A rat model of childhood diet-induced obesity: Roux-en-Y gastric bypass induced changes in metabolic parameters and gastric peptide ghrelin
- PMID: 17505835
- DOI: 10.1007/s00383-007-1944-4
A rat model of childhood diet-induced obesity: Roux-en-Y gastric bypass induced changes in metabolic parameters and gastric peptide ghrelin
Abstract
Childhood morbid obesity is reaching epidemic proportions. Roux-en-Y gastric bypass (RYGB) results in many metabolic alterations, including changes in glucose and lipid metabolism, and changes in levels of the gastric hormone, ghrelin. As more children are undergoing RYGB, an animal model would be beneficial to further study RYGB and its subsequent metabolic effects. DIO Sprague Dawley rats underwent RYGB, sham jejunojejunostomy (SH), or no operation (HFC) after 6 weeks of high-fat diet. Non-obese rats fed standard chow (SC) were a final control group. Animals were post-operatively fed standard chow for 7 days before sacrifice. At sacrifice, venous blood and gastric mucosa was collected for metabolic parameters and ghrelin determination. RYGB rats weighed less than SH and HFC (361 +/- 8.8 vs. 437 +/- 9.3 and 443 +/- 6.2 g, P < 0.05). Compared to HFC, RYGB animals had decreased plasma glucose (292 +/- 23 vs. 141 +/- 10 mg/dL), cholesterol (80 +/- 12 vs. 45 +/- 5 mg/dL), triglycerides (138 +/- 37 vs. 52 +/- 7 mg/dL), HDL (43 +/- 5 vs. 20 +/- 3 mg/dL), and free fatty acids (0.72 +/- 0.14 vs. 0.23 +/- 0.02 mEq/L), all P < 0.05. Plasma ghrelin increased in RYGB rats compared to SC and HFC (116.22 +/- 32.27 vs. 31.60 +/- 2.66 and 31.75 +/- 0.75 pg/mL, P < 0.05). In a rat model of RYGB, we demonstrated improved metabolic parameters and increased plasma and gastric mRNA ghrelin levels. The rat model for RYBG appears to be a reasonable model for future study of the cellular and molecular regulatory pathways of obesity and its surgical treatment.
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