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Study on OB-Rb, SOCS3 mRNA Expression in Liver of Obese SD Rats Fed with High-fat Diet

Author: DiNa
Tutor: LiuZhengJuan
School: Dalian Medical University
Course: Pediatrics
Keywords: Obesity Leptin resistance OB-Rb SOCS3 SD rats
CLC: R589.2
Type: Master's thesis
Year: 2007
Downloads: 200
Quote: 0
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Background: Obesity is excessive body fat accumulation, body weight over a certain range of a nutritional disorders caused due to the imbalance in the energy metabolism, calorie intake exceeds the body's long-term consumption. Due to the improvement of people's living standards, dietary patterns change, childhood obesity has shown a trend of increasing year by year. Obesity not only affects the health of children, and will also serve as incentives adult hypertension, diabetes, coronary heart disease, cholelithiasis, gout and other diseases and sudden death. The discovery of leptin (Leptin), provides a new perspective for the understanding of the mechanisms of obesity. Leptin has a wide range of biological effects: inhibition of food intake, promote energy consumption, regulates metabolism, affect hormone secretion, reproductive, immune and vascular proliferation, combined with these role play needs its specific receptor (OB-R). Animal experiments have shown that, of Leptin gene mutation leads to the lack of leptin in the blood circulation is one of the causes of obesity. However, in acquired obesity mouse model and in the vast majority of patients with obesity, elevated serum leptin levels. They leptin decreased response or no response to the phenomenon known as leptin resistance, the incidence of obesity may be related to leptin resistance. To diet-induced obesity mouse central injection of exogenous recombinant leptin treat Tip leptin resistance may occur in the receptor / post-receptor transduction level. Janus protein kinase - signal transduction and transcriptional activator protein (JAK-STAT) pathway leptin signal transduction. JAK / STAT signaling pathway negative regulator of cytokine signal transduction inhibitor -3 (SOCS3) as a leptin receptor, Leptin resistance may be involved. Cellular level, the study confirmed that leptin can cause cells SOCS3 levels, the combination of the latter with JAK2 inhibition of tyrosine phosphorylation of JAK2 and leptin receptor, thereby preventing the leptin signal conduction along the JAK / STAT pathway . And compared to the wild-type SOCS3 heterogeneity deficient mice increased sensitivity to leptin, hypothalamic leptin receptor in response to exogenous leptin signaling enhancements can resist high-fat food induced obesity and related metabolic comprehensive generation of disease. Inhibition of hypothalamic SOCS3 expression may be effective in treating obesity caused by leptin resistance. Objective: This experiment simulating the characteristics of childhood obesity (equivalent to four weeks after birth, infancy) SD rats as experimental animals, high fat diet for preparation of childhood obesity rat model to study the the obese rats surrounding tissue (liver) within long OB-R (OB-Rb) the mRNA and SOCS3mRNA expression change. From the leptin receptor gene expression and leptin receptor, JAK-STAT signaling pathway level to study the mechanisms of leptin resistance may occur, preliminary study in obese rat liver tissue the OB-RbmRNA, SOCS3mRNA with high leptin hyperlipidemia relationship as well as the relationship between of the OB-RbmRNA with SOCS3mRNA expression. Based animal model to investigate childhood obesity, leptin resistance mechanisms may occur. Methods: 4-week-old, 32 healthy male SD rats were randomly divided into two groups, a group of 20 for the experimental group, the average weight (77.47 ± 7.90) g be high fat diet-induced obesity formation; another group of 12 only for the control group, the average weight (78.83 ± 6.90) g, be a normal diet. Feeding period with free access to water, and does not limit the amount of feed, measured body weight once a week, to exceed 20% of the control group, the average weight of obesity standards determine the obese group. 8 weeks of feeding, the obese mice and control mice were fasted for 12 hours after blood collection, separation of the serum, livers were quickly put to death. Radioimmunoassay of serum leptin, insulin and C-peptide content; correlation analysis of the obese group serum leptin levels with insulin, C peptide content. By ABB OTTCCX-Ⅱ type automatic biochemical analyzer, blood sugar, blood total cholesterol and triglyceride completed; semi-quantitative RT-PCR method to?-Actin as an internal control to detect liver OB-Rb, SOCS3mRNA expression levels, and analysis of diet-induced obese rat liver OB-Rb for SOCS3mRNA expression levels and both serum leptin content relevance. Results: SD rats fed high fat diet weight gain compared with the normal diet control group significantly, up to four weeks to reach statistical significance (P lt; 0.01). Feeding weekend to exceed the average weight of 20% of the control group as obesity standards, the experimental group, a total of 15 rats become obese model (75%), the average body weight (416.33 ± 23.01) g, the average weight of the control group (321.92 ± 19.65) g, the difference between the two groups was statistically significant (P lt; 0.01). Obese rats glucose, triglyceride and cholesterol levels were significantly higher, statistically significant. 2 obese rats serum leptin, insulin, C-peptide levels were significantly higher than those in the normal control group, the difference between the two groups was statistically significant (P lt; 0.01). Serum leptin content of obese rats with serum insulin, C-peptide concentration showed a significant positive correlation (r = 0.608, P lt; 0.05 and r = 0.686, P lt; 0.01). 3 obese rats OB-Rb mRNA levels in the liver (relative gray value) was 0.79 ± 0.29, significantly lower than the normal control group, 1.63 ± 0.62, the difference between the two groups was significant (P lt; 0.01). OB-Rb mRNA levels of serum leptin content and liver of obese group showed a significant negative correlation coefficient of determination r 2 0.523 (P lt; 0.01). SOCS3 mRNA levels in the liver of obese rats (relative gray value) was significantly higher than the normal control group was 1.42 ± 0.65, 0.54 ± 0.12, the difference between the two groups was significant (P lt; 0.01). Obesity, serum leptin content SOCS3 mRNA levels in the liver was significantly positively related to the coefficient of determination r2 of 0.624 (P lt; 0.01). Fat diet induced obese rats liver OB-Rb mRNA levels (relative gray value) SOCS3mRNA level (relative gray value) no obvious correlation coefficient of determination r2 was 0.154 (P gt; 0.05). Conclusion: The high-fat diet-induced obese rats serum leptin levels increased and insulin, C-peptide levels were positively correlated, suggesting that high-fat diet can induce leptin resistance occurs. Hyperleptinemia may be involved in the formation of insulin resistance. In the surrounding tissues (liver) long form leptin receptor mRNA expression in obese rats was significantly lower than the control group, and was significantly negatively correlated with the level of Leptin, suggesting that diet-induced obese rats by peripheral tissue leptin The gene involved in the mechanism of leptin resistance silence. 3 the obese rats SOCS3 mRNA expression was significantly higher, and Leptin levels showed a significant positive correlation. Tip peripheral tissues SOCS3 expression raised the leptin receptor, JAK-STAT signal transduction pathway may also be involved in the mechanism of leptin resistance.

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CLC: > Medicine, health > Internal Medicine > Endocrine diseases and metabolic diseases > Metabolic diseases > Lipodystrophy
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