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Related Concept Videos

Glucose Transporters01:27

Glucose Transporters

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Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
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Glycolysis: Preparatory Phase01:21

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In cellular metabolism (the complete breakdown of glucose to extract energy),  glycolysis is the first step. Glycolysis takes place in the cytoplasm of both prokaryotic and eukaryotic cells. Glucose enters heterotrophic cells in two ways. One method is through secondary active transport, where the transport takes place against the glucose concentration gradient. The other mechanism uses a group of integral proteins called GLUT proteins, also known as glucose transporter proteins. These...
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Fructose-induced ROS generation impairs glucose utilization in L6 skeletal muscle cells.

N Jaiswal1, C K Maurya, J Pandey

  • 1Division of Biochemistry, CSIR-Central Drug Research Institute , Lucknow, Uttar Pradesh , India.

Free Radical Research
|May 14, 2015
PubMed
Summary

High fructose intake impairs skeletal muscle glucose uptake and insulin signaling by increasing oxidative stress. Antioxidants can prevent these negative effects, suggesting a potential therapeutic target for metabolic dysfunction.

Keywords:
insulin resistancenutrient signaloxidative stressstress kinase

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Syndrome Research

Background:

  • High fructose consumption is linked to insulin resistance and metabolic syndrome.
  • Fructose significantly impacts liver metabolism and has broader metabolic consequences.
  • Skeletal muscle is crucial for glucose disposal, making its response to fructose critical.

Purpose of the Study:

  • To investigate the effects of fructose exposure on glucose utilization in skeletal muscle cells.
  • To elucidate the molecular mechanisms underlying fructose-induced impairment of skeletal muscle function.

Main Methods:

  • Utilized L6 skeletal muscle cells for in vitro studies.
  • Assessed glucose uptake, glucose transporter type 4 (GLUT4) translocation, and insulin signaling pathways.
  • Measured reactive oxygen species (ROS) production and stress/inflammation markers (JNK, ERK1/2, IκBα).

Main Results:

  • Fructose exposure diminished glucose uptake and GLUT4 translocation in L6 myotubes.
  • Impaired insulin signaling was observed following fructose exposure.
  • Fructose elevated ROS production, activating JNK and ERK1/2 pathways and degrading IκBα.
  • Antioxidant treatment prevented fructose-induced impairments.

Conclusions:

  • Fructose exposure triggers an intrinsic oxidative stress response in skeletal muscle cells.
  • This oxidative stress, mediated by ROS, leads to impaired insulin signaling and reduced glucose utilization.
  • The findings highlight a mechanism by which fructose contributes to metabolic dysfunction in skeletal muscle.