Brain glucose overexposure and lack of acute metabolic flexibility in obesity and type 2 diabetes: a PET-[ F]FDG study in Zucker and ZDF rats

Brain glucose exposure may complicate diabetes and obesity. We used positron emission tomography with 18F-fluorodeoxyglucose in Zucker obese, diabetic, and control rats to determine the contributions of blood glucose mass action versus local mechanisms in regulating central glucose disposal in faste...

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Bibliographic Details
Published in:Journal of cerebral blood flow and metabolism 2010-05, Vol.30 (5), p.895-899
Main Authors: Liistro, Tiziana, Guiducci, Letizia, Burchielli, Silvia, Panetta, Daniele, Belcari, Nicola, Pardini, Silvia, Del Guerra, Alberto, Salvadori, Piero A, Iozzo, Patricia
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood Glucose - metabolism
Brain - anatomy & histology
Brain - metabolism
Brief Communication
Diabetes Mellitus, Type 2 - diagnostic imaging
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - physiopathology
Fasting
Fluorodeoxyglucose F18 - metabolism
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
Male
Medical sciences
Nervous system (semeiology, syndromes)
Neurology
Obesity - diagnostic imaging
Obesity - metabolism
Obesity - physiopathology
Positron-Emission Tomography
Rats
Rats, Zucker
Vascular diseases and vascular malformations of the nervous system
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Summary:Brain glucose exposure may complicate diabetes and obesity. We used positron emission tomography with 18F-fluorodeoxyglucose in Zucker obese, diabetic, and control rats to determine the contributions of blood glucose mass action versus local mechanisms in regulating central glucose disposal in fasted and acutely glucose-stimulated states, and their adaptations in obesity and diabetes. Our study data indicate that brain glucose uptake is dependent on both local and mass action components, and is stimulated by acute glucose intake in healthy rats. In diseased animals, the organ was chronically overexposed to glucose, due to high fasting glucose uptake, almost abolishing the physiologic response to glucose loading.
ISSN:0271-678X
1559-7016
DOI:10.1038/jcbfm.2010.27