Effect of Leptin on Cold Restraint-Induced Gastric Lesions in Albino Rats | ||||
| Bulletin of Egyptian Society for Physiological Sciences | ||||
| Article 5, Volume 28, Issue 1, June 2008, Page 47-58 PDF (179.83 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/besps.2008.36819 | ||||
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| Authors | ||||
| Selim Abdel-Hakim* 1; Yehia Mahmoud2 | ||||
| 1Department of Physiology, Faculty of Medicine, El-Minia University | ||||
| 2Department of Internal Medicine, Faculty of Medicine, El-Minia University | ||||
| Abstract | ||||
| Leptin, 167 amino acid peptide hormone, is secreted by adipocytes, has been found to be present in the gastric mucosa. The locally secreted leptin was proved to have a cytoprotective effect. To investigate whether exogenous leptin may be implicated in gastric mucosal protection, male albino rats were randomly assigned to six groups of six rats each. The rats of control (C) group were left freely wandering in their cages. The rats of cold restraint stress (CRS) group were exposed to cold restraint stress for three hours. The rats of leptin (L) group were given leptin subcutaneously (SC) in a dose of 10 g/kg/rat 30 minutes before subjection to CRS. The rats of famotidine (F) group were given famotidine SC in a dose of 50 mg/kg/rat just before subjection to CRS. The rats of L-NAME group were injected with N G -nitro-L-arginine methyl ester in a dose of 25 mg/kg/rat SC 15 minutes before giving leptin and 45 minutes before being exposed to CRS. The rats of indomethacin (I) group were injected with indomethacin SC in a dose of 10 mg/kg/rat followed 30 minutes later by leptin (10 g/kg/rat, SC) and exposure to CRS. Pyloric ligation was done in all animals at the beginning of the experiment to collect the gastric juice for analysis. The juice was analysed to determine its volume, pH, free and total acid concentration (FAC and TAC), proteolytic activity and mucin concentration. Lesions of gastric mucosa were scored, the ulcer index (UI) and preventive index (PI) were calculated. Gastric mucosa was scrapped and stored at –80 o C until used for assay of gastric mucosal prostaglandin E2(PGE2). Exposure to CRS significantly reduced gastric juice volume, pH and mucin concentration and gastric mucosal PGE2and significantly increased gastric juice proteolytic activity and acidity (FAC and TAC) in CRS group compared with C group. CRS induced ulcerative lesions in all rats achieving an UI of 19.25. Administration of leptin or famotidine before exposure to CRS significantly increased gastric juice volume, pH and mucin concentration and gastric mucosal PGE2 and significantly decreased gastric juice proteolytic activity in L and F groups compared with CRS group. Both leptin and famotidine exhibited profound protection of gastric mucosa against CRS-induced lesions achieving an UI of 9.5 and 9.75 in L and F groups respectively. This was evident from the PI which was 50.65 and 49.35 in L and F groups respectively. Administration of L-NAME or indomethacin before exposure to CRS aggravated CRS-induced gastric mucosal lesion achieving an UI of 10.75 and 14 in L-NAME and I groups respectively. It could be concluded from the present study that exogenous leptin has an ulcer preventing ability in case of CRS which is comparable to that of famotidine, the famous H2antagonist. The mechanism of ulcer prevention of leptin may involve the cyclooxygenase and nitric oxide pathways. These results may have consequence for the clinical practice. | ||||
| Keywords | ||||
| leptin; cold restrained stress (CRS); gastric mucosa; N G-nitroarginine methyl ester (L-NAME); famotidine; Indomethacin; nitric oxide synthase (NOS) | ||||
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