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Glucose-induced norepinephrine levels and obesity resistance
The American Journal of Physiology
|September 1, 1987
Summary
Rats resistant to diet-induced obesity show dampened sympathetic responses to glucose. This suggests altered sympathetic activation may predict obesity development in rats fed a high-calorie diet.
Area of Science:
- Physiology
- Metabolic Research
- Obesity Research
Background:
- Diet-induced obesity (DIO) is a significant health concern.
- Understanding factors predicting obesity development is crucial.
- Sympathetic nervous system (SNS) activity plays a role in metabolic regulation.
Purpose of the Study:
- To investigate the role of glucose-stimulated sympathetic activation in differentiating rats that resist or develop DIO.
- To determine if pre-existing differences in sympathetic response predict obesity susceptibility.
Main Methods:
- Male Sprague-Dawley rats were given an intravenous glucose load.
- Plasma glucose, insulin, and norepinephrine (NE) levels were measured.
- Rats were subsequently fed a high-calorie diet (CM) for 14 weeks to assess DIO development.
Main Results:
- Rats that developed DIO showed significantly higher weight gain and retroperitoneal fat pad weights compared to diet-resistant (DR) rats.
- NE levels after glucose load were 54% lower in DR rats compared to DIO rats.
- A positive correlation was found between NE levels and subsequent weight gain on the CM diet.
Conclusions:
- Dampened sympathetic activation following a glucose load may predispose rats to DIO.
- Heightened end-organ responsiveness to NE could underlie this dampened sympathetic response in diet-resistant rats.
- Glucose-stimulated sympathetic response is a potential biomarker for predicting obesity susceptibility.