Glucose Supplementation Enhances Hypoxia-Induced Cardiac VEGF and PGC-1a Expression

Abstract

Listen

Translate article

PURPOSE: Altitude expedition is a popular recreational activity in Taiwan. However, hypoxia inhibits aerobic metabolism and increases glucose transport in cardiac muscle. This study determined the interactive effect of moderate hypoxia and glucose supplementation on vascular endothelial growth factor (VEGF) and glucose transporter (GLUT) expressions in heart. METHODS: Rats were randomly separated into control and glucose-supplemented groups, and both were subjected to 0, 30, 60, 120, and 240 min of 14% systemic hypoxia. The mRNA levels of glucose transporters and VEGF were measured by quantitative real-time PCR. AMP-activated protein kinase (AMPK) phosphorylation (Thr 172) and peroxisome proliferator activated receptor co-activator 1a (PGC-1a) mRNA were also determined. RESULTS: While hypoxia did not change cardiac glycogen levels in the control rats, glucose supplementation significantly elevated cardiac glycogen. GLUT1 and GLUT4 mRNA levels were not altered with hypoxia for both groups. VEGF mRNA levels were transiently elevated by hypoxia and returned to basal level within 240 min, and glucose supplementation led to greater VEGF mRNA increase above control level. Intriguingly, moderate hypoxia lowered Thr 172 phosphorylation of AMPK and suppressed HIF-1a mRNA level, whereas glucose supplementation partially blocked these changes. PGC1-a was continuously increased within the 240 min period of hypoxia only in the glucose-supplemented group. CONCLUSIONS: The current study demonstrates that glucose supplementation enhanced moderate hypoxia-induced increases in cardiac VEGF and PGC-1a mRNAs.