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Glucocorticoids and hypothalamic obesity.

B M King1

  • 1Department of Psychology, University of New Orleans, LA 70148.

Neuroscience and Biobehavioral Reviews
|January 1, 1988
PubMed
Summary
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Adrenal glucocorticoid hormones play a permissive role in ventromedial hypothalamus (VMH) lesion-induced obesity. Glucocorticoids are necessary for hyperphagia, but their effects occur outside the medial hypothalamus.

Area of Science:

  • Neuroendocrinology
  • Obesity Research
  • Behavioral Neuroscience

Background:

  • Ventromedial hypothalamus (VMH) lesions induce hyperphagia and obesity.
  • Adrenal glucocorticoid hormones are implicated in this process.
  • VMH-lesioned animals show heightened sensitivity to glucocorticoids.

Purpose of the Study:

  • To investigate the role of adrenal glucocorticoid hormones in VMH lesion-induced hyperphagia and obesity.
  • To determine the mechanism and site of action of glucocorticoids in this model.

Main Methods:

  • Surgical lesions of the ventromedial hypothalamus (VMH) and paraventricular nuclei (PVN).
  • Adrenalectomy and hypophysectomy to manipulate corticosterone levels.
  • Intracerebroventricular and intraperitoneal administration of glucocorticoids.

Related Experiment Videos

  • Measurement of feeding behavior and body weight.

    • Main Results:

    • VMH lesions elevate corticosterone but this is not the primary cause of obesity.
    • Hyperphagia and obesity were prevented/reversed by adrenalectomy/hypophysectomy and restored by glucocorticoid replacement.
    • Glucocorticoids act centrally in a permissive manner, with effects observed after central administration but not peripheral.
    • PVN stimulation elicits feeding, but PVN lesions do not abolish VMH-lesion-induced obesity.

    Conclusions:

    • Adrenal glucocorticoid hormones are essential for VMH lesion-induced hyperphagia and obesity.
    • Glucocorticoids exert permissive effects on feeding behavior centrally, likely outside the medial hypothalamus.
    • The septo-hippocampal complex is a potential site for glucocorticoid action in this model.