| The animal model of hypothalamus obese rats was constructed by single or bilateral electrical damage of hypothalamic arch nucleus,ventral nucleus and dorsal medial nucleus,and the changes of feeding,weight gain and serum Nesfatin-1 expression levels after single lateral injury and bilateral injury in rats were observed.To collate and analyze the correlation between the occurrence of hypothalamic obesity and the changes of serum Nesfatin-1,to investigate whether the expression of Nesfatin-1 in unilateral hypothalamus injury group and bilateral hypothalamus injury Group was consistent,and to identify whether unilateral hypothalamic injury had compensation for lateral hypothalamus.Based on our previous research,it is preliminarily verified that there is an essential difference between unilateral hypothalamic injury and bilateral hypothalamic injury,and the relevant areas of neurons expressing Nesfatin-1 in the hypothalamus are understood,which give a foundation in the future for study of functional reconstruction of hypothalamic obesity.It provides a theoretical basis for evaluating the range of hypothalamus injury and the choice of surgical route in perioperative period.Methods:Two different hypothalamic obese rat models were created by microelectrode injury of unilateral or bilateral hypothalamus dorsal medial nucleus,arch nucleus and ventral nucleus,and the success of modeling was demonstrated through the discovery of HE staining,weight and feeding.Enzyme-linked immunosorbent test was used to detect the change of serum nesfatin-1 concentration in mold-making animals within 7 weeks and to record the results,the Western blot method was used to determine the content of hypothalamic nesfatin-1 after 7 weeks of molding.Results:1.Compare with the blank control group,the weight gain and food intake were significantly reduced within 4 days after modeling(P<0.05).After 1 week of hypothalamic injury,the body weight and food intake increased considerably.In the unilateral injury group,the dietary intake and weight gain at week 1-3 were considerably upper than those in the control group,reaching a peak at week 2(P<0.05),and the dietary intake and weight gain at week 4 were gradually reduced,almost approaching the normal control group at week 7.2.In the bilateral hypothalamus injury group,the intake and weight gain were considerably upper than those sham group at 1-6 Weeks(P <0.05),with the highest in the 2nd week and the relative decrease in the 4th week,and close to the normal control group level at 7 weeks.Compared with the blank control group,the weight and food intake of the conditioned control group did not change significantly.3.In the early stage of hypothalamus injury(4 days),the serum Nesfatin-1 of single and bilateral hypothalamus injury groups and sham groups were significantly higher than those in normal control group(P<0.05).The Nesfatin-1 of the single and bilateral hypothalamus injury group began to decline after 1 week of hypothalamic injury,reaching the lowest point after 2 weeks(P<0.05)and recovering gradually in 3-7 weeks.After 7 weeks of hypothalamic injury,there was no significant difference in serum nesfatin-1 expression level between the unilateral hypothalamus injury group and the normal control group(P > 0.05),while the nesfatin-1 of bilateral hypothalamus injury group was lesser(P<0.05).4.After 2 weeks of hypothalamic injury,the content of Nesfatin-1 in the hypothalamus of single and bilateral hypothalamus injury group decreased significantly compared with that of conditional control group(P<0.05),and the decrease of nesfatin-1 in bilateral hypothalamus injury group was more obvious than that of unilateral hypothalamus injury group.(P<0.05),but compared with the blank control group,nesfatin-1 of the conditioned control group did not change significantly.(P>0.05).After 7 weeks of molding,the nesfatin-1 in the thalamus was significantly higher than that of the single and bilateral hypothalamus injury group(P<0.05),and there was no significant difference in nesfatin-1 expression level between unilateral hypothalamus injury Group and normal control group,while the expression level of nesfatin-1 in the bilateral injury group was still low(P>0.05).Conclusion:1.From the above results,it can be seen that after unilateral or bilateral hypothalamic injury,the concentration of serum nesfatin-1 changes with the changes of food intake and body weight,indicating that nesfatin-1 and hypothalamic injury after the production of obesity.2.After 7 weeks of hypothalamic injury,compared with normal control,the expression of lateral hypothalamus nesfatin-1 in the unilateral hypothalamus injury group increased obviously,and the corresponding feeding,weight and serum nesfatin-1 concentrations were restored to normal level,suggesting that unilateral hypothalamic injury had compensatory effect on lateral hypothalamus.3.After 2 weeks of single and bilateral hypothalamic injury,the changes of feeding,weight gain and serum nesfatin-1 concentration were most obvious,while 7 weeks of after hypothalamic injury,these indexes were close to the normal control group level,indicating that there may be other compensatory mechanisms in the body to maintain the balance of energy metabolism in vivo. |
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