Glucose transporter 4 (GLUT4) expression in adipose tissue decreases during fasting. In skeletal muscle, we hypothesized that GLUT4 expression might be maintained in a beta-adrenergic-dependent way to ensure energy disposal for contractile function. Herein we investigate beta-blockade or beta-stimulation effects on GLUT4 expression in oxidative (soleus) and glycolytic [extensor digitorum longus (EDL)] muscles of fasted rats. Fasting increased GLUT4 mRNA in soleus (24%) and EDL (40%), but the protein content increased only in soleus (30%). beta1-beta2-, and beta1-beta2-beta3-blockade decreased (20-30%) GLUT4 mRNA content in both muscles, although GLUT4 protein decreased only in EDL. When mRNA and GLUT4 protein regulations were discrepant, changes in the mRNA poly(A) tail length were detected, indicating a posttranscriptional modulation of gene expression. These results show that beta-adrenergic activity regulates GLUT4 gene expression in skeletal muscle during fasting, highlighting its participation in preservation of GLUT4 protein in glycolytic muscle.
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http://dx.doi.org/10.1002/mus.21359 | DOI Listing |
J Chromatogr B Analyt Technol Biomed Life Sci
December 2024
The College of Life Sciences, Northwest University, Xi'an, China. Electronic address:
Zhi Bai Heye Fang (AR-PCC-NF) exerts a positive effect on glycolipid metabolic disorders in the clinical setting; however, its efficacy components and mechanisms of action remain unclear. Glycolipid metabolic disorders in mice were used to evaluate the therapeutic effects of AR-PCC-NF and its individual components, and the chemical components of AR-PCC-NF were detected by HPLC. An insulin-resistant cell model was then treated with 12 biological components in vitro, and seven candidate active components were administered to mice with glycolipid metabolic disorders to investigate the efficacy and mechanism of AR-PCC-NF.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Indian Institute of Technology, Gandhinagar, India.
Background: Diabetes is a modifiable risk factor for Alzheimer's disease, and GLUT4, an insulin-dependent transporter, plays a crucial role in insulin-resistant conditions and, consequently, in diabetes development. The study aimed to investigate the relationship between tau pathology and insulin resistance by quantifying GLUT4 expression and glucose concentration.
Method: Initially, SH-SY5Y cells underwent transfection with either a wild-type tau plasmid or a mutant tau plasmid.
Sci Adv
January 2025
Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine University, Düsseldorf, Germany.
The athlete's paradox states that intramyocellular triglyceride accumulation associates with insulin resistance in sedentary but not in endurance-trained humans. Underlying mechanisms and the role of muscle lipid distribution and composition on glucose metabolism remain unclear. We compared highly trained athletes (ATHL) with sedentary normal weight (LEAN) and overweight-to-obese (OVWE) male and female individuals.
View Article and Find Full Text PDFNutr Metab (Lond)
December 2024
College of Physical Education and Health Sciences, Zhejiang Normal University, 688 Yingbin Road, Jinhua, 321004, Zhejiang Province, China.
Objective: Impaired skeletal muscle glycogen synthesis contributes to insulin resistance (IR). Aerobic exercise reported to ameliorate IR by augmenting insulin signaling, however the detailed mechanism behind this improvement remains unclear. This study investigated whether aerobic exercise enhances glycogen anabolism and insulin sensitivity via EGR-1/PTP1B signaling pathway in skeletal muscle of rats.
View Article and Find Full Text PDFPLoS One
December 2024
Metabolic Research Laboratories, Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, Cambridge, United Kingdom.
Objective: A biallelic missense mutation in mitofusin 2 (MFN2) causes multiple symmetric lipomatosis and partial lipodystrophy, implicating disruption of mitochondrial fusion or interaction with other organelles in adipocyte differentiation, growth and/or survival. In this study, we aimed to document the impact of loss of mitofusin 1 (Mfn1) or 2 (Mfn2) on adipogenesis in cultured cells.
Methods: We characterised adipocyte differentiation of wildtype (WT), Mfn1-/- and Mfn2-/- mouse embryonic fibroblasts (MEFs) and 3T3-L1 preadipocytes in which Mfn1 or 2 levels were reduced using siRNA.
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