| Objective:More and more the incidence rate of obesity in the worldwide is obvious. Obesity can lead to insulin resistance, which makes insulin not able to decrease blood sugar, even to induce type 2 diabetes mellitus. The pathogenesis that why obesity can lead to insulin resistance is still unclear. An unique signaling molecule-resistin maybe answer the question. In the beginning, people found that resistin resisted insulin action, so that insulin and blood sugar were higher than usual. Whereas the anti-resistin antibody produced the opposite effect. Resistin is thus a hormone that potentially links obesity with insulin resistiance to type 2 diabetes mellitus. Because it is a short time for resistin being found, people need more work to know it. In other experiments, the opposite effect was found.Today, the studies mainly aim at adult mice and adult people about the expression of resistin, whereas it hardly has no reports about young creatures in the foreign countries and no reports in China. The objective of the study is that we build the obesity model of young SD rat. The resistin expression was studied in the white adipose tissue of perirenal and epididymal of young obese rats, the rats having a normal diet were as controls. The correlation was al so studied between the resistin expression and the related factors. The factors that influenced significantly on resistin were also found. The study was to give a proof to the pathogenesis between obesity and insulin resistance.Methods:30 SI) rats were divided into two groups, each group had 15 rats. One group had a normal diet, the other had a high fat diet. The rats were weighed once a week. After 5 weeks,the rats were sacrificed. Their blood samples were taken, the plasma was separated by centri fugation for assaying glucose, insulin, triglycerides, free fatty acids and total cholesterol. The perirenal and epididymal fat pads were disected, too. Total RNA from fat pads tissue was extracted by TRIzol method and then the cDNAs were obtained by RT-PCR. Resistin and 0-actin were amplified simultaneously in a multiple-PCR. The co-amplification products were separated on 1.5% agarose gel and then analyzed by GelBase/Gelbiot-Pro software of UVP system. The ratio of resistin and 3~actin was calculated in order to normalize the data.Results:1. In normal group and high fat diet group, the body weight after 5 week'diet was 183. 33 ±49. 34k 225.33+ 41.810; the fasting glucose was 4.240+ 1.145k 5.440 +0.8542; the total cholesterol was 1.747 ± 0.2066, 1.993 ±0.3081: the fasting insulin was 7. 6953± 1. 56794. 9. 7820±2. 066268; the free fatty acids was 0. 7020±0. 15442, 0.8673 ±0. 15229; the triglycerides was 0. 5253±0. 19164, 0. 9427±0. 34675c2. The Kesistin/P-actin in the white adipose tissue in the two groups was 0. 9544±0. 09749, 1.0435 + 0.11021 in perirenal and 0.9324 ±0.13290, 1.1533 + 0.30340 in epididymal.3. The differences between the normal group and the high fat diet group were analyzed using t test. The results exsit significant difference (P<0. 05 or P<0. 01) .But there was no difference between the perirenal and the epididymal adipose tissue in two groups(P>0. 05).
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