Mice lacking ghrelin receptors resist the development of diet-induced obesity.

By J. Zigman, Y. Nakano, R. Coppari, N. Balthasar, Jacob N. Marcus, Charlotte E. Lee, Juli E. Jones, Amy E Deysher, Amanda R. Waxman, Ryan D. White and 5 more. Journal of Clinical Investigation, 2005

621 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Nutrition and Dietetics, Physiology

View Paper: https://www.semanticscholar.org/paper/260b2a6d4df9e9ff201201075b01f66bde219d58

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrine and Autonomic Systems

1. Nick V. Grishin
2. Michael S. Brown
3. Jing Yang
4. J. Goldstein
5. Matthias Tschöp
6. G. Liang
7. Roger Cone

In Nutrition and Dietetics

1. Nick V. Grishin
2. Matthias Tschöp
3. Roger Cone

In Physiology

1. William A. Banks
2. J. Morley
3. Matthias Tschöp
4. T. Horvath

Citations in the corpus

• Ghrelin controls hippocampal spine synapse density and memory performance (2006, background): “Ghrelin- or GHS-R null mutant animals show no obvious metabolic phenotyp”
• Identification of the acyltransferase that octanoylates ghrelin, an appetite-stimulating peptide hormone. (2008, positive): “Available data suggest that a reduction in ghrelin or its receptor can reduce food intake and partially ameliorate obesity in fat-fed mice (Zorrilla et al., 2006; Zigman et al., 2005; Wortley et al., 2005).”
• Ghrelin octanoylation mediated by an orphan lipid transferase (2008, background): “Specifically, GHSR-null mice eat less food, metabolize more fat, become less adipose, and remain more insulin-sensitive (21).”