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Related Concept Videos

Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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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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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.
Insulin and C-peptide are...
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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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Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

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The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
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Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

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Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1...
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Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

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Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
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Related Experiment Video

Updated: May 4, 2026

Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets
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Virus-induced decrease of insulin receptors in cultured human cells.

F Shimizu, J J Hooks, C R Kahn

    The Journal of Clinical Investigation
    |November 1, 1980
    PubMed
    Summary

    Viral infections can decrease insulin receptors, impacting glucose metabolism. This study shows viruses alter cell membranes, reducing insulin binding and potentially causing diabetic complications.

    Area of Science:

    • Virology
    • Cell Biology
    • Endocrinology

    Background:

    • Viral infections can disrupt normal carbohydrate metabolism and glucose homeostasis, particularly in individuals with diabetes.
    • The precise mechanisms by which viruses affect glucose regulation are not fully understood.

    Purpose of the Study:

    • To investigate the impact of viral infections on insulin receptors.
    • To determine if viral infections alter insulin receptor concentration or affinity.

    Main Methods:

    • Utilized an in vitro radio-receptor assay with 125I-labeled insulin and human-amnion (WISH) cells.
    • Examined the effects of herpes simplex virus and vesicular stomatitis virus on insulin binding.

    Main Results:

    • Herpes simplex virus and vesicular stomatitis virus caused a 50% decrease in insulin binding.

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  • The reduction in binding was due to decreased insulin receptor concentration, not altered receptor affinity.
  • Decreased receptors correlated with viral antigen insertion into the plasma membrane.

    • Conclusions:

    • Viral infections can alter cell membranes, leading to reduced insulin receptor concentration.
    • These changes in insulin receptors may contribute to glucose metabolism abnormalities observed during viral infections.
    • The insulin receptor assay is a valuable tool for studying virus-induced changes in cell membranes.