Treatment of diabetic mice with the SGLT2 inhibitor TA-1887 antagonizes diabetic cachexia and decreases mortality
Metabolic syndrome: SGLT2i prevents diabetic cachexia and prolongs survival Sodium-glucose cotransporter 2 inhibitor (SGLT2i) has a favorable effect on mortality of diabetic subjects, but the mechanism stays unclear. Taichi Sugizaki at Kumamoto University examined SGLT2i effects in severe diabetic o...
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| Autores principales: | , , , , , , , , , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Nature Portfolio
2017
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/a2c42276f5e74aac86a47284b4a91626 |
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| Sumario: | Metabolic syndrome: SGLT2i prevents diabetic cachexia and prolongs survival Sodium-glucose cotransporter 2 inhibitor (SGLT2i) has a favorable effect on mortality of diabetic subjects, but the mechanism stays unclear. Taichi Sugizaki at Kumamoto University examined SGLT2i effects in severe diabetic obese mice, and discovered that they showed prolonged survival without pathological weight loss, or cachexia. As with SGLT2i, Insulin also prevented cachexia, improved pancreatic beta cell function, insulin sensitivity and some organ damages. However, what makes SGLT2i important was to suppress cellular aging or vessel inflammation, while insulin accelerated those developments, which may lead to a result that SGLT2i has contributed to prolonged survival more than insulin. SGLT2i demonstrates an association with survival period upon maintaining good condition of pancreatic beta cells and insulin target organs, providing insight into strategies for treatment of severe diabetes. |
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