| Objective:The incidence rate of obesity and fatty liver continues to increase in middle-aged and elderlypopulation. Meanwhile, exercise is widely recognized as one of the most effective ways toreduce the body fat, and improve/reverse fatty liver.However, the mechanism of its action has notbeen fully understood.Through an8-week exercise intervention on diet-induced obese rats, thisstudy aims to explore the impact of long-term aerobic exercise intervention on liver’sLKB1-AMPK-ACC signal transduction pathway of high-fat diet-induced obese aged male ratsand provide experimental evidence for expounding that the long-term aerobic exercise canimprove obesity conditions and the molecular biological mechanisms that can alleviate fataccumulation in liver.Methods:1.The author randomly selects10rats as the control group (CON) from4815-month-old maleSD rats. After obesity-model-making experiment with high fat diet on the remaining38rats, theauthor selects30obese rats which are consistent with obesity model according to body weightfrom high to low, and then randomly divides them into three groups: obesity group for10rats(OB), obesity-continuous exercise group1for10rats (OB+CE1), and obesity-continuousexercise group2for10rats (OB+CE2).2.After obesity-model-making experiment, the author implements eight weeks’ swimmingtraining for rats in OB+CE1group and OB+CE2group.3. At the end of the experiment’s16th week, the author takes rats in each group for sampling todetermine the content of blood lipid and triglyceride TG in liver, free fatty acid (FFA) and theprotein expression level and kinase phosphorylation level of LKB1-AMPK-ACC signaltransduction pathway in liver.Results:1.For rats in OB group, their body weight, abdominal fat weight, serum TG, TC, LDL-C level forsampling are significantly higher than that of CON group (P<0.01), serum HDL-C level issignificantly lower than that of CON group (P<0.01); for rats in OB+CE1group and OB+CE2group, their body weight, abdominal fat weight, serum TG, LDL-C level for sampling aresignificantly lower than that of OB group (P<0.05-P<0.01), serum HDL-C level is significantlyhigher than that of OB group (P<0.01); but there is no significant changes for body weight, abdominal fat weight, TG, TC, LDL-C and HDL-C (P>0.05) for sampling when comparing ratsin OB+CE2group with rats in OB+CE1group.2.Compared with rats in CON group, TG and FFA content in liver tissue for rats in OB groupsignificantly increases (P<0.01); compared with rats in OB group, TG and FFA content in theliver tissue for rats in OB+CE1group and OB+CE2significantly decreases (P<0.05, P<0.01);but there is no significant changes for TG and FFA content in liver tissue compared to liver tissuewhen comparing rats in OB+CE2group and rats in OB+CE1group(P>0.05).3.Compared with rats in CON group, liver LKB1protein expression level and phosphorylationlevel, and protein expression and phosphorylation level of AMPKα1, α2and α1/2for rats in OBgroup are significantly lower (P <0.05-P <0.01); compared with rats in OB group, LKB1phosphorylation level, AMPKα1, AMPKα2and AMPKα1/2protein expression andphosphorylation level for rats in OB+CE1group are significantly higher (P <0.01); for rats inOB+CE2group, their LKB1phosphorylation level, AMPKα1phosphorylation level and proteinexpression and phosphorylation level for AMPKα2and AMPKα1/2also significantly increase(P<0.05-P<0.01). Liver ACC protein expression for rats in OB group is significantly higher thanthat of CON group while ACC phosphorylation level is significantly lower than that of rats inCON group (P<0.01); compared with rats in OB group, ACC protein expression level for rats inOB+CE1group and OB+CE2group is significantly lower while their ACC phosphorylationlevel is significantly higher (P<0.01). Meanwhile, compared with rats in OB+CE1group, thereis no significant changes for any other indicators (P>0.05) except that phosphorylation level ofAMPKα1and AMPKα2for rats in OB+CE2group is significantly lower (P <0.05).Conclusion:1. Each protein kinase expression and phosphorylation level in Liver LKB1-AMPK-ACC signaltransduction pathway of high-fat diet-induced obese rats are exposed to different degrees ofdamage. It is speculated that the damage to the pathway is connected with fat metabolismdisorder.2. Long-term aerobic exercise can significantly improve each damaged protein kinasephosphorylation and expression of LKB1-AMPK-ACC signal transduction pathway and alleviatefat metabolism disorder of liver and body, and the effect of aerobic exercise can continue for46-48hours at least. |
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