ArticleThe Journal of biological chemistry2017
A systems biology analysis connects insulin receptor signaling with glucose transporter translocation in rat adipocytes.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- QSP Modeling Shows Pathological Synergism Between Insulin Resistance and Amyloid-Beta Exposure in Upregulating VCAM1 Expression at the BBB Endothelium.CPT: pharmacometrics & systems pharmacology · 2025Article
- Assessment of distinct effects ofPeerJ · 2025Article
- Insulin Signaling Pathway Model in Adipocyte Cells.Current pharmaceutical design · 2023Article
- Computational Analysis of Insulin-Glucagon Signalling Network: Implications of Bistability to Metabolic Homeostasis and Disease states.Scientific reports · 2019Article
- Insulin Receptor Trafficking: Consequences for Insulin Sensitivity and Diabetes.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes is characterized by insulin resistance, which arises from malfunctions in the intracellular insulin signaling network. Knowledge of the insulin signaling network is fragmented, and because of the complexity of this network, little consensus has emerged for the structure and importance of the different branches of the network. To help overcome this complexity, systems biology mathematical models have been generated for predicting both the activation of the insulin receptor (IR) and the redistribution of glucose transporter 4 (GLUT4) to the plasma membrane. Although the insulin signal transduction between IR and GLUT4 has been thoroughly studied with modeling and time-resolved data in human cells, comparable analyses in cells from commonly used model organisms such as rats and mice are lacking. Here, we combined existing data and models for rat adipocytes with new data collected for the signaling network between IR and GLUT4 to create a model also for their interconnections. To describe all data (>140 data points), the model needed three distinct pathways from IR to GLUT4: (i) via protein kinase B (PKB) and Akt substrate of 160 kDa (AS160), (ii) via an AS160-independent pathway from PKB, and (iii) via an additional pathway from IR,
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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.