ArticleThe Journal of clinical investigation2021
Electrogenic sodium bicarbonate cotransporter NBCe1 regulates pancreatic β cell function in type 2 diabetes.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- AWmeta Empowers Adaptively Weighted Transcriptomic Meta-Analysis.Current issues in molecular biology · 2026Article
- Toll of Chronic Metabolic Acidosis at Molecular, Cellular, and Systemic Levels: A Conceptual Framework to Revisit Type 2 Diabetes (T2D) Pathophysiology.Biomedicines · 2026Review
- Selective Deletion of NBCe1 in Reactive Astrocytes Attenuates Ischemic Stroke Brain Damage.Glia · 2025Article
- Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes.Experimental & molecular medicine · 2025Article
- Endogenous cell membrane interactome mapping for the GLP-1 receptor in different cell types.Nature chemical biology · 2025Article
- Succinylation-related molecular activities in cancer: metabolic adaptations, immune landscape, and prognostic significance in colorectal cancer.Frontiers in immunology · 2025Article
- The role of NaPflugers Archiv : European journal of physiology · 2024Review
- The versatile multi-functional substance NMN: its unique characteristics, metabolic properties, pharmacodynamic effects, clinical trials, and diverse applications.Frontiers in pharmacology · 2024Review
- Comprehensive Analysis of CircRNA Expression Profiles in Multiple Tissues of Pigs.International journal of molecular sciences · 2023Article
- Potential Theranostic Roles of SLC4 Molecules in Human Diseases.International journal of molecular sciences · 2023Review
- Hidden chronic metabolic acidosis of diabetes type 2 (CMAD): Clues, causes and consequences.Reviews in endocrine & metabolic disorders · 2023Review
- FALCON systematically interrogates free fatty acid biology and identifies a novel mediator of lipotoxicity.Cell metabolism · 2023Article
- FALCON systematically interrogates free fatty acid biology and identifies a novel mediator of lipotoxicity.bioRxiv : the preprint server for biology · 2023Article
- Genome-wide placental DNA methylations in fetal overgrowth and associations with leptin, adiponectin and fetal growth factors.Clinical epigenetics · 2022Article
- Uncoupling protein 2 and aldolase B impact insulin release by modulating mitochondrial function and CaiScience · 2022Article
- Prevalence and clinical characteristics of T2DM patients with OTUD3 gene rs78466831 SNP at a single academic center in China.Frontiers in endocrinology · 2022Article
- It's What and When You Eat: An Overview of Transcriptional and Epigenetic Responses to Dietary Perturbations in Pancreatic Islets.Frontiers in endocrinology · 2022Review
- Time-restricted feeding prevents deleterious metabolic effects of circadian disruption through epigenetic control of β cell function.Science advances · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Pancreatic β cell failure in type 2 diabetes mellitus (T2DM) is attributed to perturbations of the β cell's transcriptional landscape resulting in impaired glucose-stimulated insulin secretion. Recent studies identified SLC4A4 (a gene encoding an electrogenic Na+-coupled HCO3- cotransporter and intracellular pH regulator, NBCe1) as one of the misexpressed genes in β cells of patients with T2DM. Thus, in the current study, we set out to test the hypothesis that misexpression of SLC4A4/NBCe1 in T2DM β cells contributes to β cell dysfunction and impaired glucose homeostasis. To address this hypothesis, we first confirmed induction of SLC4A4/NBCe1 expression in β cells of patients with T2DM and demonstrated that its expression was associated with loss of β cell transcriptional identity, intracellular alkalinization, and β cell dysfunction. In addition, we generated a β cell-selective Slc4a4/NBCe1-KO mouse model and found that these mice were protected from diet-induced metabolic stress and β cell dysfunction. Importantly, improved glucose tolerance and enhanced β cell function in Slc4a4/NBCe1-deficient mice were due to augmented mitochondrial function and increased expression of genes regulating β cell identity and function. These results suggest that increased β cell expression of SLC4A4/NBCe1 in T2DM plays a contributory role in promotion of β cell failure and should be considered as a potential therapeutic target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.