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Tumor-host wasting not explained by adrenal hyperfunction in tumor-bearing animals
G Svaninger1, J Gelin, K Lundholm
1Department of Surgery I and II, University of Gothenburg, Sahlgrenska Hospital, Sweden.
Journal of the National Cancer Institute
|November 1, 1987
Summary
Cancer cachexia, characterized by body wasting, can occur independently of adrenal gland function. Elevated corticosteroids in tumor-bearing animals do not cause this wasting, suggesting other mechanisms are at play.
Area of Science:
- Endocrinology
- Oncology
- Physiology
Background:
- Cancer cachexia involves significant body mass loss, including skeletal muscle.
- The role of hypercorticism (elevated corticosteroids) in cancer cachexia is debated.
- Adrenal glands are a primary source of corticosteroids.
Purpose of the Study:
- To investigate if hypercorticism contributes to body wasting in tumor-bearing animals.
- To determine if adrenalectomy affects cancer cachexia.
- To examine the relationship between corticosteroid levels and specific wasting markers.
Main Methods:
- Used adrenalectomized and sham-operated, tumor-bearing, and control mice.
- Administered hydrocortisone to mice.
- Measured body composition, food intake, urinary corticosteroid excretion, and liver tyrosine aminotransferase (TAT) activity.
Main Results:
- Tumor-bearing mice exhibited wasting regardless of adrenal gland presence.
- Adrenalectomy did not alter body composition in normal mice.
- Elevated corticosteroids in tumor-bearing mice did not correlate with body fat or lean mass loss.
- Physiological hydrocortisone doses affected muscle RNA activity, but tumor-induced wasting occurred independently.
Conclusions:
- Cancer cachexia can develop independently of adrenal gland hyperfunction.
- Elevated corticosteroid production is not the primary cause of experimental cancer cachexia.
- Anorexia-induced cancer cachexia is not directly driven by adrenal hyperfunction.