2004
DOI: 10.1016/j.jss.2004.07.203
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Leptin administration increases small intestinal response to cholecystokinin in leptin-deficient obese mice

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Cited by 5 publications
(8 citation statements)
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“…Barrenetxe and coworkers [11] have demonstrated the presence of the long leptin receptor isoform in the brush border, basolateral membrane and cytoplasm of enterocytes from rat, mouse, and human small intestine. Leptin increases the duodenal secretion of cholecystokinin and acts on vagal mechanoreceptors in the regulation of small intestinal motility [12]. Systemic leptin administration enhances mucosal mass and absorptive function in normal rat intestine [13].…”
Section: Discussionmentioning
confidence: 99%
“…Barrenetxe and coworkers [11] have demonstrated the presence of the long leptin receptor isoform in the brush border, basolateral membrane and cytoplasm of enterocytes from rat, mouse, and human small intestine. Leptin increases the duodenal secretion of cholecystokinin and acts on vagal mechanoreceptors in the regulation of small intestinal motility [12]. Systemic leptin administration enhances mucosal mass and absorptive function in normal rat intestine [13].…”
Section: Discussionmentioning
confidence: 99%
“…The present study comprises one in a series of studies examining the role of leptin in the intestine and during the process of intestinal adaptation [17,27,28]. To be compatible with these studies and to have a complete data set, we therefore chose the single 48-hour time-point.…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, exogenous administration of recombinant human leptin in doses sufficient to achieve physiological and pharmacological leptin levels does not regulate PYY in the short term, suggesting that, similar to our previous findings on the lack of regulation of ghrelin by leptin [14], the adipocyte-derived leptin and the gut-derived PYY systems act independently of each other. The question of whether leptin alters the response to PYY, as it does for the intestinal response to cholecystokinin in leptin-deficient mice [15], and/or whether more long-term administration of leptin alters either the PYY levels or the PYY response, requires further evaluation. Short-term gut-derived appetite signals such as PYY and long-term adipostatic signals such as leptin may play different roles in the complex system of energy homeostasis that tightly defends body weight over the long term despite short-term variations in food intake.…”
Section: Discussionmentioning
confidence: 99%