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Related Experiment Videos

Glucocorticoid blockade does not abrogate tumor-induced cachexia.

D E Rivadeneira1, H A Naama, M D McCarter

  • 1Department of Surgery, New York Presbyterian Hospital-Cornell Campus, NY, USA.

Nutrition and Cancer
|February 29, 2000
PubMed
Summary
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Cancer-induced cachexia involves significant body composition changes. High glucocorticoid levels correlate with these changes, but blocking their receptors did not prevent muscle and fat wasting in mice.

Area of Science:

  • Oncology
  • Endocrinology
  • Metabolism

Background:

  • Cancer-induced cachexia is a prevalent condition in cancer patients.
  • Elevated circulating glucocorticoids and interleukin-6 (IL-6) are implicated in cachexia.
  • The precise role of glucocorticoids as primary mediators requires further investigation.

Purpose of the Study:

  • To investigate the role of circulating glucocorticoid levels as primary mediators in cancer-induced cachexia.
  • To determine if inhibiting glucocorticoids with RU-486 can prevent tissue wasting in a murine cachexia model.

Main Methods:

  • Utilized a murine tumor-induced cachexia model.
  • Groups included control, tumor-bearing, control + vehicle, and tumor-bearing + glucocorticoid receptor antagonist (RU-486).

Related Experiment Videos

  • Measured serum glucocorticoid and IL-6 levels, body weight, lean body mass, and adipose tissue.

    • Main Results:

    • Tumor-bearing mice exhibited significant detrimental changes in body composition.
    • A significant correlation was found between elevated glucocorticoid levels and altered body composition.
    • Administration of the glucocorticoid receptor antagonist RU-486 did not abrogate these cachexia-related defects.

    Conclusions:

    • The detrimental effects of tumor-induced cachexia are not primarily mediated by peripheral glucocorticoid action.
    • Cachexia may involve complex interactions between glucocorticoids and other factors like IL-6.