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Identification of ALOX5 as a gene regulating adiposity and pancreatic function
M Mehrabian1, F T Schulthess, M Nebohacova
1Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Diabetologia
|April 19, 2008
Summary
Mice lacking 5-lipoxygenase (5-LO) showed increased fat mass but impaired insulin secretion. This suggests 5-LO plays a key role in regulating both adiposity and pancreatic islet function.
Area of Science:
- Metabolic research
- Cardiovascular research
- Endocrinology
Background:
- 5-lipoxygenase (5-LO) deficiency in mice (Alox5 (-/-)) previously protected against atherosclerosis.
- This protection occurred despite increased lipid levels and fat mass in Alox5 (-/-) mice.
Purpose of the Study:
- To investigate the role of 5-lipoxygenase (5-LO) in adiposity.
- To examine the impact of 5-LO on pancreatic function.
Main Methods:
- Characterized Alox5 (-/-) and wild-type (WT) mice for adiposity and glucose/insulin metabolism.
- Assessed ALOX5's role in human islets using short interfering RNA (siRNA) knockdown.
Main Results:
- Alox5 (-/-) mice exhibited increased fat mass, leptin, and fasting glucose, with lower fasting insulin.
- Impaired insulin secretion was observed in Alox5 (-/-) mice, despite no insulin resistance.
- Reduced insulin and PDX1 gene expression and secretion were found in Alox5 (-/-) islets and human islets with ALOX5 knockdown.
Conclusions:
- 5-lipoxygenase has pleiotropic metabolic effects on adiposity and pancreatic function.
- These findings have implications for therapeutic strategies targeting 5-LO in cardiovascular disease.
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