Reduced islet function contributes to impaired glucose homeostasis in fructose-fed mice
| Autor: | Zeenat Asghar, Andrew Cusumano, Kelle H. Moley, Maria S. Remedi, Zihan Yan |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty endocrine system endocrine system diseases Physiology Endocrinology Diabetes and Metabolism Down-Regulation 030209 endocrinology & metabolism Fructose Carbohydrate metabolism 03 medical and health sciences chemistry.chemical_compound Islets of Langerhans Mice 0302 clinical medicine Physiology (medical) Internal medicine Glucose Intolerance medicine Hyperinsulinemia Dietary Carbohydrates Glucose homeostasis Animals Homeostasis Pancreatic islet function Hyperuricemia Cells Cultured geography geography.geographical_feature_category biology nutritional and metabolic diseases medicine.disease Islet Mice Inbred C57BL 030104 developmental biology Endocrinology Glucose chemistry biology.protein GLUT5 Research Article |
| Popis: | Increased sugar consumption, particularly fructose, in the form of sweetened beverages and sweeteners in our diet adversely affects metabolic health. Because these effects are associated with features of the metabolic syndrome in humans, the direct effect of fructose on pancreatic islet function is unknown. Therefore, we examined the islet phenotype of mice fed excess fructose. Fructose-fed mice exhibited fasting hyperglycemia and glucose intolerance but not hyperinsulinemia, dyslipidemia, or hyperuricemia. Islet function was impaired, with decreased glucose-stimulated insulin secretion and increased glucagon secretion and high fructose consumption leading to α-cell proliferation and upregulation of the fructose transporter GLUT5, which was localized only in α-cells. Our studies demonstrate that excess fructose consumption contributes to hyperglycemia by affecting both β- and α-cells of islets in mice. |
| Databáze: | OpenAIRE |
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