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Updated: Jun 3, 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 induces apelin expression in human adipocytes.

K Geiger¹, A Muendlein, N Stark

¹Vorarlberg Institute for Vascular Investigation and Treatment, Feldkirch, Austria.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme

|March 31, 2011

Summary

Hypoxia, or low oxygen, significantly increases the expression and secretion of the adipokine apelin in human fat cells. This response is mediated by HIF-1α, offering new insights into obesity and insulin resistance.

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Area of Science:

Endocrinology and Metabolism
Cellular Biology
Physiology

Background:

Adipokines are crucial in obesity and insulin resistance.
Adipose tissue hypoxia disrupts adipokine expression.
The impact of hypoxia on apelin in human adipocytes is not well understood.

Purpose of the Study:

To investigate the effect of hypoxia on apelin expression in human adipocytes.
To elucidate the role of hypoxia-inducible factor 1-alpha (HIF-1α) in this process.

Main Methods:

Differentiated human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were exposed to hypoxic conditions (1% O2) or chemical hypoxia (CoCl2).
Gene expression was analyzed using real-time PCR.
Apelin secretion was quantified via ELISA.

Main Results:

Hypoxia significantly upregulated mRNA expression of leptin and apelin.
Hypoxia significantly downregulated adiponectin mRNA expression.
Secreted apelin protein levels were elevated under hypoxic conditions.
Hypoxia-induced apelin mRNA expression was dependent on HIF-1α.

Conclusions:

Apelin expression and secretion are strongly induced by hypoxia in human adipocytes.
The early hypoxic response of apelin induction is mediated by HIF-1α.
Findings provide novel insights into adipokine regulation in metabolic diseases.