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Alterations in sympathetic nervous system activity do not regulate adipsin gene expression in mice
A Napolitano1, B B Lowell, J S Flier
1Charles A. Dana Research Institute, Boston, MA.
International Journal of Obesity
|March 1, 1991
Summary
Sympathetic nervous system (SNS) activity does not regulate adipsin gene expression in mice. However, atypical beta-adrenergic agonists suppressed adipsin levels, suggesting a novel regulatory pathway.
Area of Science:
- Adipose tissue biology
- Neuroendocrinology
- Obesity research
Background:
- Adipsin gene expression is reduced in rodent obesity models with decreased sympathetic nervous system (SNS) activity.
- Sympathomimetic drugs reversed obesity and restored adipsin levels in obese mice, suggesting SNS regulation of adipsin.
Purpose of the Study:
- To investigate the role of the sympathetic nervous system (SNS) in regulating adipsin gene expression.
- To determine if altered SNS activity impacts adipsin levels in normal mice.
Main Methods:
- Mice were exposed to cold (4°C) to activate SNS.
- Mice underwent chemical sympathectomy using 60H-dopamine.
- Lean mice were treated with an atypical beta-adrenoreceptor agonist (BRL 26830A).
- Adipsin mRNA levels in white (WAT) and brown adipose tissue (BAT) and serum adipsin concentrations were measured.
Main Results:
- Cold exposure and sympathectomy did not alter serum adipsin or adipsin mRNA levels in normal mice.
- Treatment with BRL 26830A significantly decreased both serum adipsin concentrations and adipsin mRNA levels.
- These findings contradict the initial hypothesis that SNS activity regulates adipsin expression.
Conclusions:
- SNS activity does not appear to regulate adipsin gene expression in normal mice.
- Atypical beta-adrenoreceptor agonists may suppress adipsin expression in vivo.
- Further research is needed to elucidate the mechanisms and physiological significance of BRL 26830A-induced adipsin suppression.