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Related Concept Videos

Insulin: The Receptor and Signaling Pathways01:28

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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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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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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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Type II Diabetes II: Pathophysiology01:24

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PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
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Regulation of Food Intake01:30

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Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
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Glucose Homeostasis: Regulation of Blood Glucose01:02

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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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Related Experiment Video

Updated: May 1, 2026

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
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The brain modulates insulin sensitivity in multiple tissues.

Edwin T Parlevliet1, Claudia P Coomans, Patrick C N Rensen

  • 1Department of Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Frontiers of Hormone Research
|April 16, 2014
PubMed
Summary
This summary is machine-generated.

Insulin sensitivity involves direct and indirect effects, including the central nervous system. Targeting central insulin resistance offers therapeutic potential for metabolic disorders.

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Area of Science:

  • Endocrinology
  • Metabolic Research
  • Neuroscience

Background:

  • Insulin sensitivity is regulated by direct insulin actions on tissues and indirect effects via the central nervous system.
  • Insulin's dose-response effects vary across physiological functions, impacting glucose and fatty acid metabolism.

Purpose of the Study:

  • To investigate the dual role of direct and indirect insulin signaling in metabolic regulation.
  • To explore the contribution of central insulin resistance to overall metabolic dysfunction.
  • To assess the therapeutic potential of targeting central insulin resistance.

Main Methods:

  • Analysis of dose-dependent insulin effects on glucose and fatty acid metabolism.
  • Induction of high-fat diet to model central nervous system insulin resistance.
  • Evaluation of therapeutic interventions (topiramate, GLP-1) in insulin-resistant mouse models.

Main Results:

  • Lower insulin concentrations inhibit endogenous glucose production via direct and indirect pathways.
  • Higher insulin concentrations promote glucose and fatty acid uptake in adipose tissue.
  • High-fat diet-induced central insulin resistance significantly impacts liver and peripheral tissues; this central resistance is therapeutically responsive.

Conclusions:

  • Central insulin resistance is a significant contributor to overall metabolic dysfunction.
  • Therapeutic interventions targeting the central nervous system show promise in ameliorating hepatic and peripheral insulin resistance.