PDF(Pubmed)
Abstract：
UNASSIGNED: To investigate the specific effects of s odium-glucose transporter 2 inhibitor (SGLT2i) on cardiac energy metabolism.
UNASSIGNED: A systematic literature search was conducted in eight databases. The retrieved studies were screened according to the inclusion and exclusion criteria, and relevant information was extracted according to the purpose of the study. Two researchers independently screened the studies, extracted information, and assessed article quality.
UNASSIGNED: The results of the 34 included studies (including 10 clinical and 24 animal studies) showed that SGLT2i inhibited cardiac glucose uptake and glycolysis, but promoted fatty acid (FA) metabolism in most disease states. SGLT2i upregulated ketone metabolism, improved the structure and functions of myocardial mitochondria, alleviated oxidative stress of cardiomyocytes in all literatures. SGLT2i increased cardiac glucose oxidation in diabetes mellitus (DM) and cardiac FA metabolism in heart failure (HF). However, the regulatory effects of SGLT2i on cardiac FA metabolism in DM and cardiac glucose oxidation in HF varied with disease types, stages, and intervention duration of SGLT2i.
UNASSIGNED: SGLT2i improved the efficiency of cardiac energy production by regulating FA, glucose and ketone metabolism, improving mitochondria structure and functions, and decreasing oxidative stress of cardiomyocytes under pathological conditions. Thus, SGLT2i is deemed to exert a benign regulatory effect on cardiac metabolic disorders in various diseases.
UNASSIGNED: https://www.crd.york.ac.uk/, PROSPERO (CRD42023484295).
UNASSIGNED: A systematic literature search was conducted in eight databases. The retrieved studies were screened according to the inclusion and exclusion criteria, and relevant information was extracted according to the purpose of the study. Two researchers independently screened the studies, extracted information, and assessed article quality.
UNASSIGNED: The results of the 34 included studies (including 10 clinical and 24 animal studies) showed that SGLT2i inhibited cardiac glucose uptake and glycolysis, but promoted fatty acid (FA) metabolism in most disease states. SGLT2i upregulated ketone metabolism, improved the structure and functions of myocardial mitochondria, alleviated oxidative stress of cardiomyocytes in all literatures. SGLT2i increased cardiac glucose oxidation in diabetes mellitus (DM) and cardiac FA metabolism in heart failure (HF). However, the regulatory effects of SGLT2i on cardiac FA metabolism in DM and cardiac glucose oxidation in HF varied with disease types, stages, and intervention duration of SGLT2i.
UNASSIGNED: SGLT2i improved the efficiency of cardiac energy production by regulating FA, glucose and ketone metabolism, improving mitochondria structure and functions, and decreasing oxidative stress of cardiomyocytes under pathological conditions. Thus, SGLT2i is deemed to exert a benign regulatory effect on cardiac metabolic disorders in various diseases.
UNASSIGNED: https://www.crd.york.ac.uk/, PROSPERO (CRD42023484295).
摘要：
■研究葡萄糖转运蛋白2抑制剂（SGLT2i）对心脏能量代谢的具体影响。
■在8个数据库中进行了系统的文献检索。根据纳入和排除标准对检索到的研究进行筛选，并根据研究目的提取相关信息。两名研究人员独立筛选了这些研究，提取的信息，并评估文章质量。
■34项纳入研究（包括10项临床研究和24项动物研究）的结果表明，SGLT2i抑制心脏葡萄糖摄取和糖酵解，但在大多数疾病状态下促进脂肪酸（FA）代谢。SGLT2i上调酮代谢，改善了心肌线粒体的结构和功能，在所有文献中都能减轻心肌细胞的氧化应激。SGLT2i增加了糖尿病（DM）中的心脏葡萄糖氧化和心力衰竭（HF）中的心脏FA代谢。然而,SGLT2i对DM中心脏FA代谢和HF中心脏葡萄糖氧化的调节作用因疾病类型而异，阶段,和SGLT2i的干预持续时间。
■SGLT2i通过调节FA提高了心脏能量产生的效率，葡萄糖和酮代谢，改善线粒体结构和功能，在病理条件下降低心肌细胞的氧化应激。因此，SGLT2i被认为对各种疾病中的心脏代谢紊乱发挥良性调节作用。
■https://www.crd.约克。AC.英国/,PROSPERO（CRD42023484295）。
■在8个数据库中进行了系统的文献检索。根据纳入和排除标准对检索到的研究进行筛选，并根据研究目的提取相关信息。两名研究人员独立筛选了这些研究，提取的信息，并评估文章质量。
■34项纳入研究（包括10项临床研究和24项动物研究）的结果表明，SGLT2i抑制心脏葡萄糖摄取和糖酵解，但在大多数疾病状态下促进脂肪酸（FA）代谢。SGLT2i上调酮代谢，改善了心肌线粒体的结构和功能，在所有文献中都能减轻心肌细胞的氧化应激。SGLT2i增加了糖尿病（DM）中的心脏葡萄糖氧化和心力衰竭（HF）中的心脏FA代谢。然而,SGLT2i对DM中心脏FA代谢和HF中心脏葡萄糖氧化的调节作用因疾病类型而异，阶段,和SGLT2i的干预持续时间。
■SGLT2i通过调节FA提高了心脏能量产生的效率，葡萄糖和酮代谢，改善线粒体结构和功能，在病理条件下降低心肌细胞的氧化应激。因此，SGLT2i被认为对各种疾病中的心脏代谢紊乱发挥良性调节作用。
■https://www.crd.约克。AC.英国/,PROSPERO（CRD42023484295）。
