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HPA-axis responses during experimental colitis in the rat
Kensaku Kojima1, Yoshihisa Naruse, Norio Iijima
1Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-0841, Japan.
Summary
In experimental colitis, hypothalamic-pituitary-adrenal (HPA) axis responses were investigated. Glucocorticoid feedback inhibited corticotropin-releasing hormone (CRH) mRNA expression, suggesting HPA axis alterations in inflammatory bowel disease.
Area of Science:
- Neuroendocrinology
- Gastroenterology
- Stress Physiology
Background:
- The hypothalamic-pituitary-adrenal (HPA) axis is crucial for stress response.
- Inflammatory bowel disease (IBD) involves chronic inflammation of the digestive tract.
- HPA axis dysregulation is implicated in IBD pathogenesis.
Purpose of the Study:
- To investigate HPA axis activity during experimental colitis.
- To determine the role of glucocorticoid feedback and food intake in HPA axis response to colitis.
Main Methods:
- Induction of experimental colitis using 2,4,6-trinitrobenzenesulfonic acid in rats.
- Measurement of corticotropin-releasing hormone (CRH) mRNA, plasma ACTH, and plasma corticosterone (Cort) levels.
- Adrenalectomy with corticosterone pellet replacement and pair-feeding were used to control for confounding factors.
Main Results:
- Colitis led to reduced CRH mRNA, basal ACTH, and high Cort levels.
- Adrenalectomized rats with corticosterone replacement showed increased CRH mRNA during colitis.
- Pair feeding did not alter CRH mRNA, ACTH, or Cort levels compared to controls.
Conclusions:
- Glucocorticoid feedback inhibits CRH mRNA expression in experimental colitis.
- Reduced food intake during colitis is not the primary driver of CRH mRNA changes.
- The HPA axis, including CRH levels, is likely altered in patients with inflammatory bowel disease.