type 1 Diabetes.
- To determine if Olfr1393 influences hyperglycemia and glucose tolerance in a mouse model of Type 1 Diabetes.
Main Methods:
- Utilized Olfr1393 wildtype (WT) and knockout (KO) mice.
- Induced Type 1 Diabetes using streptozotocin (STZ) to cause pancreatic beta-cell depletion.
- Monitored diabetic mice over a 12-week period.
Main Results:
- Diabetic male Olfr1393 KO mice exhibited significantly improved hyperglycemia and glucose tolerance compared to WT controls.
- Olfr1393 expression was confirmed in the renal proximal tubule and additionally found in the glomerulus.
- Mice remained susceptible to STZ-induced pancreatic damage despite improved glucose control.
Conclusions:
- Loss of renal Olfr1393 provides protection against streptozotocin-induced Type 1 Diabetes in male mice.
- Olfr1393 may function as a general regulator of glucose handling in both healthy and diseased states.
- Olfr1393 warrants further investigation as a potential therapeutic target for diabetes management.
More Related Videos
08:32Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
Published on: January 4, 2018
06:21Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid
Published on: April 7, 2023