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Related Experiment Video

Updated: May 15, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

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Published on: June 3, 2016

Hypoxia and adipose tissue function and dysfunction in obesity.

Paul Trayhurn¹

¹Obesity Biology Research Unit, Institute of Ageing and Chronic Diseases, University of Liverpool, Liverpool, UK.

Physiological Reviews

|January 11, 2013

Summary

This summary is machine-generated.

Hypoxia, or low oxygen, in white adipose tissue drives inflammation and insulin resistance, contributing to obesity-associated diseases. This impacts fat cell function and adipose tissue fibrosis.

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Area of Science:

Adipose tissue biology
Endocrinology
Metabolic disease research

Background:

Obesity is linked to increased white adipose tissue (WAT) mass and inflammation.
WAT functions as an endocrine organ, secreting adipokines.
Hypoxia is increasingly recognized as a factor in WAT dysfunction during obesity.

Purpose of the Study:

To investigate the effects of hypoxia on white adipocytes and adipose tissue.
To understand the role of hypoxia in obesity-associated inflammation and metabolic dysfunction.

Main Methods:

In vitro studies exposing white adipocytes to hypoxic conditions.
Analysis of gene expression changes (>1,000 genes).
Assessment of adipokine secretion, metabolism, and insulin resistance.

Main Results:

Hypoxia upregulates inflammation-related adipokines and switches metabolism to anaerobic glycolysis.
Hypoxic adipocytes exhibit increased glucose utilization, lactate production, and insulin resistance.
Hypoxia also induces adipose tissue fibrosis and alters preadipocyte differentiation.

Conclusions:

Hypoxia is a key driver of white adipose tissue dysfunction in obesity.
Hypoxia contributes to inflammation, insulin resistance, and fibrosis in adipose tissue.
Understanding hypoxia's role is crucial for developing treatments for obesity-related diseases.