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Hexosamines stimulate leptin production in transgenic mice
D A McClain1, T Alexander, R C Cooksey
1Department of Medicine, University of Utah, Salt Lake City 84132, USA. donald.mcclain@hsc.utah.edu
Endocrinology
|June 1, 2000
Summary
Increased hexosamine flux in mice, driven by GFA enzyme overexpression, led to higher leptin levels and leptin mRNA in fat tissue. This suggests hexosamine flux regulates leptin synthesis and secretion.
Area of Science:
- Metabolism
- Endocrinology
- Molecular Biology
Background:
- Hexosamine flux is implicated in nutrient sensing and may act as a satiety signal.
- Previous studies suggest hexosamines and glucosamine stimulate leptin secretion in vitro and acutely in vivo.
Purpose of the Study:
- To investigate the effects of chronic, physiological increases in hexosamine flux on leptin levels.
- To examine the role of the hexosamine synthesis pathway enzyme, GFA, in regulating leptin.
Main Methods:
- Mice overexpressing the GFA enzyme in muscle and fat were generated.
- Levels of UDP-N-acetylglucosamine, leptin mRNA, and serum leptin were measured.
- Body weight and body fat content were assessed.
Main Results:
- Transgenic mice showed increased UDP-N-acetylglucosamine in fat, confirming GFA overexpression.
- Hyperleptinemia was observed in fasted transgenic mice compared to controls.
- Leptin mRNA levels were significantly elevated in the fat tissue of transgenic mice.
Conclusions:
- Chronic, physiological increases in hexosamine flux regulate leptin synthesis and secretion.
- Hexosamine flux in adipose tissue plays a key role in controlling leptin production.
- Despite elevated leptin, increased hexosamine flux did not alter body fat content in this model.