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Miguel J.M. Lewin

Researcher at French Institute of Health and Medical Research

Publications -  63
Citations -  3434

Miguel J.M. Lewin is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Somatostatin & Receptor. The author has an hindex of 23, co-authored 63 publications receiving 3369 citations.

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The stomach is a source of leptin

TL;DR: It is shown 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, indicating that gastric leptin may be involved in early CCK-mediated effects activated by food intake, possibly including satiety.
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Leptin secretion and leptin receptor in the human stomach

TL;DR: These data provide the first evidence of the presence of leptin and leptin receptor proteins in the human stomach and suggest that gastric epithelial cells may be direct targets for leptin.
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PepT1-mediated epithelial transport of dipeptides and cephalexin is enhanced by luminal leptin in the small intestine

TL;DR: It is shown here that PepT1 and leptin receptors are expressed in Caco-2 and rat intestinal mucosal cells and an unexpected action of gastric leptin in controlling ingestion of dietary proteins is revealed.
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Expression and regulation of leptin receptor proteins in afferent and efferent neurons of the vagus nerve

TL;DR: It is speculated that vagal leptin receptors, apart from being activated by adipocyte‐derived leptin, may also be influenced by leptin produced by the stomach, which may explain the synergistic action of leptin and CCK on neuronal activity in the NTS and on food intake.
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Hepatocyte growth factor induces colonic cancer cell invasiveness via enhanced motility and protease overproduction. Evidence for PI3 kinase and PKC involvement.

TL;DR: Evidence is provided that the process of HGF-activated invasiveness of Caco-2 cells involves PI3 kinase and PKC and results from close association of two events, stimulation of cell motile activity and concomitant overproduction of proteases, which permits cell migration through a degraded extracellular matrix.