Prostaglandin E2-induced anorexia involves hypothalamic brain-derived neurotrophic factor and ghrelin in chicks

Area of Science:

• Neuroscience
• Endocrinology
• Appetite Regulation

Background:

• Central administration of prostaglandin E2 (PGE2) induces anorexia in rodents and chicks.
• The precise hypothalamic mechanisms underlying this effect remain incompletely understood.

Purpose of the Study:

• To identify hypothalamic nuclei and appetite-related factors involved in PGE2-induced anorexia using chickens as a model.
• To elucidate the role of PGE2 in acute appetite regulation.

Main Methods:

• Intracerebroventricular injection of varying doses of PGE2 in broiler chicks.
• Measurement of food and water intake.
• Analysis of c-Fos immunoreactivity in hypothalamic nuclei.
• Quantitative assessment of mRNA expression for appetite-related factors (melanocortin receptor 3, ghrelin, neuropeptide Y receptor subtype 5, TrkB, BDNF, CRFR1, CRFR2) in the hypothalamus and paraventricular nucleus (PVN).

Main Results:

• PGE2 dose-dependently suppressed food and water intake.
• Increased c-Fos immunoreactivity in the PVN following PGE2 injection.
• Upregulation of hypothalamic melanocortin receptor 3 and ghrelin mRNA.
• Downregulation of hypothalamic neuropeptide Y receptor subtype 5 and TrkB mRNA.
• In the PVN, PGE2 increased BDNF and ghrelin mRNA, while decreasing CRFR1, CRFR2, and TrkB mRNA expression.

Conclusions:

• PGE2 injection leads to reduced food and water intake.
• The anorexigenic effect of PGE2 likely involves brain-derived neurotrophic factor (BDNF) and ghrelin originating in the PVN.
• Similarities in hypothalamic mechanisms between chickens and rodents suggest PGE2's role in appetite regulation may have implications for human eating and metabolic disorders.