miR-483 deficiency promotes loss of pancreatic beta-cell identity and aberrant glucagon production under metabolic stress

Clicks: 2
ID: 329898
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #316 of 316 articles by views in american journal of physiology endocrinology and metabolism

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 316 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Abstract Pancreatic β-cell dedifferentiation is a pathological mechanism that contributes to β-cell dysfunction and loss during type 2 diabetes (T2D), but the underlying mechanisms remain incompletely understood. MicroRNAs (miRNAs) are key post-transcriptional regulators of cellular identity and function. We previously identified miR-483 as a β-cell-enriched miRNA that promotes β-cell function by targeting Aldh1a3. Here, we investigated its role under high-fat diet (HFD)/multiple low-dose streptozotocin (STZ)-induced metabolic stress. β-cell-specific miR-483 deficiency exacerbated hyperglycemia and impaired glucose tolerance, accompanied by increased ALDH1A3 expression and reduced insulin expression in GFP-labeled cells. Under HFD/STZ-induced metabolic stress, miR-483 deficiency also increased glucagon production and the abundance of GFP+GCG+ and ALDH1A3+GCG+ cells, consistent with loss of β-cell identity and emergence of α-cell-like characteristics. Single-cell RNA sequencing revealed increased β-cells heterogeneity, including a subpopulation with glucagon expression and an altered endocrine phenotype. In addition, miR-483 deficiency was associated with mitochondrial fragmentation, impaired respiratory function, and increased oxidative stress. Together, these findings suggest that miR-483-ALDH1A3 axis contributes to the coordination of β-cell identity with mitochondrial and metabolic homeostasis during metabolic stress.
Reference Key
openalex_W7214451723 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Katy Matson, Aaron MacLeod, Ellie Sempek, Jordan Noble, Bryce Tapert, Farhad Alipour, Xiaohu Tang, Aimee Marceau, Leslie S. Satin, Xiaoqing Tang
Journal american journal of physiology endocrinology and metabolism
Year 2026
DOI
10.1210/endocr/bqag110
URL
https://doi.org/10.1210/endocr/bqag110
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.