2006/07/26 by Hongxia Lei, Rolf Gruetter · 37 citations
Chemistry · Medicine · #Advanced MRI Techniques and Applications #Advanced NMR Techniques and Applications #Biology #Blood–brain barrier #Carbohydrate #Carbohydrate metabolism #Central nervous system #Chemistry #Endocrinology #GLUT1 #Glucose transporter #Glycogen #In vivo #Insulin #Internal medicine #Medicine #Neurological disorders and treatments
paper · open access · doi:10.1111/j.1471-4159.2006.04115.x
published in Journal of Neurochemistry 99(1), 260-268 (Wiley)
openalex publication_date 2006/07/26 · openalex created_date 2016/06/24 · openalex updated_date 2026/08/01
While chronic hypoglycaemia has been reported to increase unidirectional glucose transport across the blood-brain barrier (BBB) and to increase GLUT1 expression at the endothelium, the effect on steady-state brain d-glucose and brain glycogen content is currently unknown. Brain glucose and glycogen concentrations were directly measured in vivo using localized 13C magnetic resonance spectroscopy (MRS) following 12-14 days of hypoglycaemia. Brain glucose content was significantly increased by 48%, which is consistent with an increase in the maximal glucose transport rate, Tmax, by 58% compared with the sham-treated animals. The localized 13C NMR measurements of brain glucose were directly validated by comparison with biochemically determined brain glucose content after rapid focused microwave fixation (1.4 s at 4 kW). Both in vivo MRS and biochemical measurements implied that brain glycogen content was not affected by chronic hypoglycaemia, consistent with brain glucose being a major factor controlling brain glycogen content. We conclude that the increased glucose transporter expression in chronic hypoglycaemia leads to increased brain glucose content at a given level of glycaemia. Such increased brain glucose concentrations can result in a lowered glycaemic threshold of counter-regulation observed in chronic hypoglycaemia.