ArticleMolecular and cellular endocrinology2011
Differential muscle gene expression as a function of disease progression in Goto-Kakizaki diabetic rats.
Article in Molecular and cellular endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Revealing the critical state and identifying individualized dynamic network biomarker for type 2 diabetes through advanced analysis methods on individual basis.Scientific reports · 2025Article
- Current advancement in the preclinical models used for the assessment of diabetic neuropathy.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Animal models for induction of diabetes and its complications.Journal of diabetes and metabolic disorders · 2023Review
- Experimental animal models for diabetes and its related complications-a review.Laboratory animal research · 2021Review
- Small intestine remodeling in male Goto-Kakizaki rats.Physiological reports · 2021Article
- Article
- Quantification of Mitochondrial Oxidative Phosphorylation in Metabolic Disease: Application to Type 2 Diabetes.International journal of molecular sciences · 2019Review
- Skeletal muscle energetics are compromised only during high-intensity contractions in the Goto-Kakizaki rat model of type 2 diabetes.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Article
- Article
- Transcriptomic responses of hypothalamus to acute exercise in type 2 diabetic Goto-Kakizaki rats.PeerJ · 2019Article
- Multi-Level Comparative Framework Based on Gene Pair-Wise Expression Across Three Insulin Target Tissues for Type 2 Diabetes.Frontiers in genetics · 2019Article
- Transcriptomic Responses of Skeletal Muscle to Acute Exercise in Diabetic Goto-Kakizaki Rats.Frontiers in physiology · 2019Article
- Effects of High-Fat Feeding on Skeletal Muscle Gene Expression in Diabetic Goto-Kakizaki Rats.Gene regulation and systems biology · 2017Article
- 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
- Transcriptomic alterations in the heart of non-obese type 2 diabetic Goto-Kakizaki rats.Cardiovascular diabetology · 2016Article
- Sexual dimorphism in myocardial acylcarnitine and triglyceride metabolism.Biology of sex differences · 2016Article
- Effects of High Fat Feeding on Adipose Tissue Gene Expression in Diabetic Goto-Kakizaki Rats.Gene regulation and systems biology · 2015Article
- The expression of PHO92 is regulated by Gcr1, and Pho92 is involved in glucose metabolism in Saccharomyces cerevisiae.Current genetics · 2014Article
- Variability in Zucker diabetic fatty rats: differences in disease progression in hyperglycemic and normoglycemic animals.Diabetes, metabolic syndrome and obesity : targets and therapy · 2014Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The Goto-Kakizaki (GK) rat, a polygenic non-obese model of type 2 diabetes, is a useful surrogate for study of diabetes-related changes independent of obesity. GK rats and appropriate controls were killed at 4, 8, 12, 16 and 20 weeks post-weaning and differential muscle gene expression along with body and muscle weights, plasma hormones and lipids, and blood cell measurements were carried out. Gene expression analysis identified 204 genes showing 2-fold or greater differences between GK and controls in at least 3 ages. Array results suggested increased oxidative capacity in GK muscles, as well as differential gene expression related to insulin resistance, which was also indicated by HOMA-IR measurements. In addition, potential new biomarkers in muscle gene expression were identified that could be either a cause or consequence of T2DM. Furthermore, we demonstrate here the presence of chronic inflammation evident both systemically and in the musculature, despite the absence of obesity.
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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.