Journal of Biosciences

, 44:19 | Cite as

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

  • R CarbóEmail author
  • E Rodríguez


Among the last consequences of metabolic syndrome are cardiovascular complications such as infarcts. The hypoxic heart switches its lipid-based metabolism to carbohydrates, and a glucose-insulin-potassium (GIK) solution can be the metabolic support to protect the organ. Due to the physiology and cardiac risks associated with the metabolic syndrome, we studied the effect 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 rats for 24 weeks. The GIK solution’s effect on myocyte glucose uptake during hypoxia and oxygenation was observed using a colorimetric method, and Western blot technique visualized the GLUT participation. Oxygenated control myocytes consumed 1.7 ± 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 metabolic syndrome myocytes uptake was similar to control cells but achieved by both carriers in oxygenation and hypoxia. Also, the GIK solution had a better response in both oxygenation (113%) and hypoxia (71%). Despite the metabolic energy disorders of this 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.


Cardiac myocytes GIK solution glucose transporters metabolic syndrome model 





glucose transporters


homeostasis model assessment



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Copyright information

© Indian Academy of Sciences 2019

Authors and Affiliations

  1. 1.Departamento de Biomedicina CardiovascularInstituto Nacional de Cardiología ‘Ignacio Chávez’Ciudad de MéxicoMéxico
  2. 2.Laboratorio de Biología Celular, Departamento de FisiologíaInstituto Nacional de Cardiología ‘Ignacio Chávez’Ciudad de MéxicoMéxico

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