| Purpose:Insulin resistance (IR) is the basic of the common pathological physiology, namely common risk factors, and it is related to many endocrine metabolic abnormalities, such as:diabetes, atherosclerosis and cardiovascular disease. IR refers to the pathological state that the amount of insulin produced by the body is less than the normal amount required, or that the unit insulin concentration in the cell biological effects is reduced, and compensatory results in increasing of insulin byβ-cell, then followed by insulin hyperlipidemia.It is a common sense that exercises can improve insulin resistance; however, its molecular mechanism still needs to be further elucidated. At present, it is believed that one of the reasons leading to IR is the abnormal state of insulin signaling pathway. As a negative signal of insulin transduction feedback, TRB3 (tribbles homologue 3) plays an important role in the exercise of improving insulin resistance. More and more people pay attention to it. This research article is done to unravel the relationship between TRB3 and IR, as well as the improvement of IR by exercises. This study focuses on the exercise and the progress of the TRB3 gene expression research.The affects of treadmill training and high fat fed on the rats hepatic TRB3 are discussed by using treatment of the 8-weeks-treadmill-training, and the observation of the development process of insulin resistance in high fat diet.Methods:40 Sprague-Dawley (SD) inbred male rats which weighing 176.36±16.33g and randomly divided into four groups:control group (group C,10), high-fat diet group (group H,10), high fat fed and exercise group (group HE,10) and exercise group (group E, 10). Group HE and H are fed in high fat diet, where as group C and group E are fed with normal diet. Fat exercise group and exercise group begin treadmill from eight or nine a.m., five days a week for eight weeks. Blood glucose is tested by glucose oxidase method. Serum insulin is tested by radioactive immunoassay. TRB3, PI3K and PKB protein content of the hepatic tissue is determined by using Western Blot's method.Results:①After the treatment of group H with eight weeks feeding of high fat diet, the average of the body weight was significantly higher than those with eight weeks of normal diet group (P<0.05); The body weight average of group HE was significantly lower than the group H (P<0.01) after 8 weeks of treatment with both high fat diets and treadmill training, while there were no significant differences compared to group E and C (P>0.05). After 8-week-treadmill training, there were also no considerable differences between the weight average of group E and group C, however, there was a trend of decreasing in group E.②After eight weeks of fat diet treatment, group C of the visceral fat pad weight and relative weight of visceral fat pad (%) were notablely lower than the group H (P<0.01), while the group HE average was significantly lower than the group H (P<0.01), and no differences between the groups HE and E, but the group HE is slightly higher.③fter the experiment, group H hepatic weight and hepatic index were higher than group C, whereas group HE was higher than group E, with a significant difference (P<0.01); compared with the group H, group HE hepatic weight hepatic index decreased significantly (P <0.01); group E hepatic weight and hepatic index was also lower than group C (P<0.05).④At the end of the 8th week, there were no significant changes of glucose concentration between these four groups (P> 0.05); compared with groups C and HE, there was a increasing trend of group H serum insulin concentration, but with little difference, and group HE was higher in concentration of serum insulin than group E (P<0.05), whereas group E was lower than group C (P<0.05); The insulin sensitivity index and insulin resistance index of group H had significant differences (respectively P<0.01 and P<0.05) compared with the group C. The insulin sensitivity index of HE rats was higher than group H, but lower than the group E, which was lower than C rats, though the differences were not significant; group H has the highest insulin resistance index, and group E was lower than the group C, and group HE was higher than the group E, but the differences were not significant.⑤After 8 weeks of high fat feeding, H group's TRB3 protein expression in the liver was higher than group C (P<0.05), while the hepatic TRB3 protein expression of group HE was lower than group H (P<0.05), and there were no significant differences between group E and group C; PEPCK protein expression by group H was higher than group C with great differences (P<0.05). HE group's PEPCK protein expression was lower than H group with significant differences (P<0.05).⑥After 8 weeks of high fat diet, H rats PKB protein expression in the liver was lower than group C (P<0.05), and lower than group HE (P<0.05), while little difference was observed between groups C and E; PI3K protein expression in group H was lower than group C (P<0.05), but slightly lower than HE, although with no significant changes, and differences between groups E and C were also not significant.Conclusion:1. With eight weeks of high fat diet feeding, SD rats showed decreasing of hepatic insulin, resulting rats IR, and the possible mechanisms were:①the over expression of hepatic TRB3 restrains the activation of PKB/Akt in PI3K/PKB hepatic signal pathway.②as hepatic PEPCK expression increased, the gluconeogenesis was improved, which affected the stability of blood glucose concentration.2. Eight weeks of treadmill training can prevent the occurrence of IR induced by high fat feeding, and the possible mechanisms were:①decrease the hepatic TRB3 expression and improve the activation of PKB/Akt in PI3K/PKB hepatic signal pathway.②decrease the expression of PEPCK as well as the gluconeogenesis in order to keep blood glucose stable. |
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