HIGH FAT DIET =>> REDUCED GLUCOSE for BRAIN ==> Slow Learning and impaired memory.
How high fat junk diet reduces potential of your brain to support mind? And in turn, shape you as future moron.
A high-fat diet of three days in mice leads to a reduction in the amount of glucose that reaches the brain.
High-fat-content foods throw our bodies out of kilter. Obesity and diseases such as type 2 diabetes can be the result. But what does a high-fat diet actually do to our brain? Scientists from the Max Planck Institute for Metabolism Research in Cologne have looked into the brains of mice to understand how obesity and diabetes develop.
Myeloid-Cell-Derived VEGF Maintains Brain Glucose Uptake and Limits Cognitive Impairment in Obesity
“A high-fat diet reduces the uptake of blood glucose into the brain in as little as three days. So the brain is starving, even though the mice are consuming a lot of calories daily. Responsible for this is the protein GLUT-1, which is the most important glucose transporter at the blood-brain barrier,” explained Alexander Jais, author of the study. Possible triggers for the reduction of the GLUT-1 transporter are free saturated fatty acids that have a toxic effect on the cells of the blood-brain barrier. The brain lacks glucose in significant areas: the hypothalamus, which controls metabolism, and the cerebral cortex, responsible for learning and memory.
- •Acute high-fat feeding suppresses GLUT1 expression at the blood-brain barrier (BBB)
- •Macrophages at the BBB increase VEGF expression upon prolonged HFD feeding
- •Inducible GLUT1 deletion in brain endothelial cells leads to increased VEGF secretion
- •Myeloid-cell-specific disruption of VEGF impairs cognitive function in obesity
High-fat diet (HFD) feeding induces rapid reprogramming of systemic metabolism. Here, we demonstrate that HFD feeding of mice downregulates glucose transporter (GLUT)-1 expression in blood-brain barrier (BBB) vascular endothelial cells (BECs) and reduces brain glucose uptake. Upon prolonged HFD feeding, GLUT1 expression is restored, which is paralleled by increased expression of vascular endothelial growth factor (VEGF) in macrophages at the BBB. In turn, inducible reduction of GLUT1 expression specifically in BECs reduces brain glucose uptake and increases VEGF serum concentrations in lean mice. Conversely, myeloid-cell-specific deletion of VEGF in VEGFΔmyel mice impairs BBB-GLUT1 expression, brain glucose uptake, and memory formation in obese, but not in lean mice. Moreover, obese VEGFΔmyel mice exhibit exaggerated progression of cognitive decline and neuroinflammation on an Alzheimer’s disease background. These experiments reveal that transient, HFD-elicited reduction of brain glucose uptake initiates a compensatory increase of VEGF production and assign obesity-associated macrophage activation a homeostatic role to restore cerebral glucose metabolism, preserve cognitive function, and limit neurodegeneration in obesity.