Gastroprotective effect of leptin on gastric mucosal injury induced by ischemia–reperfusion is related to gastric histamine content in rats

Erkasap, Nilüfer; Uzuner, Kubi̇lay; Serteser, Mustafa; Köken, Tülay; Aydın, Yasemin

doi:10.1016/j.peptides.2003.06.007

Cited by 27 publications

(18 citation statements)

References 22 publications

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“…It has been shown that leptin can reduce colonic injury caused by exposure to acetic acid (5,11). This is close to those data showing that leptin has gastroprotective effects, accelerating the healing of ethanol-induced gastric ulcers (14,24). Interestingly, one study (36) reported that, in humans with ulcerative colitis, colonic epithelial cells in the inflamed zone are leptin IR, whereas normal colon epithelial cells are not.…”

Section: Discussionsupporting

confidence: 88%

“…This contrasts with the results of a study (39) suggesting the involvement of leptin in the protective mechanisms that allow an organism to cope with potentially autoaggressive effects of its immune system. In this line, leptin has been shown to exert gastroprotective effects by accelerating the healing of ethanol-induced gastric ulcers (14,24). Furthermore, exogenous leptin has been shown to reduce the severity of acetic acid-induced colitis in rats (11).…”

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confidence: 99%

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Luminal leptin activates mucin-secreting goblet cells in the large bowel

Plaisancié¹,

Ducroc²,

Homsi³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Leptin has been suggested to be involved in tissue injury and/or mucosal defence mechanisms. Here, we studied the effects of leptin on colonic mucus secretion and rat mucin 2 (rMuc2) expression. Wistar rats and ob/ ob mice were used. Secretion of mucus was followed in vivo in the rat perfused colon model. Mucus secretion was quantified by ELISA, and rMuc2 mRNA levels were quantified by real-time RT PCR. The effects of leptin alone or in association with protein kinase C (PKC) and phosphatidylinositol 3-kinase (PI3K) inhibitors on mucin secreted by human mucus-secreting HT29-MTX cells were determined. Leptin was detected in the rat colonic lumen at substantial levels. Luminal perfusion of leptin stimulates mucus-secreting goblet cells in a dose-dependent manner in vivo in the rat. Leptin (10 nmol/l) increased mucus secretion by a factor of 3.5 and doubled rMuc2 mRNA levels in the colonic mucosa. There was no damage to mucosa 24 h after leptin, but the number of stained mucus cells significantly increased. Leptin-deficient ob/ ob mice have abnormally dense mucus-filled goblet cells. In human colonic goblet-like HT29-MTX cells expressing leptin receptors, leptin increased mucin secretion by activating PKC- and PI3K-dependent pathways. This is the first demonstration that leptin, acting from the luminal side, controls the function of mucus-secreting goblet cells. Because the gel layer formed by mucus at the surface of the intestinal epithelium has a barrier function, our data may be relevant physiologically in defence mechanisms of the gastrointestinal tract.

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Section: Discussionsupporting

confidence: 88%

mentioning

confidence: 99%

Luminal leptin activates mucin-secreting goblet cells in the large bowel

Plaisancié¹,

Ducroc²,

Homsi³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…The presence of leptin as well as the expression of its receptors was also detected in rat [8] and human [9] stomach but little is known about the role of leptin produced in the gastric mucosa. However, central or peripheral application of leptin was shown to have a protective action in several models of gastric injury [10][11][12]. It was demonstrated that exogenous as well as endogenous leptin released by CCK, gastrin and meal exerts a potent gastroprotective action depending upon vagal activity, intact sensory nerves and increased gastric microcirculation [10].…”

Section: Introductionmentioning

confidence: 99%

Gastroprotective effect of leptin in indomethacin-induced gastric injury

2008

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This study investigated the involvement of neutrophil infiltration, disturbances in nitric oxide (NO) generation and oxidative stress in indomethacin-induced gastric ulcer, and the possible gastroprotective potentials of leptin, known for its angiogenic effect. Male Wistar albino rats (180-220 g) were allocated into a normal control group, ulcer control group (received a single dose of indomethacin 40 mg/kg p.o.) and an ulcer group pretreated with leptin (10 microg/kg i.p. 30 min before ulcer induction). The animals were killed 6 h after indomethacin administration and their gastric juice, serum and mucosal tissue were used for gastric injury evaluation. Indomethacin produced multiple lesions in glandular mucosa, evidenced by marked increase in gastric ulcer index (GUI) accompanied by significant increases in gastric juice acidity, tissue myeloperoxidase (MPO) activity, serum NO and tissue conjugated diene (CD), and marked decreases in tissue NO and glutathione (GSH) as well as glutathione reductase (GR) and superoxide dismutase (SOD) activities, while gastric juice mucin and tissue glutathione peroxidase (GPx) were not affected. Leptin exerted significant gastroprotection as evidenced by significantly decreased GUI and attenuated neutrophil infiltration. Leptin significantly increased mucin and tissue NO, restored GR and SOD activities and up-regulated GPx activity. It failed to affect acidity, serum NO, GSH and CD. These results suggest that leptin confers significant gastroprotection against indomethacin-induced injury through interfering with neutrophil infiltration, NO production and oxidative stress.

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“…Lep tin is re ported to ha ve a pro tec ti ve ef fect aga inst da ma ge in duced by isc he mi a re per fu si on in jury in the gas tro in tes ti nal system. 13 This may be at tri bu ted to the tis su e spe ci fic ef fects of lep tin. 26,27 We sho wed that sti mu la ted NO synthe sis in a me di a rich of oxy gen in cre a sed da ma ge whi le the in tro duc ti on of L-NA ME dec re a sed re ti nal nitrosy la ti on sig ni fi cantly.…”

Section: Discussionmentioning

confidence: 99%

“…Mo re o ver, lep tin is a hor mo ne re por ted to ha ve a pos sib le cytop ro tec ti ve ef fect in isc he mi a re per fu si on in jury. 13,14 Alt ho ugh many stu di es exist abo ut OIR, no ne of them has des cri bed the ro le of NO, lep tin and L-NA ME in oxy gen-de pen dent re ti no pathy. The prin ci pal to pic of this re se arch was to ref lect so me pers pec ti ve in to the bi oc he mistry of oxy gen-re lated re ti no pathy.…”

Section: Itmentioning

confidence: 99%