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Objective:To investigate the effects of enteral nutrition support in inoperable advanced gastric cancer patients during chemotherapy.Methods:This was a prospective randomized study.A total of 62 patients with advanced gastric cancer were firsted evaluated according to the Nutritional Risk Screening 2002 (NRS 2002) scale,and were randomly divided into two groups.All patients received oxaliplatin combined with tegefur gimeracil oteraci.Patients in the control group (n =30) received chemotherapy along with nutrition consultation,and patients in the treatment group (n =32) were provided enteral nutrition-additionally.NRS 2002 assessment was conducted before and after chemotherapy,The body weight,BMI,serum albumin,and the efficacy and toxicity were collected during the study.Results:Patients in the treatment group had significantly higher serum albumin levels,body weight and BMI than those of the control group (P ＜ 0.05).No differences were found as for the efficacy and toxicity of chemotherapy between two groups.Conclusion:Enteral nutrition support therapy can improve the nutrition status of gastric cancer patients who received chemotherapy and reduce the risk of malnutrition.
RESUMEN
<p><b>OBJECTIVE</b>To investigate the regulation of leptin on insulin secretion and expression of ATP-sensitive potassium channel subunit sulfonulurea receptor 1 (SUR1) mRNA, and to determine whether the effects of leptin are mediated through known intracellular signaling transduction.</p><p><b>METHODS</b>Pancreatic islets were isolated by the collagenase method from male SD rats. The purified islets were incubated with different concentrations of leptin for 2 h in the presence of different concentrations of glucose. Insulin release was measured using radioimmunoassay. Expression of SUR1 mRNA was detected by RT-PCR.</p><p><b>RESULTS</b>In the presence of leptin 2 nmol/L, insulin release was significantly inhibited at either 11.1 or 16.7 mmol/L glucose concentration (both P < 0.05), but insulin release was not altered at glucose of 5.6 mmol/L physiological concentration. The dose-response experiment showed that the maximal effect of leptin on insulin secretion achieved at 2 nmol/L. Exposure of islets to 2 nmol/L leptin induced a significant increase of SUR1 transcription levels by 71% (P < 0.01) at 11.1 mmol/L glucose and by 56% (P < 0.05) at 16.7 mmol/L glucose concentration. Selective phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin significantly prevented the leptin effect on insulin secretion and SUR1 mRNA expression.</p><p><b>CONCLUSIONS</b>Regulatory effects of leptin on insulin secretion could be biphasic at different concentrations of glucose and leptin. The stimulatory regulation of SUR1 transcription levels may be mediated through activation of PI 3-kinase pathway, which may be a possible mechanism of leptin in regulating insulin secretion.</p>