TY - JOUR
T1 - Drosophila insulin release is triggered by adipose Stunted ligand to brain Methuselah receptor
AU - Delanoue, Renald
AU - Meschi, Eleonora
AU - Agrawal, Neha
AU - Mauri, Alessandra
AU - Tsatskis, Yonit
AU - McNeill, Helen
AU - Léopold, Pierre
N1 - Publisher Copyright:
© 2016, American Association for the Advancement of Science. All rights reserved.
PY - 2016/9/30
Y1 - 2016/9/30
N2 - Animals adapt their growth rate and body size to available nutrients by a general modulation of insulin-insulin-like growth factor signaling. In Drosophila, dietary amino acids promote the release in the hemolymph of brain insulin-like peptides (Dilps), which in turn activate systemic organ growth. Dilp secretion by insulin-producing cells involves a relay through unknown cytokines produced by fat cells. Here, we identify Methuselah (Mth) as a secretin-incretin receptor subfamily member required in the insulin-producing cells for proper nutrient coupling. We further show, using genetic and ex vivo organ culture experiments, that the Mth ligand Stunted (Sun) is a circulating insulinotropic peptide produced by fat cells. Therefore, Sun and Mth define a new cross-organ circuitry that modulates physiological insulin levels in response to nutrients.
AB - Animals adapt their growth rate and body size to available nutrients by a general modulation of insulin-insulin-like growth factor signaling. In Drosophila, dietary amino acids promote the release in the hemolymph of brain insulin-like peptides (Dilps), which in turn activate systemic organ growth. Dilp secretion by insulin-producing cells involves a relay through unknown cytokines produced by fat cells. Here, we identify Methuselah (Mth) as a secretin-incretin receptor subfamily member required in the insulin-producing cells for proper nutrient coupling. We further show, using genetic and ex vivo organ culture experiments, that the Mth ligand Stunted (Sun) is a circulating insulinotropic peptide produced by fat cells. Therefore, Sun and Mth define a new cross-organ circuitry that modulates physiological insulin levels in response to nutrients.
UR - http://www.scopus.com/inward/record.url?scp=84988984913&partnerID=8YFLogxK
U2 - 10.1126/science.aaf8430
DO - 10.1126/science.aaf8430
M3 - Article
C2 - 27708106
AN - SCOPUS:84988984913
SN - 0036-8075
VL - 353
SP - 1553
EP - 1556
JO - Science
JF - Science
IS - 6307
ER -