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Sympathoadrenal function in genetically obese Zucker rats
A J Scheurink1, A B Steffens, B Roossien
1Department of Animal Physiology, University of Groningen, Haren, The Netherlands.
Physiology & Behavior
|October 1, 1992
Summary
Obese Zucker rats show normal sympathetic nervous system activation during exercise but altered responses to catecholamines. This suggests underlying changes in adrenoceptor mechanisms contribute to obesity-related metabolic dysfunction.
Area of Science:
- Physiology
- Endocrinology
- Metabolic Research
Background:
- Genetic obesity in Zucker rats (fa/fa) impacts sympathetic nervous system (SNS) function.
- Understanding SNS alterations is crucial for metabolic disease research.
Purpose of the Study:
- To investigate the effects of genetic obesity on SNS activity and catecholamine responses.
- To compare exercise and infused catecholamine effects in obese vs. lean Zucker rats.
Main Methods:
- Utilized 10-12-month-old obese (fa/fa) and lean (Fa/-) Zucker rats.
- Measured blood glucose, insulin, epinephrine (E), norepinephrine (NE), and free fatty acids (FFA) via heart catheter.
- Administered exercise (swimming) and intravenous infusions of E and NE.
Main Results:
- Obese rats had higher baseline FFA and insulin. Exercise increased glucose and decreased insulin in both, but exaggeratedly in obese rats.
- Infused E increased glucose more in obese rats; infused NE decreased insulin in obese rats but not lean.
- Exercise-induced plasma catecholamine levels were similar between groups, indicating normal SNS activation.
Conclusions:
- Sympathetic nervous system activation during exercise is normal in obese Zucker rats.
- Postsynaptic receptor responses to catecholamines (epinephrine, norepinephrine) differ, suggesting altered adrenoceptor mechanisms in obesity.
- These findings highlight potential permanent changes in adipocyte, hepatocyte, and muscle cell adrenoceptors contributing to obesity.