目的观察有氧运动和抗阻运动对糖尿病前期人群胰高血糖素样肽1(GLP-1)及血糖水平的影响。方法105例糖尿病前期人群,随机分为A组34例、B组35例、C组36例。A组接受中等强度的有氧运动训练,B组接受抗阻运动训练,C组不进行运动干预,在干预...目的观察有氧运动和抗阻运动对糖尿病前期人群胰高血糖素样肽1(GLP-1)及血糖水平的影响。方法105例糖尿病前期人群,随机分为A组34例、B组35例、C组36例。A组接受中等强度的有氧运动训练,B组接受抗阻运动训练,C组不进行运动干预,在干预前和干预第3、6、12、18个月,检测三组空腹血糖(FPG)、血清GLP-1、餐后2 h血糖(2 h PG),干预第18个月计算血清GLP-1变化率及血糖变化率。结果与干预前相比,A组干预第12、18个月时血清GLP-1水平升高,B组干预第6个月时降低、第18个月时升高,C组干预第6、12、18个月时降低(P均<0.05);与C组相比,A、B组干预第12、18个月时血清GLP-1水平升高(P均<0.05);与B组相比,A组干预第6、12个月时血清GLP-1水平升高(P均<0.05)。与干预前相比,A组干预第3、6、12、18个月时FPG水平降低,B组干预第3、18个月时降低,C组干预第18个月时升高(P均<0.05);与C组相比,A、B组干预第3、6、12、18个月时FPG水平降低(P均<0.05)。与干预前相比,C组干预第3个月时2 h PG水平升高(P<0.05);与C组相比,除B组干预第12个月外,A、B组干预各时点2 h PG水平降低(P均<0.05)。105例研究对象干预18个月后GLP-1变化率与FPG变化率和2 h PG变化率均呈负相关(r分别为-0.537、-0.314,P均<0.05)。结论有氧运动和抗阻运动均能减缓糖尿病前期人群血清GLP-1的下降趋势、降低血糖水平,有氧运动对GLP-1的改善效果优于抗阻运动。展开更多
Background Although the insulinotropic role of glucagon-like peptide-1 （GLP-1） in type 2 diabetes mellitus has been substantiated, its role in cardioprotection remains largely unknown. This study aimed to determine ...Background Although the insulinotropic role of glucagon-like peptide-1 （GLP-1） in type 2 diabetes mellitus has been substantiated, its role in cardioprotection remains largely unknown. This study aimed to determine the effects of GLP-1 on injury of rats cardiac myocytes induced by hypoxia-reoxygenation （H/R） and the possible mechanisms. Methods The cultured neonatal rats cardiac myocytes were randomly divided into seven groups： the normal control group, the H/R group, the GLP-1＋H/R group, the GLP-1＋H/R＋UO126 （the p42/44 mitogen-activated protein kinase （MAPK） inhibitor） group, the GLP-1＋H/R＋LY294002 （phosphatidylinositol 3-kinase （PI3K） inhibitor） group, the H/R＋UO126 group, and the H/R＋LY294002 group. The lactate dehydrogenase （LDH） activity, apoptosis rate of cardiac myocytes, and caspase-3 activity were detected after the injury of H/R. Results Compared with the normal control group, the activity of LDH, cardiac myocyte apoptosis rate, and caspase-3 activity all increased significantly in the H/R group （P 〈0.01）. Compared with the H/R group, these three indices all decreased in the H/R＋GLP-1 group （P 〈0.01）. However, the changes of LDH activity, apoptosis rate, and caspase-3 activity were inhibited by LY294002 and UO126 respectively. Conclusions GLP-1 can directly act on cardiac myocytes and protect them from H/R injury mainly by inhibiting their apoptosis. Its mechanism may be through the PI3K-Akt pathway and the MAPK signaling pathway.展开更多
文摘目的观察有氧运动和抗阻运动对糖尿病前期人群胰高血糖素样肽1(GLP-1)及血糖水平的影响。方法105例糖尿病前期人群,随机分为A组34例、B组35例、C组36例。A组接受中等强度的有氧运动训练,B组接受抗阻运动训练,C组不进行运动干预,在干预前和干预第3、6、12、18个月,检测三组空腹血糖(FPG)、血清GLP-1、餐后2 h血糖(2 h PG),干预第18个月计算血清GLP-1变化率及血糖变化率。结果与干预前相比,A组干预第12、18个月时血清GLP-1水平升高,B组干预第6个月时降低、第18个月时升高,C组干预第6、12、18个月时降低(P均<0.05);与C组相比,A、B组干预第12、18个月时血清GLP-1水平升高(P均<0.05);与B组相比,A组干预第6、12个月时血清GLP-1水平升高(P均<0.05)。与干预前相比,A组干预第3、6、12、18个月时FPG水平降低,B组干预第3、18个月时降低,C组干预第18个月时升高(P均<0.05);与C组相比,A、B组干预第3、6、12、18个月时FPG水平降低(P均<0.05)。与干预前相比,C组干预第3个月时2 h PG水平升高(P<0.05);与C组相比,除B组干预第12个月外,A、B组干预各时点2 h PG水平降低(P均<0.05)。105例研究对象干预18个月后GLP-1变化率与FPG变化率和2 h PG变化率均呈负相关(r分别为-0.537、-0.314,P均<0.05)。结论有氧运动和抗阻运动均能减缓糖尿病前期人群血清GLP-1的下降趋势、降低血糖水平,有氧运动对GLP-1的改善效果优于抗阻运动。
文摘Background Although the insulinotropic role of glucagon-like peptide-1 （GLP-1） in type 2 diabetes mellitus has been substantiated, its role in cardioprotection remains largely unknown. This study aimed to determine the effects of GLP-1 on injury of rats cardiac myocytes induced by hypoxia-reoxygenation （H/R） and the possible mechanisms. Methods The cultured neonatal rats cardiac myocytes were randomly divided into seven groups： the normal control group, the H/R group, the GLP-1＋H/R group, the GLP-1＋H/R＋UO126 （the p42/44 mitogen-activated protein kinase （MAPK） inhibitor） group, the GLP-1＋H/R＋LY294002 （phosphatidylinositol 3-kinase （PI3K） inhibitor） group, the H/R＋UO126 group, and the H/R＋LY294002 group. The lactate dehydrogenase （LDH） activity, apoptosis rate of cardiac myocytes, and caspase-3 activity were detected after the injury of H/R. Results Compared with the normal control group, the activity of LDH, cardiac myocyte apoptosis rate, and caspase-3 activity all increased significantly in the H/R group （P 〈0.01）. Compared with the H/R group, these three indices all decreased in the H/R＋GLP-1 group （P 〈0.01）. However, the changes of LDH activity, apoptosis rate, and caspase-3 activity were inhibited by LY294002 and UO126 respectively. Conclusions GLP-1 can directly act on cardiac myocytes and protect them from H/R injury mainly by inhibiting their apoptosis. Its mechanism may be through the PI3K-Akt pathway and the MAPK signaling pathway.
