At present， the remodeling of host metabolism by viral infection has been studied in a variety of viruses. As a porcine intestinal pathogenic coronavirus， the interaction between porcine epidemic diarrhea virus （PEDV） and host metabolic system has not been reported. Studies have shown that angiotensin-converting enzyme 2 （ACE2） is involved in the regulation of glucose metabolism in the pathophysiological state of the body and plays a role in anti-PEDV infection. In order to explore the regulatory effect of PEDV infection on intestinal glucose metabolism in piglets and the possible role of ACE2， the relationship between ACE2， PEDV infection and intestinal glucose metabolism in piglets was clarified. In this experiment， healthy and PED piglets were used as the research objects. By collecting blood， duodenum， jejunum and ileum tissue samples were isolated and intercepted for the following experiments： 1） The expression of PEDV M gene and N gene and protein in each segment of small intestine was detected. 2） Detection of glucose and lactic acid in blood； western blot was used to detect the expression of glucose transporter SGLT-1 and GLUT-2 protein. 3） RT-qPCR was used to detect the gene transcription of key enzymes in glycolysis and TCA cycle pathway in each intestinal segment； 4） ELISA and Western blot were used to analyze the content of Ang1-7， AngII and the protein expression of ACE2 and MasR in each intestinal segment； 5） Spearman method was used to analyze the correlation between ACE2 and PEDV infection and glucose metabolism-related enzyme expression changes.The results showed that ： 1） There was M gene expression in the jejunum tissue of diarrhea piglets， and a positive band appeared at about 552 bp. PEDV-N protein was expressed in duodenum， jejunum and ileum of piglets， with the highest expression in jejunum （P<0.01）. 2） Compared with the normal healthy group， the contents of glucose （P<0.05） and lactic acid （P<0.01） in the blood of PEDV-infected piglets were significantly or extremely significantly increased； the protein expressions of SGLT-1 and GLUT-2 in duodenum and jejunum were significantly or extremely significantly up-regulated （P<0.05 & P<0.01）. 3） The results demonstrated that the transcriptional levels of key glycolytic enzymes （HK2， PFK， PKM， and LDHA） were markedly elevated （P<0.01） in the small intestinal tissues of PEDV-infected piglets， whereas those of key TCA cycle enzymes （CS， OGDH， and IDH） were significantly suppressed （P<0.05 & P<0.01）.； 4） In the small intestinal tissues of PEDV-infected piglets， the protein expressions of ACE2 and MasR were significantly down-regulated （P<0.01）. In conjunction with these changes， the level of Ang1-7 was markedly decreased （P<0.01）， whereas that of AngII was considerably increased （P<0.01）； 5） PEDV infection was positively correlated with SGLT-1， GLUT-2， HK2， PKM and PFK in the small intestine of piglets， and negatively correlated with ACE2-Ang1-7-MasR axis. The results suggest that PEDV infection in intestinal tissues activates glycolysis and suppresses the TCA cycle， concomitant with a weakened ACE2-mediated ACE2-Ang1-7-MasR pathway. This metabolic rewiring manifests as a Warburg effect， characterized by increased glucose uptake and lactate production. Furthermore， this PEDV-induced remodeling of intestinal glucose metabolism is negatively correlated with ACE2 expression.