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Delayed response to 2-deoxy-D-glucose in hypothalamic obese rats
Pharmacology, Biochemistry, and Behavior
|March 1, 1978
Summary
2-deoxy-D-glucose (2-DG) increases food intake in normal rats, with effects intensifying at higher doses. Obese rats show delayed feeding responses to 2-DG, with higher doses inhibiting intake.
Area of Science:
- Neuroscience
- Endocrinology
- Behavioral Science
Background:
- The ventromedial hypothalamus (VMH) plays a critical role in regulating energy balance and feeding behavior.
- Glucoreceptors in peripheral tissues signal glucose levels to the brain, influencing appetite.
- 2-deoxy-D-glucose (2-DG) is a glucose analog used to probe central glucoregulatory mechanisms.
Purpose of the Study:
- To establish a dose-response relationship for 2-deoxy-D-glucose (2-DG)-induced food intake in normal and obese rats with VMH lesions.
- To investigate the impact of VMH lesions on the effects of 2-DG on feeding behavior.
Main Methods:
- Rats, both normal and with VMH lesions (obese), were administered varying doses of 2-DG (0-400 mg/kg).
- Food intake was measured over a 4-hour period following 2-DG injection.
- Latency to the first feeding bout and the magnitude of food intake were analyzed.
Main Results:
- In normal rats, 2-DG significantly increased food intake starting at 100 mg/kg, with dose-dependent augmentation.
- Obese VMH-lesioned rats exhibited delayed increases in food intake at doses of 150-400 mg/kg 2-DG.
- Higher doses of 2-DG (300-400 mg/kg) inhibited food intake in obese rats during the first hour post-injection.
Conclusions:
- VMH lesions alter the sensitivity and temporal dynamics of 2-DG-induced feeding.
- The findings suggest that VMH lesions disrupt the processing of signals from peripheral glucoreceptors, affecting 2-DG's satiating or appetite-stimulating effects.
- These results contribute to understanding the neurobiological basis of obesity and appetite regulation.