Short-term caloric restriction in db/db mice improves myocardial function and increases high molecular weight (HMW) adiponectin.
Short-term caloric restriction in db/db mice improves myocardial function and increases high molecular weight (HMW) adiponectin.
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db/db 小鼠的短期热量限制可改善心肌功能并增加高分子量 (HMW) 脂联素。
DOI：
10.1016/j.ijcme.2016.10.002
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Colucci,WilsonS
中科院分区：
文献类型：
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作者：
Xu,XJulia;Babo,Erma;Qin,Fuzhong;Croteau,Dominique;Colucci,WilsonS
背景肥胖和代谢综合征导致代谢性心脏病（MHD）的发展，其特征是左心室肥厚（LVH）、舒张功能障碍和线粒体ROS增加。热量限制 (CR) 是一种营养干预措施，可预防肥胖、糖尿病和心血管疾病。健康的脂肪组织通过释放脂联素等脂肪因子来保护心脏。我们测试了 CR 可以改善 MHD 的假设，并且它与改善脂肪组织功能相关，这反映在高分子量 (HMW) 脂联素和 AMP 激活蛋白激酶 (AMPK) indb/dbmice 循环水平的增加。方法对遗传性 obesedb/dband Leandb/+ 雄性小鼠喂食 30% CR 的任意肿瘤细胞 5 周。在研究期结束时，进行超声心动图以评估舒张功能。采集血液、心脏和附睾脂肪垫用于线粒体研究、ELISA 和蛋白质印迹分析。结果CR 逆转了 LVH 的发展，预防了舒张功能障碍，并减少了小鼠心脏线粒体 H2O2indb/db（与 ad lib 相比）。这些对心脏的有益作用与 HMW 脂联素循环水平的增加有关。此外，CR 增加了 db/db 小鼠白色脂肪组织中的 AMPK 和 eNOS 激活，但在心脏中却没有。结论这些发现表明，即使是短期 CR 也能保护心脏免受 MHD 的影响。 CR 对心脏的有益作用是否与改善脂肪组织功能有关，值得进一步研究。
BackgroundObesity and metabolic syndrome lead to the development of metabolic heart disease (MHD) that is characterized by left ventricular hypertrophy (LVH), diastolic dysfunction, and increased mitochondrial ROS. Caloric restriction (CR) is a nutritional intervention that protects against obesity, diabetes, and cardiovascular disease. Healthy adipose tissue is cardioprotectiveviareleasing adipokines such as adiponectin. We tested the hypothesis that CR can ameliorate MHD and it is associated with improved adipose tissue function as reflected by increased circulating levels of high molecular weight (HMW) adiponectin and AMP-activated protein kinase (AMPK) indb/dbmice.MethodsGenetically obesedb/dband leandb/+ male mice were fed eitherad libitumor subjected to 30% CR for 5 weeks. At the end of the study period, echocardiography was carried out to assess diastolic function. Blood, heart, and epididymal fat pads were harvested for mitochondrial study, ELISA, and Western blot analyses.ResultsCR reversed the development of LVH, prevented diastolic dysfunction, and decreased cardiac mitochondrial H2O2indb/db(vs. ad lib) mice. These beneficial effects on the heart were associated with increased circulating level of HMW adiponectin. Furthermore, CR increased AMPK and eNOS activation in white adipose tissue ofdb/dbmice, but not in the heart.ConclusionsThese findings indicate that even short-term CR protects the heart from MHD. Whether the beneficial effects of CR on the heart could be related to the improved adipose tissue function warrants future investigation.