ArticleScientific reports2016
Adipose- and muscle-derived Wnts trigger pancreatic β-cell adaptation to systemic insulin resistance.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Voglibose Attenuates Amyloid Beta-Induced Memory Deficits in a Rodent Model: A Potential Alzheimer's Therapy via Wnt Signaling Modulation.Molecular neurobiology · 2025Article
- The Role of Wnt3a/β-Catenin/TCF7L2 Pathway in Diabetes and Cardiorenal Complications.Cardiorenal medicine · 2025Review
- Complement C3 promotes islet β-cell dedifferentiation by activating Wnt/β-catenin pathway.iScience · 2024Article
- Human Placental LRP5 and Sclerostin are Increased in Gestational Diabetes Mellitus Pregnancies.The Journal of clinical endocrinology and metabolism · 2023Article
- Review
- Androgen Deprivation Therapy Differentially Impacts Bone and Muscle in the Short Term in Physically Active Men With Prostate Cancer.JBMR plus · 2022Article
- The complex role of Wnt ligands in type 2 diabetes mellitus and related complications.Journal of cellular and molecular medicine · 2021Review
- A Comparative Peptidomic Characterization of Cultured Skeletal Muscle Tissues Derived FromFrontiers in endocrinology · 2019Article
- Myokine Regulation of Insulin Secretion: Impact of Inflammation and Type 2 Diabetes.Frontiers in physiology · 2019Article
- (Re)generating Human Beta Cells: Status, Pitfalls, and Perspectives.Physiological reviews · 2018Review
- Wnt signaling in cardiovascular disease: opportunities and challenges.Current opinion in lipidology · 2017Review
- Mesenchymal stromal cells ameliorate oxidative stress-induced islet endothelium apoptosis and functional impairment via Wnt4-β-catenin signaling.Stem cell research & therapy · 2017Article
- Skeletal muscle-specific over-expression of the nuclear sirtuin SIRT6 blocks cancer-associated cachexia by regulating multiple targets.JCSM rapid communicationsArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Wnt signaling molecules are associated with obesity, hyperlipidemia, and type 2 diabetes (T2D). Here, we show that two Wnt proteins, WNT3a and WNT4, are specifically secreted by skeletal muscle and adipose tissue during the development of insulin resistance and play an important role in cross-talk between insulin-resistant tissues and pancreatic beta cells. The activation of Frizzled receptor and Wnt signaling in pancreatic islets via circulating WNT3a in blood resulted in higher insulin secretion and an increase in beta cell proliferation, thus leading to islet adaptation in a pre-diabetic state. Interestingly, in fully developed T2D, the expression profiles of Wnt3a and Wnt4 in adipose tissue and muscle cells and blood plasma levels of these proteins were opposite to the pre-diabetic state, thus favoring the downregulation of Wnt signaling in beta cells and resulting in dysfunctional pancreatic islets. These results demonstrate that alterations in the secretion profile of a canonical Wnt activator (WNT3a) and inhibitor (WNT4) from insulin-resistant tissues during the development of T2D are responsible for triggering progression from a pre-diabetic to a diabetic state. We also show here that WNT3a and WNT4 are potent myokines, and their expression and secretion are regulated in response to nutritional and metabolic changes.
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