Insulin-stimulated GLUT4 recruitment to the plasma membrane is impaired in insulin resistance. We recently reported that a cell permeable phosphoinositide-binding peptide induces GLUT4 recruitment as potently as insulin, but does not activate GLUT4 to initiate glucose uptake. Here we investigated whether the peptide-induced GLUT4 recruitment is intact in insulin resistance. The expression levels of GLUT1 and GLUT4 were unaffected by chronically treating 3T3-L1 adipocytes with insulin. GLUT4 recruitment by acute insulin stimulation after chronic insulin treatment was significantly reduced, but was fully restored by the peptide treatment. However, subsequent acute insulin stimulation to activate GLUT4 failed to increase glucose uptake in peptide-pretreated cells. Insulin-stimulated GLUT1 recruitment was unaffected by the peptide pretreatment. These results suggest that the GLUT4 recruitment signal caused by the peptide is intact in insulin resistance, but GLUT4 activation that occurs subsequent to recruitment is not rescued by the peptide treatment.
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http://dx.doi.org/10.1016/j.bbrc.2007.06.153 | DOI Listing |
J Diabetes Investig
December 2024
Department of Reproduction, Poznan University of Medical Sciences, Poznan, Poland.
EMBO J
October 2024
Structural and Molecular Biology, Division of Biosciences, University College London, London, WC1E 6BT, UK.
The two clathrin isoforms, CHC17 and CHC22, mediate separate intracellular transport routes. CHC17 performs endocytosis and housekeeping membrane traffic in all cells. CHC22, expressed most highly in skeletal muscle, shuttles the glucose transporter GLUT4 from the ERGIC (endoplasmic-reticulum-to-Golgi intermediate compartment) directly to an intracellular GLUT4 storage compartment (GSC), from where GLUT4 can be mobilized to the plasma membrane by insulin.
View Article and Find Full Text PDFJ Neurochem
September 2024
Instituto de Fisiología, Biología Molecular y Neurociencias. CONICET. Departamento de Fisiología y Biología Molecular y Celular. Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires, Buenos Aires, Argentina.
Dynamins are large GTPases whose primary function is not only to catalyze membrane scission during endocytosis but also to modulate other cellular processes, such as actin polymerization and vesicle trafficking. Recently, we reported that centronuclear myopathy associated dynamin-2 mutations, p.A618T, and p.
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August 2024
Systems Toxicology Group, FEST Division, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), 31, Vishvigyan Bhawan, Mahatma Gandhi Marg, Lucknow 226001, India; Academy of Scientific and Innovative Research (AcSIR), Ghaziabad 201002, India. Electronic address:
The global prevalence of Metabolic Syndrome (MetS) is continuously rising and exposure to environmental toxicants such as arsenic could be contributing to this rapid surge. In this study, we have assessed the effects of prenatal arsenic exposure on insulin resistance and MetS parameters in a mouse model, and an underlying mechanism was identified. We found that prenatal arsenic exposure promotes insulin resistance and adipocyte dysfunction which leads to the early onset of MetS in male offspring.
View Article and Find Full Text PDFAutophagy
November 2024
International Institutes of Medicine, The Fourth Affiliated Hospital of Zhejiang University School of Medicine, Yiwu, China.
Macroautophagic/autophagic and endocytic pathways play essential roles in maintaining homeostasis at different levels. It remains poorly understood how both pathways are coordinated and fine-tuned for proper lysosomal degradation of diverse cargoes. We and others recently identified a Golgi-resident RAB GTPase, RAB2A, as a positive regulator that controls both autophagic and endocytic pathways.
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