ArticleFrontiers in cell and developmental biology2021
CFTR Deficiency Affects Glucose Homeostasis via Regulating GLUT4 Plasma Membrane Transportation.
Article in Frontiers in cell and developmental biology, 2021. 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, 10 citations in OpenAlex.
- ETI corrector therapy suppresses mitochondrial respiration independently of CFTR mutational status.Biochemical and biophysical research communications · 2026Article
- Identification of high-risk cells in single-cell spatially resolved transcriptomics data using Diagnostic Evidence GAuge of Single-cells with spatial smoothing.Bioinformatics (Oxford, England) · 2026Article
- Relationship between skeletal muscle indicators and clinical outcomes in cystic fibrosis is modified by adiposity and CFTR modulator use: a cross-sectional analysis.The American journal of clinical nutrition · 2025Article
- Negative energy balance by feed deprivation affects the adipose miRNome in the lactating goat.Journal of animal science · 2025Article
- Cystic Fibrosis-Related Diabetes Workshop: Research Priorities Spanning Disease Pathophysiology, Diagnosis, and Outcomes.Diabetes · 2023Review
- Cystic Fibrosis-Related Diabetes Workshop: Research Priorities Spanning Disease Pathophysiology, Diagnosis, and Outcomes.Diabetes care · 2023Review
- Short-Term Effects of Elexacaftor/Tezacaftor/Ivacaftor Combination on Glucose Tolerance in Young People With Cystic Fibrosis-An Observational Pilot Study.Frontiers in pediatrics · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic Fibrosis (CF) is an autosomal recessive disorder caused by mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene. CF-related diabetes (CFRD) is one of the most prevalent comorbidities of CF. Altered glucose homeostasis has been reported in CF patients. The mechanism has not been fully elucidated. Besides the consequence of pancreatic endocrine dysfunction, we focus on insulin-responsive tissues and glucose transportation to explain glucose homeostasis alteration in CFRD. Herein, we found that CFTR knockout mice exhibited insulin resistance and glucose tolerance. Furthermore, we demonstrated insulin-induced glucose transporter 4 (GLUT4) translocation to the cell membrane was abnormal in the CFTR knockout mice muscle fibers, suggesting that defective intracellular GLUT4 transportation may be the cause of impaired insulin responses and glucose homeostasis. We further demonstrated that PI(4,5)P
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