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Hypothalamic obesity after hypophysectomy or adrenalectomy: dependence on corticosterone
The American Journal of Physiology
|November 1, 1985
Summary
Complete adrenalectomy prevents hypothalamic obesity in rats by suppressing adrenal glucocorticoid hormones. Even minimal hormone levels are sufficient to manifest obesity after ventromedial hypothalamus lesions.
Area of Science:
- Neuroendocrinology
- Physiology
- Obesity Research
Background:
- Ventromedial hypothalamus (VMH) lesions cause hyperphagia and obesity.
- Complete adrenalectomy prevents VMH-induced obesity, but effects of hypophysectomy are less clear.
- Adrenal glucocorticoids are implicated in the VMH obesity syndrome.
Purpose of the Study:
- To directly compare the effects of hypophysectomy and adrenalectomy on VMH-induced obesity in rats.
- To elucidate the role of adrenal glucocorticoid hormones in the manifestation of hypothalamic obesity.
Main Methods:
- Adult female rats underwent VMH lesions or sham lesions.
- Rats were subjected to complete adrenalectomy or hypophysectomy.
- Plasma corticosterone and ACTH levels were measured.
- Intracranial self-stimulation was assessed.
Main Results:
- Complete adrenalectomy completely suppressed VMH-induced weight gain but did not affect intracranial self-stimulation.
- Hypophysectomy suppressed weight gain, but HYPOX-VMH rats gained more weight than controls.
- Low levels of corticosterone and ACTH in HYPOX-VMH rats correlated with significant weight gain.
- Incompletely adrenalectomized rats with low corticosterone levels also showed VMH-induced weight gain.
Conclusions:
- Adrenal glucocorticoid hormones play a permissive role in the VMH obesity syndrome.
- Only minimal levels of adrenal glucocorticoids are required for the development of hypothalamic obesity.
- The pituitary's role in VMH obesity is likely mediated through adrenal glucocorticoid secretion.