ArticleAmerican journal of physiology. Endocrinology and metabolism2017
Reduced islet function contributes to impaired glucose homeostasis in fructose-fed mice.
Article in American journal of physiology. Endocrinology and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Excess Fructose Intake Activates Hyperinsulinemia and Mitogenic MAPK Pathways in Association With Cellular Stress, Inflammation, and Apoptosis in the Pancreas of Rats.Molecular nutrition & food research · 2025Article
- Pancreatic β-Cell Apoptosis in Normoglycemic Rats is Due to Mitochondrial Translocation of p53-Induced by the Consumption of Sugar-Sweetened Beverages.Cell biochemistry and biophysics · 2023Article
- It's What and When You Eat: An Overview of Transcriptional and Epigenetic Responses to Dietary Perturbations in Pancreatic Islets.Frontiers in endocrinology · 2022Review
- Article
- Glucose but Not Fructose Alters the Intestinal Paracellular Permeability in Association With Gut Inflammation and Dysbiosis in Mice.Frontiers in immunology · 2021Article
- Pancreatic stone protein/regenerating protein is a potential biomarker for endoplasmic reticulum stress in beta cells.Scientific reports · 2019Article
- Impact of Fish Oil Supplementation and Interruption of Fructose Ingestion on Glucose and Lipid Homeostasis of Rats Drinking Different Concentrations of Fructose.BioMed research international · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
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.
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Registered trials
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