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. 2012 Mar 8;4:4. doi: 10.3389/fnene.2012.00004

Figure 1.

Figure 1

A conceptual diagram that shows key physiological mechanisms, which fulfill the brain-pull function of cerebral insulin suppression (CIS). The flux of glucose is either directed to the brain or to muscle and fat. If neuronal ATP concentrations fall, activation of neurons in the amygdala, in the ventromedial hypothalamus (VMH), and in the paraventricular nucleus (PVN) occurs, which in turn activates the sympathetic nervous system and the hypothalamus pituitary adrenal system (SNS and HPA). Both the SNS and the HPA system suppress insulin release from pancreatic beta cells, thereby decreasing glucose transporter 4 (GLUT-4) mediated glucose uptake into muscle and fat. In this way the brain limits glucose uptake in peripheral tissues and procures itself with glucose on demand. Finally, the CIS-brain-pull system is hierarchically organized and adaptive. The strength of the central glucocorticoid feedback determines whether the CIS-brain-pull system reacts in a high or low reactive manner. ACTH, Adrenocorticotropic hormone; E, epinephrine; NE, norepinephrine.