ArticleJournal of pharmacokinetics and pharmacodynamics2011
Mechanism-based disease progression modeling of type 2 diabetes in Goto-Kakizaki rats.
Article in Journal of pharmacokinetics and pharmacodynamics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- OLED catheters for inner-body phototherapy: A case of type 2 diabetes mellitus improved via duodenal photobiomodulation.Science advances · 2023Article
- A data integration approach unveils a transcriptional signature of type 2 diabetes progression in rat and human islets.PloS one · 2023Observational
- Attenuation of diabetic cardiomyopathy by relying on kirenol to suppress inflammation in a diabetic rat model.Journal of cellular and molecular medicine · 2019Article
- Abnormal myosin phosphatase targeting subunit 1 phosphorylation and actin polymerization contribute to impaired myogenic regulation of cerebral arterial diameter in the type 2 diabetic Goto-Kakizaki rat.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- ROK and Arteriolar Myogenic Tone Generation: Molecular Evidence in Health and Disease.Frontiers in pharmacology · 2017Review
- Modeling the Disease Progression from Healthy to Overt Diabetes in ZDSD Rats.The AAPS journal · 2016Article
- Sleeve gastrectomy, but not duodenojejunostomy, preserves total beta-cell mass in Goto-Kakizaki rats evaluated by three-dimensional optical projection tomography.Surgical endoscopy · 2016Article
- Modeling Disease Progression: Angiotensin II Indirectly Inhibits Nitric Oxide Production via ADMA Accumulation in Spontaneously Hypertensive Rats.Frontiers in physiology · 2016Article
- The effect of duodenojejunostomy and sleeve gastrectomy on type 2 diabetes mellitus and gastrin secretion in Goto-Kakizaki rats.Surgical endoscopy · 2015Article
- Population pharmacodynamic modeling of exenatide after 2-week treatment in STZ/NA diabetic rats.Journal of pharmaceutical sciences · 2013Article
- Multimodal Highlighting of Structural Abnormalities in Diabetic Rat and Human Corneas.Translational vision science & technology · 2013Article
- Modeling disease progression and rosiglitazone intervention in type 2 diabetic Goto-Kakizaki rats.The Journal of pharmacology and experimental therapeutics · 2012Article
- Modeling diabetes disease progression and salsalate intervention in Goto-Kakizaki rats.The Journal of pharmacology and experimental therapeutics · 2011Article
- Pharmacokinetic and pharmacodynamic modeling of exendin-4 in type 2 diabetic Goto-Kakizaki rats.The Journal of pharmacology and experimental therapeutics · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The dynamics of aging and type 2 diabetes (T2D) disease progression were investigated in normal [Wistar-Kyoto (WKY)] and diabetic [Goto-Kakizaki (GK)] rats and a mechanistic disease progression model was developed for glucose, insulin, and glycosylated hemoglobin (HbA1c) changes over time. The study included 30 WKY and 30 GK rats. Plasma glucose and insulin, blood glucose and HbA1c concentrations and hematological measurements were taken at ages 4, 8, 12, 16 and 20 weeks. A mathematical model described the development of insulin resistance (IR) and β-cell function with age/growth and diabetes progression. The model utilized transit compartments and an indirect response model to quantitate biomarker changes over time. Glucose, insulin and HbA1c concentrations in WKY rats increased to a steady-state at 8 weeks due to developmental changes. Glucose concentrations at 4 weeks in GK rats were almost twice those of controls, and increased to a steady-state after 8 weeks. Insulin concentrations at 4 weeks in GK rats were similar to controls, and then hyperinsulinemia occurred until 12-16 weeks of age indicating IR. Subsequently, insulin concentrations in GK rats declined to slightly below WKY controls due to β-cell failure. HbA1c showed a delayed increase relative to glucose. Modeling of HbA1c was complicated by age-related changes in hematology in rats. The diabetes model quantitatively described the glucose/insulin inter-regulation and HbA1c production and reflected the underlying pathogenic factors of T2D--IR and β-cell dysfunction. The model could be extended to incorporate other biomarkers and effects of various anti-diabetic drugs.
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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.