TY - JOUR
T1 - The stomach is a source of leptin
AU - Bado, André
AU - Levasseur, Sandrine
AU - Attoub, Samir
AU - Kermorgant, Stéphanie
AU - Laigneau, Jean Pierre
AU - Bortoluzzi, Marie Noëlle
AU - Moizo, Laurent
AU - Lehy, Thérèse
AU - Guerre-Millo, Michèle
AU - Marchand-Brustel, Yannick Le
AU - Lewin, Miguel J.M.
PY - 1998/8/20
Y1 - 1998/8/20
N2 - The circulating peptide leptin, which is the product of the ob gene, provides feedback information on the size of fat stores to central Ob receptors that control food intake and body-weight homeostasis. Leptin has so far been reported to be secreted only by adipocytes and the placenta. Here we show that leptin messenger RNA and leptin protein are present in rat gastric epithelium, and that cells in the glands of the gastric fundic mucosa are immunoreactive for leptin. The physiological function of this previously unsuspected source of leptin is unknown. However, both feeding and administration of CCK-8 (the biologically active carboxy-terminal end of cholecystokinin) result in a rapid and large decrease in both leptin cell immunoreactivity and the leptin content of the fundic epithelium, with a concomitant increase in the concentration of leptin in the plasma. These results indicate that gastric leptin may be involved in early CCK-mediated, effects activated by food intake, possibly including satiety.
AB - The circulating peptide leptin, which is the product of the ob gene, provides feedback information on the size of fat stores to central Ob receptors that control food intake and body-weight homeostasis. Leptin has so far been reported to be secreted only by adipocytes and the placenta. Here we show that leptin messenger RNA and leptin protein are present in rat gastric epithelium, and that cells in the glands of the gastric fundic mucosa are immunoreactive for leptin. The physiological function of this previously unsuspected source of leptin is unknown. However, both feeding and administration of CCK-8 (the biologically active carboxy-terminal end of cholecystokinin) result in a rapid and large decrease in both leptin cell immunoreactivity and the leptin content of the fundic epithelium, with a concomitant increase in the concentration of leptin in the plasma. These results indicate that gastric leptin may be involved in early CCK-mediated, effects activated by food intake, possibly including satiety.
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U2 - 10.1038/29547
DO - 10.1038/29547
M3 - Article
C2 - 9723619
AN - SCOPUS:0032552112
SN - 0028-0836
VL - 394
SP - 790
EP - 793
JO - Nature
JF - Nature
IS - 6695
ER -