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Related Concept Videos

Regulation of Food Intake01:30

Regulation of Food Intake

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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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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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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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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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Diencephalon: Hypothalamus and Coordination01:23

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The hypothalamus is a small yet highly complex and essential brain region that plays a crucial role in regulating various bodily functions. Anatomically, it is located at the base of the brain, just above the brainstem and below the thalamus, forming part of the limbic system.
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Related Experiment Video

Updated: Aug 25, 2025

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
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Hindbrain insulin controls feeding behavior.

Kim Eerola1, Francesco Longo2, Thomas M Reinbothe2

  • 1Institute for Neuroscience and Physiology, University of Gothenburg, Sweden; Unit of Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Finland.

Molecular Metabolism
|October 16, 2022
PubMed
Summary
This summary is machine-generated.

Brain insulin, particularly in the hindbrain's dorsal vagal complex (DVC), plays a key role in regulating feeding and metabolism. This study reveals that DVC insulin production increases with diet-induced obesity and influences appetite.

Keywords:
Diet-induced obesityDorsal vagal complexFood intakeHindbrainInsulin

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Area of Science:

  • Neuroscience
  • Metabolism
  • Endocrinology

Background:

  • Insulin, primarily known for its pancreatic role in glucose regulation, is also suggested to be produced in the brain.
  • The specific functions and locations of brain-derived insulin, especially in the hindbrain, remain poorly understood.
  • Understanding brain insulin is crucial for metabolic and feeding behavior research.

Purpose of the Study:

  • To investigate insulin expression in the dorsal vagal complex (DVC) of the hindbrain.
  • To determine the role of DVC-derived insulin in regulating feeding behavior and metabolism.
  • To examine how diet-induced obesity affects insulin expression in the DVC.

Main Methods:

  • Utilized transgenic mice (RipHER-cre) for optogenetic stimulation of insulin-producing neurons.
  • Employed in situ hybridization to confirm insulin expression in DVC cells.
  • Administered a central insulin receptor antagonist to block insulin signaling.
  • Used virogenetic knockdown to reduce insulin gene expression in the hindbrain.

Main Results:

  • Detected insulin gene expression in the DVC, with increased levels in diet-induced obesity, contrasting with hypothalamic changes.
  • Optogenetic activation of DVC insulin neurons induced hyperphagia, which was blocked by an insulin receptor antagonist.
  • Insulin gene knockdown in the DVC reduced food intake in mice on a high-fat diet.

Conclusions:

  • Hindbrain insulin and its producing cells are significantly involved in energy homeostasis.
  • DVC insulin plays a critical role in modulating feeding behavior, particularly under conditions of obesity.
  • These findings highlight a novel role for hindbrain insulin in metabolic regulation.