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Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

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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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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.
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Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
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Insulin preparations are categorized by their duration of action into short-acting and long-acting types. Two strategies are used to modify insulin's absorption and pharmacokinetic profile: slowing the absorption post-subcutaneous injection, or altering human insulin's amino acid sequence or protein structure. These changes retain the insulin's ability to bind to the insulin receptor, but alter its behavior in solution or after injection.
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Related Experiment Video

Updated: Feb 5, 2026

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test OGTT and Insulin Tolerance Test ITT
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Chronic NH4Cl loading improves glucose tolerance without modifying insulin sensitivity in mice.

Nawel Zaibi1,2, Jessica Montaigne3, Jennifer Baraka-Vidot4

  • 1Inserm UMR1283, CNRS UMR8199, European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille University Hospital, Lille, France. nawel.zaibi@univ-lille.fr.

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Summary

Chronic metabolic acidosis (MA) in mice improved glucose tolerance without altering insulin levels. This metabolic shift was linked to kidney changes, including reduced glucose production and increased energy use.

Keywords:
Gene expressionGluconeogenesisGlucose homeostasisMetabolic parametersRenal functionpH regulation

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Area of Science:

  • Nephrology
  • Endocrinology
  • Metabolic Physiology

Background:

  • Metabolic acidosis (MA), common in chronic kidney disease, impacts glucose metabolism.
  • The long-term effects of chronic MA on glucose homeostasis are not well understood.

Purpose of the Study:

  • To investigate the impact of chronic metabolic acidosis on glucose homeostasis and metabolic parameters in male mice.

Main Methods:

  • Chronic metabolic acidosis was induced in mice using long-term ammonium chloride (NH4Cl) administration.
  • Evaluated glucose tolerance, insulin sensitivity, basal glycemia, and energy expenditure.
  • Analyzed hepatic, intestinal, and renal gluconeogenesis, glucose uptake, and renal sodium/glucose co-transporter expression.
  • Utilized transcriptomic analysis of kidney tissue.

Main Results:

  • Chronic MA led to lower body weight, increased energy expenditure, and reduced basal glycemia.
  • Improved glucose tolerance was observed without changes in insulin secretion or sensitivity.
  • Decreased hepatic and intestinal gluconeogenesis, but increased renal endogenous glucose production.
  • Elevated urinary glucose excretion correlated with lower renal sodium/glucose co-transporter expression.
  • Kidney transcriptomics indicated enhanced anion transport, glucose/lipid metabolism, and oxidative phosphorylation.

Conclusions:

  • Chronic MA improves glucose tolerance in mice, independent of insulin changes.
  • This improvement is attributed to reduced hepatic gluconeogenesis, decreased renal glucose reabsorption, and increased kidney energy demands.