游泳运动对胰岛素抵抗大鼠脂肪组织中MEK/ERK1磷酸化水平的影响

目的探究慢性和急性游泳运动对肥胖诱导的胰岛素抵抗大鼠脂肪组织中丝裂原活化细胞外信号调节激酶(MEK)和细胞外信号调节激酶(ERK1)磷酸化水平的影响。方法 100只清洁级雄性SD大鼠随机分为对照组(10只,普通饲料喂养)和高脂组(90只,高脂饲料喂养)。喂养8周后,从高脂组中筛选出体重上游1/3大鼠(30只)并随机分为3组:高脂安静组、高脂慢性运动组和高脂急性运动组,每组10只,高脂饲料再喂养8周,并根据运动方案进行运动干预;对照组继续喂食普通饲料8周。运动干预后,取内脏脂肪组织,Western Blot方法检测MEK和ERK1的磷酸化水平。结果慢性运动干预显著降低了胰岛素抵抗大鼠的体重、内脏脂肪质量和脂体比(P<0.01),急性运动对大鼠体重、内脏脂肪质量和脂体比影响无统计学意义。两种运动干预均显著改善了机体胰岛素敏感性(P<0.05),降低了脂肪组织MEK和ERK1的磷酸化水平(P<0.01)。结论运动改善肥胖诱导的胰岛素抵抗可能与抑制脂肪组织中MEK和ERK1的磷酸化有关。

Effect of swimming exercise on MEK and ERK1 phosphorylation level in adipose tissue of insulin resistance rats

OBJECTIVE To investigate the effect of chronic and acute swimming exercise intervention on the mitogen-activated extracellular signal-regulated kinase(MEK) and extracellular signal-regulated kinase 1(ERK1) phosphorylation level in adipose tissues of obesityinduced insulin resistance rats. METHODS A total of 100 SD rats were randomly divided into control group(n=10) fed with normal diet and high-fat diet group(n=90) fed with high fat diet. After 8 weeks, one third rats(n=30) with upper weight in high-fat diet group were selected and randomly divided into high-fat diet sedentary group(n=10), chronic exercise group(n=10) and acute exercise group(n=10). Under another 8-week high-fat diet feeding, exercise intervention was performed according to the exercise procedure;control group was fed with normal diet for 8 weeks. After exercise intervention, visceral adipose tissues were separated and MEK and ERK1 phosphorylation level in adipose tissue was detected by Western blot method. RESULTS Chronic exercise intervention significantly reduced body weight, visceral fat weight and visceral fat weight/body weight ratio(P<0.01), and acute exercise intervention had no significant effect on body weight, visceral fat weight and visceral fat weight/body weight ratio. Both chronic and acute exercise intervention significantly increased body insulin sensitivity(P<0.05), as well as significantly decreased MEK and ERK1 phosphorylation level in adipose tissues(P<0.01). CONCLUSION The improvement of obesity-induced insulin resistance by exercise might be related to inhibited phosphorylation of MEK and ERK1 in adipose tissues.