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Related Concept Videos

Glucose Homeostasis: Regulation of Blood Glucose01:02

Glucose Homeostasis: Regulation of Blood Glucose

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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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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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Receptor-mediated Endocytosis01:39

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Receptor-mediated Endocytosis01:20

Receptor-mediated Endocytosis

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Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
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Glucose Absorption Into the Small Intestine01:26

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Complex carbohydrates consumed cannot be absorbed into the small intestine in their original form. First, they must be hydrolyzed to a monosaccharide form such as glucose or galactose. These monosaccharides are then transported across the intestinal membrane and into the blood via transcellular transport. The intestinal epithelial cells allow the movement of these monosaccharides with a defined 'entry' through membrane transporter proteins present on their apical membrane and...
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Hormones Regulating Blood Glucose01:16

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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction
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TRAF6 mediates high glucose-induced endothelial dysfunction.

Rong Liu1, Hong Shen1, Tao Wang2

  • 1Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Rd, Shanghai 200233, China.

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|July 19, 2018
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Tumor necrosis factor-associated factor 6 (TRAF6) drives high glucose-induced endothelial cell dysfunction. Targeting TRAF6 may prevent vascular complications in diabetes and atherosclerosis.

Keywords:
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Area of Science:

  • Vascular Biology
  • Endocrinology
  • Molecular Medicine

Background:

  • Endothelial cell dysfunction is a key factor in vascular diseases.
  • High glucose levels in diabetes mellitus contribute to endothelial damage.
  • The specific role of TRAF6 in high glucose-induced endothelial dysfunction requires elucidation.

Purpose of the Study:

  • To investigate the role of TRAF6 in high glucose-induced endothelial cell dysfunction.
  • To explore the underlying signaling pathways.
  • To assess the therapeutic potential of targeting TRAF6.

Main Methods:

  • Human aortic endothelial cells (HAECs) were cultured in high glucose conditions.
  • TRAF6 expression was analyzed using quantitative real-time PCR and western blotting.
  • Gene knockdown, cell viability, apoptosis, migration, and adhesion assays were performed.
  • A mouse model of type I diabetes was utilized.
  • Signaling pathway analysis involved IκB-α degradation and JNK phosphorylation assessments.

Main Results:

  • High glucose significantly increased TRAF6 expression in HAECs.
  • TRAF6 knockdown reversed high glucose-induced reductions in cell viability, apoptosis, and migration.
  • TRAF6 knockdown attenuated high glucose-induced endothelial-monocyte adhesion by downregulating ICAM-1 and VCAM-1.
  • Increased TRAF6, ICAM-1, and VCAM-1 were observed in diabetic mouse aortas.
  • TRAF6 knockdown inhibited NF-κB and AP-1 signaling pathways.

Conclusions:

  • TRAF6 plays a critical role in high glucose-induced endothelial cell dysfunction.
  • TRAF6 mediates endothelial damage through NF-κB and AP-1 signaling pathways.
  • Targeting TRAF6 presents a potential therapeutic strategy for vascular complications in diabetes and atherosclerosis.