ArticleThe Journal of clinical investigation1997
Muscle-specific transgenic complementation of GLUT4-deficient mice. Effects on glucose but not lipid metabolism.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
17 citing papers in PubMed, 69 citations in OpenAlex.
- Regulation of injury-induced skeletal myofiber regeneration by glucose transporter 4 (GLUT4).Skeletal muscle · 2024Article
- AIFM2 Is Required for High-Intensity Aerobic Exercise in Promoting Glucose Utilization.Diabetes · 2022Article
- Maresin 1 Alleviates Diabetic Kidney Disease via LGR6-Mediated cAMP-SOD2-ROS Pathway.Oxidative medicine and cellular longevity · 2022Article
- Maresin 1 regulates insulin signaling in human adipocytes as well as in adipose tissue and muscle of lean and obese mice.Journal of physiology and biochemistry · 2021Article
- A novel mutation in Slc2a4 as a mouse model of fatigue.Genes, brain, and behavior · 2019Article
- Enhanced GLUT4-Dependent Glucose Transport Relieves Nutrient Stress in Obese Mice Through Changes in Lipid and Amino Acid Metabolism.Diabetes · 2016Article
- Regulation of GLUT4 and Insulin-Dependent Glucose Flux.ISRN molecular biology · 2012Review
- Rodent models for metabolic syndrome research.Journal of biomedicine & biotechnology · 2011Review
- Hypotension, lipodystrophy, and insulin resistance in generalized PPARgamma-deficient mice rescued from embryonic lethality.The Journal of clinical investigation · 2007Article
- Article
- Skeletal muscle insulin resistance: is it important for the pathogenesis of type 2 diabetes after all?Journal of endocrinological investigation · 2003Article
- Control of body weight: a physiologic and transgenic perspective.Diabetologia · 2003Review
- Genetic manipulation of insulin signaling, action and secretion in mice. Insights into glucose homeostasis and pathogenesis of type 2 diabetes.EMBO reports · 2002Review
- Insights into insulin resistance and type 2 diabetes from knockout mouse models.The Journal of clinical investigation · 2000Review
- In vitro analysis of the glucose-transport system in GLUT4-null skeletal muscle.The Biochemical journal · 1999Article
- Genetic engineering in mice: impact on insulin signalling and action.The Biochemical journal · 1998Review
- Metabolic and therapeutic lessons from genetic manipulation of GLUT4.Molecular and cellular biochemistry · 1998Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
We have taken the approach of introducing the muscle-specific myosin light chain (MLC)-GLUT4 transgene into the GLUT4-null background to assess the relative role of muscle and adipose tissue GLUT4 in the etiology of the GLUT4-null phenotype. The resulting MLC-GLUT4-null mice express GLUT4 predominantly in the fast-twitch extensor digitorum longus (EDL) muscle. GLUT4 is nearly absent in female white adipose tissue (WAT) and slow-twitch soleus muscle of both sexes of MLC-GLUT4-null mice. GLUT4 content in male MLC-GLUT4-null WAT is 20% of that in control mice. In transgenically complemented EDL muscle, 2-deoxyglucose (2-DOG) uptake was restored to normal (male) or above normal (female) levels. In contrast, 2-DOG uptake in slow-twitch soleus muscle of MLC-GLUT4-null mice was not normalized. With the normalization of glucose uptake in fast-twitch skeletal muscle, whole body insulin action was restored in MLC-GLUT4-null mice, as shown by the results of the insulin tolerance test. These results demonstrate that skeletal muscle GLUT4 is a major regulator of skeletal muscle and whole body glucose metabolism. Despite normal skeletal muscle glucose uptake and insulin action, the MLC-GLUT4-null mice exhibited decreased adipose tissue deposits, adipocyte size, and fed plasma FFA levels that are characteristic of GLUT4-null mice. Together these results indicate that the defects in skeletal muscle and whole body glucose metabolism and adipose tissue in GLUT4-null mice arise independently.
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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.