ArticleCommunications biology2024
Normoglycemia and physiological cortisone level maintain glucose homeostasis in a pancreas-liver microphysiological system.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Foetal Development and Placental Health in Response to Apical Periodontitis Induced in Pregnant Wistar Rats.International endodontic journal · 2026Article
- Multidimensional Classification of Insulin Resistance (MCIR) Focused on Therapeutic Targets and Interventions-A Comprehensive Review.International journal of molecular sciences · 2026Review
- Organ-on-chip (OoC) and nano-biomaterials: next generation of precision oral and dental healthcare research.Journal of nanobiotechnology · 2026Review
- Hepatogenous diabetes in the era of precision medicine: diagnosis, management, and future directions.Clinical and experimental medicine · 2026Review
- Metabolic and biochemical profiling reveals phenotypic heterogeneity in Zucker diabetic fatty rats.Animal models and experimental medicine · 2026Article
- Lysolecithin reprogramming via LPCAT1 modulation restores endothelial function and prevents diabetes-associated dysmetabolism.Cardiovascular diabetology · 2026Article
- A convective transport-enhanced multi-organoid device for therapeutic modeling of the liver-pancreas axis in obesity.Theranostics · 2026Article
- Functional material probes and advanced technologies in organ-on-a-chip characterization.Theranostics · 2026Review
- Review
- Interplay between endocrine disorders and liver dysfunction: Mechanisms of damage and therapeutic approaches.World journal of gastroenterology · 2025Review
- Lipid Hormones at the Intersection of Metabolic Imbalances and Endocrine Disorders.Current issues in molecular biology · 2025Review
- Therapeutic Effects of Proanthocyanidins on Diabetic Erectile Dysfunction in Rats.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Current research on metabolic disorders and diabetes relies on animal models because multi-organ diseases cannot be well studied with standard in vitro assays. Here, we have connected cell models of key metabolic organs, the pancreas and liver, on a microfluidic chip to enable diabetes research in a human-based in vitro system. Aided by mechanistic mathematical modeling, we demonstrate that hyperglycemia and high cortisone concentration induce glucose dysregulation in the pancreas-liver microphysiological system (MPS), mimicking a diabetic phenotype seen in patients with glucocorticoid-induced diabetes. In this diseased condition, the pancreas-liver MPS displays beta-cell dysfunction, steatosis, elevated ketone-body secretion, increased glycogen storage, and upregulated gluconeogenic gene expression. Conversely, a physiological culture condition maintains glucose tolerance and beta-cell function. This method was reproducible in two laboratories and was effective in multiple pancreatic islet donors. The model also provides a platform to identify new therapeutic proteins, as demonstrated with a combined transcriptome and proteome analysis.
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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.