ArticleOncotarget2017
Hyperglycemia and advanced glycation end products (AGEs) suppress the differentiation of 3T3-L1 preadipocytes.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Advanced glycation end-products regulate extracellular matrix-adipocyte metabolic crosstalk in diabetes.Scientific reports · 2019Trial
- Liraglutide reduces lipid accumulation in human orbital fibroblasts in Graves' orbitopathy.Frontiers in endocrinology · 2026Article
- Interplay of Glucose Metabolism and Hippo Pathway in Chondrocytes: Pathophysiology and Therapeutic Targets.Bioengineering (Basel, Switzerland) · 2024Review
- Nuclear Factor-Kappa-B Mediates the Advanced Glycation End Product-Induced Repression ofInternational journal of molecular sciences · 2024Article
- Article
- Dietary advanced glycation end-products and their associations with body weight on a Mediterranean diet and low-fat vegan diet: a randomized, cross-over trial.Frontiers in nutrition · 2024Article
- Receptor for the Advanced Glycation End Products (International journal of molecular sciences · 2023Review
- Review
- The Effect on Inflammation of Adherence to the Mediterranean Diet in Polycystic Ovary Syndrome.Current nutrition reports · 2023Review
- Mechanobiology-informed biomaterial and tissue engineering strategies for influencing skeletal stem and progenitor cell fate.Frontiers in physiology · 2023Review
- Chronic and Transient Hyperglycemia Induces Changes in the Expression Patterns ofInternational journal of molecular sciences · 2021Article
- Cold-induced Yes-associated-protein expression through miR-429 mediates the browning of white adipose tissue.Science China. Life sciences · 2021Article
- Role of YAP/TAZ in Cell Lineage Fate Determination and Related Signaling Pathways.Frontiers in cell and developmental biology · 2020Review
- Protective effect of ISO‑1 against advanced glycation end product aggravation of PC12 cell injury induced by Aβ1‑40.Molecular medicine reports · 2019Article
- Central role of Yes-associated protein and WW-domain-containing transcriptional co-activator with PDZ-binding motif in pancreatic cancer development.World journal of gastroenterology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is characterized by mild hyperglycemia and accumulation of advanced glycation end products (AGEs). Effects of chronic exposure to hyperglycemia or AGEs on the adipogenic differentiation of 3T3-L1 preadipocytes remain unclear. We examined the chronic effect of AGEs and high glucose on the differentiation of 3T3-L1 cells by culturing 3T3-L1 cells in the presence of AGEs or 25 mM glucose for 1 month. Chronic incubation of 3T3-L1 cells with AGEs or high glucose blocked their differentiation into mature adipocytes as evidenced by reduced levels of adipocyte markers such as accumulated oil droplets, GPDH, aP2, adiponectin and of adipogenesis regulators PPARγ and C/EBPα. Levels or activities of Src, PDK1, Akt, and NF-κB were higher in AGEs- and high glucose-treated cells than those in 3T3-L1 cells. Levels of Bcl-2 were elevated in AGEs- and high glucose-treated cells, and were attenuated by inhibitors of PI3-kinase, Akt and NF-κB. Moreover, adipogenesis was attenuated in 3T3-L1 cells stably expressing Bcl-2 or YAP. These results suggest that chronic AGEs and high glucose treatments up-regulate Bcl-2 and YAP via the Akt-NF-κB pathway and impair adipogenesis.
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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 OpenQuestion graph.