Susceptibility of gastric cancer according to leptin and leptin receptor gene polymorphisms in Korea / 대한외과학회지

PURPOSE: Leptin plays an important role in the control of body weight and also has a growth-factor-like function in epithelial cells. Abnormal expression of leptin and leptin receptor may be associated with cancer development and progression. We evaluated the relationship among leptin and leptin receptors polymorphisms, body mass index (BMI), serum leptin concentrations, and clinicopathologic features with gastric cancer and determined whether they could be the risk factor of gastric cancer. METHODS: We measured the serum leptin concentrations of 48 Korean patients with gastric cancer and 48 age- and sex-matched controls. By polymerase chain reaction-restriction fragment length polymorphism, we investigated one leptin gene promoter G-2548A genotype and four leptin receptor gene polymorphisms at codons 223, 109, 343, and 656. RESULTS: There was no significant difference between the mean leptin concentrations of the patient and control groups, while BMI was significantly lower in gastric cancer cases (22.9 +/- 3.6 vs. 24.5 +/- 2.8 kg/m2, P = 0.021). There was significant association between the LEPR Lys109Arg genotype and gastric cancer risk, heterozygotes for GA genotype had been proved to increased the risk of gastric cancer, and its corresponding odds ratio was 2.926 (95% confidence interval, 1.248 to 6.861). CONCLUSION: Our results suggested that LEPR gene Lys109Arg polymorphism is associated with gastric cancer in Korean patients.

Leptin and gastrointestinal motility / 国际外科学杂志

Leptin,a peptide encoded by the obese gene,is primarily secreted by adipocytes,which is a critical hormone controlling food intake, body weight, energy expenditure and neuroendocrine function. Leptin can alter the reactivity of the gastrointestinal neuromuscular, thereby to regulate the gastric emptying and bow-el movement. Leptin seems to be a new gut hormone that has a close relationship with the function and dis-ease of gastrointestinal tract. This article reviews the relationship of leptin and gastrointestinal motility.

Mechanism of Leptin-Induced Potentiation of Catecholamine Secretion Evoked by Cholinergic Stimulation in the Rat Adrenal Medulla

The aim of the present study was to examine the effect of leptin on CA release from the isolated perfused model of the rat adrenal gland, and to establish its mechanism of action. Leptin (1~100 ng/ml), when perfused into an adrenal vein of the rat adrenal gland for 60 min, enhanced a dose-dependently the secretory responses of CA evoked by ACh (5.32x10 (-3)M), DMPP (10 (-4)M) and McN-A-343 (10 (-4)M), although it alone has weak effect on CA secretion. However, it did not affect the CA secretion evoked by excess K+ (5.6x10 (-2)M). Leptin alone produced a weak secretory response of the CA. Moreover, leptin (10 ng/ml) in to an adrenal vein for 60 min also augmented the CA release evoked by BAY-K-8644, an activator of the dihydropyridine L-type Ca2+ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic Ca2+ ATPase. However, in the presence of U0126 (1micrometer), an inhibitor of mitogen-activated protein kinase (MAPK), leptin no longer enhanced the CA secretion evoked by ACh and DMPP. Furthermore, in the presence of anti-leptin (10 ng/ml), an antagonist of Ob receptor, leptin (10 ng/ml) also no longer potentiated the CA secretory responses evoked by DMPP and Bay-K-8644. Collectively, these experimental results suggest that leptin enhances the CA secretion from the rat adrenal medulla evoked by cholinergic stimulation (both nicotininc and muscarinic receptors), but does not that by membrane depolarization. It seems that this enhanced effect of leptin may be mediated by activation of U0126-sensitive MAPK through the leptin receptors, which is probably relevant to the activation of the dihydropyridine L-type Ca2+ channels located on the rat adrenomedullary chromaffin cells.