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Related Experiment Video

Updated: Jun 26, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

Resistin and postburn insulin dysfunction.

Steve L Duffy¹, Lavenia Lagrone, David N Herndon

¹Department of Surgery, The University of Texas Medical Branch at Galveston, Galveston, Texas 77555, USA.

The Journal of Trauma

|January 10, 2009

Summary

This summary is machine-generated.

Postburn insulin resistance is linked to elevated resistin levels, a hormone produced by activated monocytes at the burn site. This finding sheds light on the mechanisms behind post-burn metabolic dysfunction.

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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

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Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes

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Published on: June 25, 2017

Area of Science:

Metabolic dysfunction
Endocrinology
Burn injury research

Background:

Postburn insulin dysfunction significantly impacts patient morbidity and mortality.
The exact mechanisms driving postburn insulin resistance remain unclear.
Resistin, initially identified as an insulin antagonist in mice, has an obscure role in human metabolic regulation.

Purpose of the Study:

To investigate the role of resistin in postburn insulin dysfunction.
To determine if resistin is produced by mononuclear cells at burn injury sites.
To explore the correlation between resistin levels and insulin resistance post-burn.

Main Methods:

Assessed plasma glucose, insulin, and resistin protein levels in burned and healthy individuals.
Analyzed resistin gene expression in adipose tissue and circulating monocytes.
Compared these levels between burn survivors and control groups.

Main Results:

Burned individuals exhibited elevated glucose, insulin, and circulating resistin levels.
A significant correlation was observed between rising resistin levels and increasing insulin resistance.
Circulating monocyte resistin gene expression was profoundly elevated in the burn population.

Conclusions:

Resistin is likely produced by activated monocytes in the adipose tissue surrounding burn wounds.
Elevated resistin from monocyte activation may adversely affect postburn insulin function.
This study implicates resistin as a key mediator in postburn metabolic complications.