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Glucose Absorption Into the Small Intestine01:26

Glucose Absorption Into the Small Intestine

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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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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.
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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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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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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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Transcellular transport of solutes is the movement of substances like monosaccharides and amino acids through polarized cells. This transport mechanism is primarily seen in epithelial and endothelial cells aided by membrane transport proteins such as channels and transporters. The tight junctions between these cells confine the membrane proteins to the two sides of the cell. The epithelial cells have distinct apical and basolateral domains. In contrast, the endothelial cells show the luminal...
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High glucose exposure drives intestinal barrier dysfunction by altering its morphological, structural and functional

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High glucose (HG) negatively impacts intestinal barrier cells, altering their structure and function. Controlling hyperglycemia is crucial for preventing intestinal barrier damage and improving therapies.

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Area of Science:

  • Cell Biology
  • Gastroenterology
  • Endocrinology

Background:

  • High glucose (HG) and hyperglycemia are linked to chronic health complications.
  • Previous research suggests HG impairs intestinal barrier function, but specific changes are not fully understood.

Purpose of the Study:

  • To investigate the long-term effects of HG on the morphological, structural, and functional characteristics of the intestinal barrier using in vitro models.
  • To compare the impact of HG on intestinal barrier cells in monoculture versus co-culture systems.

Main Methods:

  • Utilized Caco-2 and HT29-MTX cell lines in monoculture and co-culture models.
  • Exposed cells to normal (5.5 mM) and high (25 mM) glucose concentrations for 21 days.
  • Assessed morphological changes, tight junction protein expression (ZO-1, OCLN, E-cad) via mRNA, protein, and immunofluorescence, and functional parameters like permeability, mucus production, and alkaline phosphatase activity.

Main Results:

  • HG exposure led to denser, less organized cell layers, increased Caco-2 migration, and enhanced HT29-MTX proliferation.
  • While mRNA and protein levels of tight junction proteins showed minor decreases, immunofluorescence revealed significant disruption of their structural networks under HG.
  • HG negatively affected intestinal barrier functionalities, including increased permeability, reduced mucus production, and altered alkaline phosphatase activity, with more pronounced effects in co-cultures.

Conclusions:

  • Long-term high glucose exposure disrupts the intestinal barrier's morphology, structure, and function.
  • The interplay between enterocytes and goblet cells (in co-culture) exacerbates HG-induced damage.
  • Managing hyperglycemia is essential for mitigating intestinal barrier damage and enhancing therapeutic outcomes.