Related Experiment Video

Updated: Aug 11, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
11:10

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

Dexamethasone inhibition of hydrogen peroxide-stimulated glucose transport

D H Nelson, D K Murray

    Endocrinology
    |January 1, 1987
    PubMed

    Insights

    Corticosteroids, like dexamethasone, inhibit glucose transport by affecting cells after insulin binding. This study shows dexamethasone also blocks hydrogen peroxide-stimulated glucose transport, suggesting a post-receptor mechanism involving membrane lipids.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Endocrinology

    Background:

    • Corticosteroids are known to inhibit glucose transport, but the precise mechanism remains unclear.
    • Evidence suggests effects on insulin receptors or post-receptor pathways.
    • Hydrogen peroxide stimulates glucose transport via a postbinding site.

    Purpose of the Study:

    • To investigate if corticosteroids inhibit hydrogen peroxide-induced glucose transport.
    • To explore the postbinding mechanism of corticosteroid action on glucose transport.

    Main Methods:

    • Experiments were conducted using 3T3-L1 fibroblasts.
    • Cells were incubated with insulin or hydrogen peroxide to measure glucose transport.
    • The effect of dexamethasone pre-incubation on glucose transport was assessed.

    Main Results:

    • Both insulin and hydrogen peroxide significantly increased glucose transport in 3T3-L1 fibroblasts.
    • Dexamethasone pre-incubation inhibited the glucose transport stimulated by both insulin and hydrogen peroxide.
    • These findings support a postbinding effect of dexamethasone on glucose transport.

    Conclusions:

    • Dexamethasone inhibits glucose transport at a postbinding site, independent of direct insulin receptor interaction.
    • Alterations in plasma membrane lipids by dexamethasone may mediate its effects on glucose transporters.
    • The study provides further evidence for a non-genomic mechanism of corticosteroid action on glucose uptake.

    More Related Videos

    Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells10:00

    Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells

    Published on: December 11, 2020

    Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo10:35

    Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo

    Published on: April 6, 2022

    Related Concept Videos

    Peroxisomes01:24

    Peroxisomes

    Peroxisomes are specialized organelles present in fungi, plant, and animal cells. It can vary in number, size, morphology, and activity depending on the type of tissue and the nutritional state of the cell. For example, cells with active lipid metabolism, such as adipocytes, neurons, and hepatocytes, have more peroxisomes than other cells in the body. Besides their primary role in breaking down complex organic molecules, peroxisomes can also synthesize specific macromolecules and participate in...
    Hormones Regulating Blood Glucose01:16

    Hormones Regulating Blood Glucose

    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.
    In addition to accelerating glucose uptake and utilization, insulin has...
    Glucose Homeostasis: Regulation of Blood Glucose01:02

    Glucose Homeostasis: Regulation of Blood Glucose

    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.
    During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
    Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

    Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

    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 co-secreted in...
    Hypoglycemia and Glucagon01:15

    Hypoglycemia and Glucagon

    Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
    Hyperglycemia01:29

    Hyperglycemia

    Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...