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Purpose: To assess the effect of empagliflozin on the expression of SGLT-2 and GLUT-1 in the chorioretina of streptozotocin-induced diabetic rats.
Methods: An experimental study was performed on Wistar rats. After a 2-week adaptation period, the rats were allocated to one of four groups. The group allocations were as follows: (K1) negative control (no intervention); (K2) positive control injected with streptozotocin (STZ) without treatment; (K3) positive control injected with STZ and treated with metformin; and (K4) positive control injected with STZ and treated with empagliflozin. SGLT-2 and GLUT-1 expressions were examined using the Western blot technique.
Results: SGLT-2 was expressed in the chorioretinal tissue of all groups; administration of SGLT-2 inhibitors could suppress its expression. The average band thickness indicated that SGLT-2 expression was higher in diabetic rats compared to rats with normal sugar levels. GLUT-1 expression was noticed in all groups based on the chorioretinal examination. It did not change in the metformin group, whereas the empagliflozin group showed a significant decrease in the GLUT-1 expression.
Conclusion: Both metformin and empagliflozin suppress the expression of SGLT-2 and GLUT-1 in the chorioretina of diabetic rats. In comparison, empagliflozin seems to be more potent in reducing this expression.
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http://dx.doi.org/10.18502/jovr.v20.15231 | DOI Listing |
Biosci Biotechnol Biochem
September 2025
Department of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan University, Osaka 558-8585, Japan.
Glucagon dysregulation is a hallmark of type 2 diabetes mellitus (T2DM), yet its early hepatic effects remain unclear. Here, we demonstrate that glucagon-induced gluconeogenesis is markedly enhanced in primary hepatocytes from prediabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a well-established model of human T2DM. Compared to control LETO rats, OLETF hepatocytes showed significantly higher glucagon-stimulated expression of gluconeogenic genes (Pepck, G6pase, Fbp1) at both mRNA and protein levels, along with elevated glucose production.
View Article and Find Full Text PDFJ Ophthalmic Vis Res
September 2025
Faculty of Medicine, Padjadjaran University, Bandung, Indonesia.
Purpose: To assess the effect of empagliflozin on the expression of SGLT-2 and GLUT-1 in the chorioretina of streptozotocin-induced diabetic rats.
Methods: An experimental study was performed on Wistar rats. After a 2-week adaptation period, the rats were allocated to one of four groups.
Diabetes Obes Metab
September 2025
Department of Pharmacology, Kagawa University, Kagawa, Japan.
Aim: Sodium-glucose cotransporter 2 (SGLT2) inhibitors consistently demonstrate renal protection against progressive kidney disease. We hypothesised that SGLT2 inhibition reduces blood glucose levels in peri-proximal tubular capillaries by limiting reabsorption from the tubular filtrate, thereby safeguarding the renal microvasculature from hyperglycaemic stress.
Materials And Methods: In anaesthetised streptozotocin-induced type 1 and Otsuka-Long Evans fatty (OLETF) type 2 diabetic rats, we measured the arterial-to-renal venous glucose ratio (RV/A) to evaluate the effects of canagliflozin, a SGLT2 inhibitor.
Drug Deliv
December 2025
School of Pharmaceutical Sciences, Capital Medical University, Beijing, China.
Obesity is a global health crisis strongly linked to increased risk of type 2 diabetes, cardiovascular diseases, and other metabolic disorders. Glucagon-like peptide-1 (GLP-1) has emerged as an effective macromolecular therapeutic agent for weight management. This study addressed obesity management from three distinct perspectives: enhancing drug dispersion and bioavailability through a novel drug delivery device, extending drug half-life by developing sustained-release formulations, and sustaining the weight loss through implementation of structured dietary protocols.
View Article and Find Full Text PDFJ Dent Res
September 2025
Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.
The diabetic microenvironment intensifies M1-type macrophage-mediated inflammation and impairs bone regeneration. Glycophagy-a process of glycogen-selective autophagy that degrades intracellular glycogen into glucose-is essential for maintaining glucose homeostasis under metabolic stress. The role of glycophagy in regulating M1-type polarization remains unclear.
View Article and Find Full Text PDF