In vivo (Athens, Greece) · 2026
Effects of a Sodium-Glucose Cotransporter 2 Inhibitor Dapagliflozin on Pancreas in Obese Diabetic Mice.
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Sekikawa Ryoko, Uehara Hikari, Uno Kinuko, Sasase Tomohiko, Nakata Yusuke, Mori Yukina, Shinohara Masami, Sugimoto Miki, Ohta Takeshi
Аннотация
BACKGROUND/AIM: Insulin secretion deficiency is one of the factors that cause onset and progression of type 2 diabetes, and pancreatic β-cell mass is also reduced in patients with type 2 diabetes. Some anti-diabetic drugs act directly on the pancreas to promote insulin secretion. Although such drugs provide good glycemic control, there are concerns regarding secondary failure during long-term treatment. Therefore, we aimed to investigate the effects of the sodium-glucose cotransporter 2 (SGLT2) inhibitor, dapagliflozin, which does not act directly on the pancreas, using obese type 2 diabetic mice.
MATERIALS AND METHODS: Six-week-old db/db mice were administered dapagliflozin at doses equivalent to 0.3 or 1 mg/kg in their diet for nine weeks.
RESULTS: Dapagliflozin treatment increased blood insulin levels and improved hyperglycemia. Histological analysis showed an increase in islet areas and improved islet irregularity and fibrosis in a dose-dependent manner. Immunostaining also showed a dose-dependent increase in β-cell positive areas and decrease in the ratio of α-cell positive area/β-cell positive area. Furthermore, dapagliflozin treatment suppressed the expression of CD44 (an inflammation- and fibrosis-related factor) around the pancreatic islets.
CONCLUSION: Treatment with dapagliflozin for nine weeks increases insulin secretion and preserves β-cell areas in type 2 diabetic mice, suggesting that long-term administration of dapagliflozin may have a protective effect on pancreas affected by diabetes.
MATERIALS AND METHODS: Six-week-old db/db mice were administered dapagliflozin at doses equivalent to 0.3 or 1 mg/kg in their diet for nine weeks.
RESULTS: Dapagliflozin treatment increased blood insulin levels and improved hyperglycemia. Histological analysis showed an increase in islet areas and improved islet irregularity and fibrosis in a dose-dependent manner. Immunostaining also showed a dose-dependent increase in β-cell positive areas and decrease in the ratio of α-cell positive area/β-cell positive area. Furthermore, dapagliflozin treatment suppressed the expression of CD44 (an inflammation- and fibrosis-related factor) around the pancreatic islets.
CONCLUSION: Treatment with dapagliflozin for nine weeks increases insulin secretion and preserves β-cell areas in type 2 diabetic mice, suggesting that long-term administration of dapagliflozin may have a protective effect on pancreas affected by diabetes.