A Study On The Change Of GH/IGF-â…  Axis In Dietinduced Male Obese Rats

IntroductionPrevalence and severity of obesity are increasing rapidly all over the world, because the life standard is improved and man has increased ingestion of fat -rich foods. The obese velocity of our city children is increased by 9. 1% per year, obesity has become to be a worldwide health problem. It leads to the hormones and the biological factors change, including leptin, insulin, Neuropeptide Y(NPY) and tumor necrosis factor-alpha (TNF-a) et al, which levels are significantly increased.In normal physiological condition except trimester of pregnancy, growth hormone ( GH) conjugates its recipient to induce the target tissues, for instance liver and adipose tissue and so on , to secret insulin - like growth factor- I (IGF- I ). IGF- I increases accompany with GH rising . When the level of IGF- I has achieved certain degree, it can either induce hypothalamus to release growth hormone release inhibiting hormone ( GHRIH) , or inhibit anterior pituitary to secret GH directly, which can prevent GH from raising. Therefore it was called GH/IGF- I axis. Most functions of GH is modulated by IGF- I . Through the function of IGF- I , GH facilitate cartilage cell to proliferate and ossification, which leads long bone and body length to grow. In obesity, however, the level of GH decreases, the level of total IGF- I is normal or increased, accompany with the level of free IGF-1 is normal or increased. Despite GH secretion is impaired in obesity, the growth velocity of obese children is commonly normal or increased.This study is to discuss the reason of normal or high free IGF- I in serum, GH/ IGF- I axis changes.Objective1. To discuss whether GH and free IGF- I levels are comparable in diet -induced obese rats with control rats;2. To discuss whether IGF- I concentration in hepatic is comparable in dietf- induced obese rats with control rats;3. To discuss the relationship between insulin and IGF- I ;4. To discuss the change of GH/ IGF- I .Materials and MethodsAnimal and Diets. Thirty - two male weanling Wistar rats weighting 55 卤 5g were obtained from the Animal Department of China Medical University. Animals were housed in cages in a temperature - controlled room (22 5 C ) and the relative humidity is 45% 10% . Animals were given free access to diets and water over the duration of the study. 16 rats were given a high - diet and 16 rats were given a standard diet as control.Experimental protocol. 32 animals were initially fed a standard diet for 1 week before the high - fat or control diets were started. 16 rats were given a high -fat diet to induce obesity, the other 16 rats were given a standard diet as control. At every weekend in this period, body weights were measured. 16 rats (8 control, 8 experiment ) were killed in the sixth weekend, while others were killed in the twelfth weekend after sampled blood. Abdominal fat pads ( perirenal, mesenteric, epididymidis) were weighted. All blood samples were centrifuged and the serum was stored at - 701. At the end of the experiment, the livers were quickly removed, fixation and made sections of 3 - 5 m.Assays. The level of serum GH,free IGF- I and fast insulin (FINS) were determined in rats by radioimmunnoassay. The level of fast plasma glucose ( FPG) were determined in rats by toluidine. The concentration of IGF- I in theliver were detected by immunohistochemistry.Statistical method. All values are expressed as means 卤 SE. Data were analyzed across two groups by student' s t test, the relationships are analyzed by pearson correlation analysis.Results1. body weights Changes of high - fat diet group and control group rats After given 12wk of high - fat diet, body weights of high - fat diet grouprats were significantly greater than control group (P <0.01)2. Rats Abdominal fat pads depot during experimentAt the end of 6 weeks, the weights of epididymal fat pads were heavier than control rats(P < 0. 05) , mesenteric, perirenal fat pads were comparable with controls ( P >0. 05) ; At the end of 12 w...