| IntroductionObesity is thought to be a chronic disease, company with too much fat content , multietiologic nature, and can unite many other disease, which is closely correlated with cerebrovascular disease, hypertention and diabetes mellitus, disorder of fat metabolism, et al. In the world, the incidence of obesity has increased obviously. The incidence of obesity of Asian is lower than western countries , but most of those are abdomenform obesity. Accompany with the development of economy and the change of human living form, obesity has become one of the most common health problem in the twenty-one century. Every country scholar pay closely attention to the investigation of obesity. In 1994,upsurge of investigation of obese gene is uncovered after detected and cloned obese gene the first time of mice and human. The investigation of obesity entered molecular biology period.It is difficult to study mechanism of obesity in humans because of the multietiologic nature of obesity. Models have been made to acquire information which would not otherwise be obtainable. Levin found that part of the rats fed the same high fat diet was obese and part was not obese in 1983. Lauterio et al develop this model. On the basis of weight gain, the rats whose weight in the upper tertile of all rats were called diet-induced obesity ( DIO) , the rats whose weight in the lower tertile of all rats were called diet-induced obesity resistant ( DIO-R ) , those between them were abandoned. Lauterio et al investigated DIO rats. The level of serum leptin of DIO and DIO-R rats advanced, but the level of serum leptin ofDIG was higher than DIO-R rats. Watson et al thought that decreased NPY mR-NA of hypothalamus might be related to obesity-resistant. The text utilizes the a-bove animal model to extermine the change of the level of leptin and the expression of NPY mRNA, and the relationship between leptin, NPY and obesity-resis-tent in order to find the mechanism of obesity-resistent and provide theoretical basis for the study of obesity.ObjectiveThe purposes of this experiment are:1. Assessing early and late serum leptin, insulin, fat depot changes induced by high-fat diet in diet-induced obesity and diet-induced obesity resistant rats.2. Ivestigating NPY mRNA expression in the arcuate nucleus of hypothalamus of diet-induced obesity and diet-induced obesity resistant rats.3. Ivestigating the relationship between leptin and NPY.4. Ivestigating the relationship between NPY, leptin and obesity-resistant.Material and MethodsAnimal and Diets. 52 male Wistar rats weighting 200 å¤ 20g were obtained from the Animal Department of China Medical University. Animals were housed in cages in a temperature-controlled room (22 å¤3^1) with a 12-hour light-dark cycle. Animals were given free access to diets and water over the duration of the study. 39 rats were given a high-diet and 13 rats were given a standard diet as control. The composition of diets in listed on Table 1.Experimental protocol. 52 animals were initially fed a standard diet for 1 week before the high-fat or control diets were started. 39 rats were given a high-fat diet to induce obesity,the other 13 rats were given a standard diet as control. At every weeken in this period, body weights were measured. 24 rats(6 control, 18 experiment ) were killed in 2 wk,while others were killed in 12 wk by decapitation after sampled blood. The brains were quickly removed from the skulls, the hypothalamus were obtained and stored. The brain were glued to a specimenholder and placed in a cryostat at - 17 C. The serial sections of 13 m. The brain sections were placed on glass slides and stored at - 701. Abdominal fat pads (perirenal, mesenteric, epididymidis) were weighted. All blood samples were centrifuged and the serum was stored at -70 C.Over the 2 wk and 12 wk period, rats fed the high-fat diet diverged into two groups based on body weight gain. 6/7 rats with the greatest weight gain were referred to as diet-induced obesity, while 6/7 rats with the lowest weigh...
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