Leptin Mediates a Proliferative Response in Human Gastric Mucosa Cells with Functional Receptor

Schneider, RJ; Bornstein, S. R.; Chrousos, G. P.; Boxberger, Sabine; Ehninger, G.; Breidert, Matthias

doi:10.1055/s-2001-12617

Cited by 53 publications

(33 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results indicate that leptin might promote myoblast proliferation by increasing proliferating cell accumulation in the S + G2/M phase. A leptin positive effect on proliferation in endothelial and hemopoietic cells, 18) pancreaticcells, 19) gastric mucosa, 29) and breast tumor cells has also been reported. 30) However, in contrast to these studies, the results of Baratta et al indicate that only higher concentrations (1.5 and 15 mM) inhibited HC11 cell growth.…”

Section: Discussionmentioning

confidence: 99%

Leptin Promotes Proliferation and Inhibits Differentiation in Porcine Skeletal Myoblasts

Luo

Zhang

et al. 2008

Bioscience, Biotechnology, and Biochemistry

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Leptin Promotes Proliferation and Inhibits Differentiation in Porcine Skeletal Myoblasts

Luo

Zhang

et al. 2008

Bioscience, Biotechnology, and Biochemistry

View full text Add to dashboard Cite

“…Leptin is known to be a growth factor for gastrointestinal cells as well as these cancer cells (2,3). We next examined the effects of leptin on proliferation of MKN28 cells measured by MTS assay using 5 to 5,000 ng/mL leptin.…”

Section: Resultsmentioning

confidence: 99%

“…Ob-R is highly expressed in the hypothalamus but is also found in many peripheral tissues. For example, Ob-R is detected in normal gastric mucosa, especially in chief cells and parietal cells, and in some gastric cancer cells (3,4). Furthermore, in addition to adipocytes and the placenta, the gastric mucosa has been shown to produce a significant amount of leptin (5).…”

Section: Introductionmentioning

confidence: 99%

Transactivation of Epidermal Growth Factor Receptor Is Involved in Leptin-Induced Activation of Janus-Activated Kinase 2 and Extracellular Signal–Regulated Kinase 1/2 in Human Gastric Cancer Cells

et al. 2005

View full text Add to dashboard Cite

Leptin is known to act as a growth factor through the Janusactivated kinase (JAK)/signal transducer and activator of transcription signaling pathway as well as the mitogenactivated protein kinase pathway. In this study, we showed a novel signal transduction pathway using two human gastric cancer cell lines, MKN28 and MKN74. Both gastric cancer cells expressed leptin and its receptors (Ob-R) at the protein level. We found that leptin, even at as low as 0.1 ng/mL, induced significant tyrosine phosphorylation of epidermal growth factor receptor (EGFR). Time-course experiments revealed that phosphorylation was maximal after 5 minutes of stimulation and declined thereafter. We also revealed that tyrosine phosphorylation of EGFR induced by leptin was significantly attenuated by two inhibitors, an EGFR tyrosine kinase inhibitor, AG1478, and a broad-spectrum matrix metalloproteinase inhibitor, GM6001. This indicates that the pathway of EGFR transactivation induced by leptin is dependent on proteolytically released EGFR ligands. Leptin induced JAK2 activation and extracellular signal-regulated kinase (ERK) 1/2 activation in these gastric cancer cells, both of which occurred after the peak of EGFR transactivation. Pretreatment of gastric cancer cells with AG1478 significantly reduced the degree of phosphorylation of both JAK2 and ERK1/2. These findings indicate the involvement of EGFR transactivation in the activation of JAK2 and ERK1/2. Our results reveal that EGFR transactivation is involved in the leptin signaling pathway in gastric cancer cells, which extends the physiologic action of leptin beyond its central effects in the hypothalamus to regulate body weight. (Cancer Res 2005; 65(20): 9159-63)

show abstract

“…Leptin expression has also been detected in the lower half of the gastric fundic glands (21,22). This protein is thought to provide feedback information to the central nervous system (CN) regarding the size of energy stores and thus is involved in controlling food intake, energy expenditure, and body weight homeostasis (23).…”

Section: Introductionmentioning

confidence: 99%

“…This protein is thought to provide feedback information to the central nervous system (CN) regarding the size of energy stores and thus is involved in controlling food intake, energy expenditure, and body weight homeostasis (23). Leptin signals satiety to the hypothalamus, resulting in reduced food intake, increased energy expenditure, reduced gastrin and acid secretion, and increased gastric mucosal cell proliferation (22).…”

Section: Introductionmentioning

confidence: 99%

Long-term effects of Helicobacter pylori eradication on circulating ghrelin and leptin concentrations and body composition in prepubertal children

Pacifico¹,

Anania²,

Osborn³

et al. 2008

European Journal of Endocrinology

View full text Add to dashboard Cite

Background: Helicobacter pylori, and the chronic gastric inflammation that it causes, may compromise the function and survival of ghrelin-producing cells, resulting in a decrease of circulating ghrelin levels. This finding raises the possibility that the infection might affect growth in children by reducing the ghrelin production. Aims: To determine baseline circulating levels of ghrelin and leptin in prepubertal children with and without H. pylori infection and to evaluate the long-term effects of H. pylori eradication on circulating levels of ghrelin and leptin as well as on body composition. Patients: Thirty children with H. pylori-associated gastritis, 35 children with H. pylori-negative gastric mucosa, and 20 healthy controls were studied. Results: At baseline, while leptin levels were significantly lower in H. pylori-positive patients, ghrelin concentrations did not differ among the three study groups. However, a significant inverse correlation between ghrelin concentrations and histological severity of gastritis was found. Eradication of the organism was associated with a progressive decrease in ghrelin concentrations over baseline at both 6-and 12-month follow-ups. SDS-body mass index (BMI), lean and fat mass, as well as leptin concentrations, significantly increased over baseline at both follow-ups. Conclusions: In prepubertal children, serum ghrelin concentrations are inversely related to the severity of H. pylori-associated gastritis. In these youngsters, long-term eradication of H. pylori infection is associated with a significant increase in BMI, lean and fat mass along with a significant decrease in circulating ghrelin levels and an increase in leptin levels.

show abstract

Leptin Mediates a Proliferative Response in Human Gastric Mucosa Cells with Functional Receptor

Abstract: Leptin protein may not be produced but rather stored in human gastric cells. Leptin-induced increases in the proliferation of gastric mucosa cells suggests that leptin might contribute to mucosal integrity and gastroprotection.

Cited by 53 publications

References 17 publications

Leptin Promotes Proliferation and Inhibits Differentiation in Porcine Skeletal Myoblasts

Leptin Promotes Proliferation and Inhibits Differentiation in Porcine Skeletal Myoblasts

Transactivation of Epidermal Growth Factor Receptor Is Involved in Leptin-Induced Activation of Janus-Activated Kinase 2 and Extracellular Signal–Regulated Kinase 1/2 in Human Gastric Cancer Cells

Long-term effects of Helicobacter pylori eradication on circulating ghrelin and leptin concentrations and body composition in prepubertal children

Contact Info

Product

Resources

About