Ghrelin From the Stomach Stimulates Appetite and Opposes Leptin's Satiety Signal
Ghrelin, the stomach-derived GH secretagogue ligand, stimulated food intake and body weight gain in rats through vagus nerve and hypothalamic pathways, acting as an appetite signal that opposes leptin.
Quick Facts
What This Study Found
Ghrelin stimulated food intake and weight gain in rats through vagal and hypothalamic mechanisms, with ghrelin levels suppressed by feeding and increased by leptin, establishing the ghrelin-leptin axis for appetite regulation.
Key Numbers
How They Did This
Animal study examining ghrelin's effects on food intake, body weight, and interactions with leptin and vagus nerve signaling in rats. Central and peripheral ghrelin administration tested.
Why This Research Matters
Identifying ghrelin as the stomach's hunger signal complemented leptin's satiety signal, completing the peripheral hormonal framework for appetite regulation and opening new obesity treatment targets.
The Bigger Picture
Ghrelin's identification as the hunger hormone completed the leptin-ghrelin axis, providing a bidirectional hormonal framework for understanding appetite. This has driven drug development targeting both sides of this system.
What This Study Doesn't Tell Us
Rat study. Acute ghrelin effects may differ from chronic signaling. The exact mechanisms of ghrelin-leptin interaction were not fully resolved.
Questions This Raises
- ?Can ghrelin antagonists treat obesity?
- ?Does ghrelin resistance develop with chronic overeating?
- ?How do ghrelin levels change with bariatric surgery?
Trust & Context
- Key Stat:
- Hunger hormone identified Ghrelin from the stomach signals hunger through the vagus nerve and hypothalamus, directly opposing leptin's satiety message
- Evidence Grade:
- Moderate evidence from comprehensive animal studies characterizing ghrelin's appetite and energy balance effects.
- Study Age:
- Published in 2001. Ghrelin is now well-established as a key hunger hormone, with ghrelin-based drug development ongoing for obesity and cachexia.
- Original Title:
- Ghrelin is an appetite-stimulatory signal from stomach with structural resemblance to motilin.
- Published In:
- Gastroenterology, 120(2), 337-45 (2001)
- Authors:
- Asakawa, A, Inui, A(2), Kaga, T, Yuzuriha, H, Nagata, T, Ueno, N, Makino, S, Fujimiya, M, Niijima, A, Fujino, M A, Kasuga, M
- Database ID:
- RPEP-00645
Evidence Hierarchy
Tests effects in animals (usually mice or rats), not humans.
What do these levels mean? →Frequently Asked Questions
What is ghrelin?
Ghrelin is a hormone produced by the stomach that signals hunger to the brain. It's the opposite of leptin (which signals fullness). Together, they form the body's main hormonal system for controlling appetite.
Could blocking ghrelin help with weight loss?
In theory, yes — blocking the hunger signal should reduce appetite. Ghrelin antagonists are being developed for obesity. However, the body's appetite system has many backup mechanisms, which complicates this approach.
Read More on RethinkPeptides
Cite This Study
https://rethinkpeptides.com/research/RPEP-00645APA
Asakawa, A; Inui, A; Kaga, T; Yuzuriha, H; Nagata, T; Ueno, N; Makino, S; Fujimiya, M; Niijima, A; Fujino, M A; Kasuga, M. (2001). Ghrelin is an appetite-stimulatory signal from stomach with structural resemblance to motilin.. Gastroenterology, 120(2), 337-45.
MLA
Asakawa, A, et al. "Ghrelin is an appetite-stimulatory signal from stomach with structural resemblance to motilin.." Gastroenterology, 2001.
RethinkPeptides
RethinkPeptides Research Database. "Ghrelin is an appetite-stimulatory signal from stomach with ..." RPEP-00645. Retrieved from https://rethinkpeptides.com/research/asakawa-2001-ghrelin-is-an-appetitestimulatory
Access the Original Study
Study data sourced from PubMed, a service of the U.S. National Library of Medicine, National Institutes of Health.
This study breakdown was produced by the RethinkPeptides research team. We analyze and report published research findings without making health recommendations. All interpretations are based solely on the published abstract and study data.