A glucose-insulin-potassium solution improves glucose intake in hypoxic cardiomyocytes by a differential expression of glucose transporters in a metabolic syndrome model

ABSTRACT

Among the last consequences of metabolic syndrome are cardiovascular complications such as infarcts. The hypoxic heartswitches its lipid-based metabolism to carbohydrates, and a glucose-insulin-potassium (GIK) solution can be the metabolicsupport to protect the organ. Due to the physiology and cardiac risks associated with the metabolic syndrome, we studied theeffect of GIK solution during hypoxia in a metabolic syndrome model by observing the participation of glucose transporters(GLUTs). The metabolic syndrome characteristics were established by giving a 30% sucrose drinking solution to Wistar ratsfor 24 weeks. The GIK solution’s effect on myocyte glucose uptake during hypoxia and oxygenation was observed using acolorimetric method, and Western blot technique visualized the GLUT participation. Oxygenated control myocytes consumed1.7 ± 0.2 µg of glucose per gram of fresh tissue per hour using the GLUT1, and during hypoxia, they incorporated 41.1%more glucose by GLUT1 and GLUT4. The GIK solution improved glucose uptake in oxygenation by 70.5% through GLUT1.In hypoxia, the uptake was 21% more than the hypoxic control group and by both GLUTs too. Oxygenated metabolicsyndrome myocytes uptake was similar to control cells but achieved by both carriers in oxygenation and hypoxia. Also, theGIK solution had a better response in both oxygenation (113%) and hypoxia (71%). Despite the metabolic energy disorders ofthis syndrome, the GIK solution protects cardiomyocytes, in conditions of hypoxia, through the modulation of both GLUTs.So, this solution can be considered a useful resource during a heart attack in cases of metabolic syndrome.