Nathan P. Metzger

TL;DR: It is predicted that the plasma LEAP2/acyl-gh Relin molar ratio may be a key determinant modulating acyl-ghrelin activity in response to body mass, feeding status, and blood glucose.

TL;DR: The data suggest that an intact ghrelin system limits the capacity of exercise to restrict food intake following exercise, although it enhances exercise endurance.

TL;DR: Although the A203E mutation does not block ghrelin-evoked signaling as assessed using in vitro and ex vivo models, GHSR-A203E mice lack the usual acute food intake response to administered gh Relin in vivo, and that constitutive G HSR activity contributes to the native depolarizing conductance of GHSr-expressing arcuate NPY neurons.

TL;DR: The first known LEAP2-KO mouse line was generated in this paper, where the metabolic effects of genetic leaper-expressed antimicrobial peptide-2 (LEAP2) deletion were determined.

TL;DR: It is shown that 2 weeks of daily administration of the GHSR agonist HM01 to Snord116del neonates markedly improved survival, resulting in a nearly complete rescue of the excess mortality owing to loss of the paternal Snord 116 gene, which support further exploration of the therapeutic potential of GHSr agonist administration in limiting PWS mortality, especially during the period characterized by failure to thrive.