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Hypoxia increases leptin expression in human PAZ6 adipose cells
A Grosfeld1, V Zilberfarb, S Turban
1INSERM U 465, Paris, France.
Diabetologia
|May 29, 2002
Summary
Low oxygen levels (hypoxia) significantly increase leptin production in fat cells by activating the leptin gene. This finding highlights a novel regulatory pathway for leptin, a key hormone in body weight control and angiogenesis.
Area of Science:
- Cell Biology
- Endocrinology
- Molecular Biology
Background:
- Leptin, a cytokine from adipose tissue, regulates body weight and angiogenesis.
- Angiogenesis is induced by reduced oxygen availability (hypoxia).
Purpose of the Study:
- To investigate the hypothesis that low cellular oxygen tension regulates leptin expression in adipose cells.
- To determine the effect of hypoxia on leptin gene expression and production.
Main Methods:
- PAZ6 adipocytes and primary rat adipose cells were exposed to hypoxia using chemical inducers or low oxygen atmosphere.
- Gene expression (leptin, GLUT-1, GLUT-4, HSL, aP2, UCP2) was assessed by RT-PCR.
- Leptin promoter activity and secretion were measured using luciferase reporter assays and radioimmunoassay, respectively.
Main Results:
- Hypoxia increased leptin mRNA expression, promoter activity, and secretion by two- to threefold in PAZ6 adipocytes.
- Hypoxia also increased leptin mRNA and secretion in primary rat adipose cells.
- While GLUT-1 mRNA increased, GLUT-4, HSL, aP2, and UCP2 mRNAs were reduced by hypoxia.
Conclusions:
- Hypoxia specifically and markedly increases leptin gene expression via leptin gene promoter activation.
- This leads to enhanced leptin production in human PAZ6 adipocytes.
- Adipose cells' leptin production is regulated by cellular oxygen levels.