ArticleEndocrine connections2022
Txnip deficiency promotes β-cell proliferation in the HFD-induced obesity mouse model.
Article in Endocrine connections, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Thioredoxin-interacting protein is associated with obesity-induced insulin resistance in PCOS patients: a large-scale case-control study.Archives of gynecology and obstetrics · 2025Article
- Oral TIX100 protects against obesity-associated glucose intolerance and diet-induced adiposity.Diabetes, obesity & metabolism · 2025Article
- Pyroptosis in Diabetic Peripheral Neuropathy and its Therapeutic Regulation.Journal of inflammation research · 2024Review
- Integrated epigenome, whole genome sequence and metabolome analyses identify novel multi-omics pathways in type 2 diabetes: a Middle Eastern study.BMC medicine · 2023Article
- Pancreatic β-cell dysfunction in type 2 diabetes: Implications of inflammation and oxidative stress.World journal of diabetes · 2023Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elucidating the mechanisms of regulation of β-cell proliferation is key to understanding the pathogenesis of diabetes mellitus. Txnip is a tumor suppressor that is upregulated in diabetes and plays an important role in the regulation of insulin sensitivity; however, its potential effect on pancreatic β-cell proliferation remains unclear. Here, we evaluated the role of Txnip in pancreatic β-cell compensatory proliferation by subjecting WT and Txnip knockout (KO) mice to a high-fat diet (HFD). Our results demonstrate that Txnip deficiency improves glucose tolerance and increases insulin sensitivity in HFD-induced obesity. The antidiabetogenic effect of Txnip deficiency was accompanied by increased β-cell proliferation and enhanced β-cell mass expansion. Furthermore, Txnip deficiency modulated the expression of a set of transcription factors with key roles in β-cell proliferation and cell cycle regulation. Txnip KO in HFD mice also led to activated levels of p-PI3K, p-AKT, p-mTOR and p-GSK3β, suggesting that Txnip may act via PI3K/AKT signaling to suppress β-cell proliferation. Thus, our work provides a theoretical basis for Txnip as a new therapeutic target for the treatment of diabetes mellitus.
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