ArticleIn vivo (Athens, Greece)
Effects of a Sodium-Glucose Cotransporter 2 Inhibitor Dapagliflozin on Pancreas in Obese Diabetic Mice.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND/
aimInsulin 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
methodsSix-week-old
resultsDapagliflozin 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.
conclusionTreatment 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.
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