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Related Concept Videos

Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

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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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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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Insulin Secretory Vesicles01:05

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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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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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Endocrine Signaling01:45

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Endocrine cells produce hormones to communicate with remote target cells found in other organs. The hormone reaches these distant areas using the circulatory system. This exposes the whole organism to the hormone but only those cells expressing hormone receptors or target cells are affected. Thus, endocrine signaling induces slow responses from its target cells but these effects also last longer.
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Related Experiment Video

Updated: Nov 29, 2025

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
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Insulin signalling in hypothalamic neurones.

Denise D Belsham1, Prasad S Dalvi2

  • 1Departments of Physiology, Obstetrics and Gynaecology and Medicine, University of Toronto, Toronto, ON, Canada.

Journal of Neuroendocrinology
|November 23, 2020
PubMed
Summary
This summary is machine-generated.

Brain insulin resistance disrupts energy balance, leading to obesity and related diseases. Neuronal therapeutics offer hope by targeting key signaling pathways for potential treatment.

Keywords:
hypothalamusinsulin resistanceinsulin signallingneuropeptides

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Metabolic Research

Background:

  • Insulin's role in whole-body homeostasis is increasingly recognized, particularly its action in the brain.
  • The hypothalamus integrates insulin signals to regulate hunger and feeding behaviors.
  • Cellular insulin resistance in brain neurons disrupts this critical feedback loop.

Purpose of the Study:

  • To explore the mechanisms and consequences of insulin resistance in the brain.
  • To highlight the link between brain insulin signaling and metabolic disorders.
  • To discuss potential therapeutic strategies targeting neuronal insulin pathways.

Main Methods:

  • Review of current literature on insulin signaling in the hypothalamus.
  • Analysis of factors contributing to neuroinflammation and blood-brain barrier alterations.
  • Examination of cell models for investigating insulin resistance mechanisms.

Main Results:

  • Disruption of hypothalamic insulin signaling leads to neuroinflammation and endoplasmic reticulum stress.
  • Altered blood-brain barrier function impairs insulin transport into the brain.
  • Impaired insulin sensing in neurons contributes to weight gain, obesity, and comorbidities like type 2 diabetes.

Conclusions:

  • Brain insulin resistance is a significant factor in metabolic dysfunction and obesity.
  • Neurone-specific therapeutics targeting signal transduction pathways offer promising treatment avenues.
  • Continued research into novel targets is crucial for advancing diabetes and metabolic disorder treatments.