Hypometabolic state

Fat is generally considered an ideal fuel for this kind of hypometabolic state because it supplies glycerol as a precursor for glucogenesis (glucose usually remains the main fuel for cells of the CNS, for RBCs, and for some cells in the kidney, to mention three well-known examples). Additionally, fat catabolism yields metabolic end products no more noxious than C02 and... 

Amino acids (and precursor proteins) also are frequently used to variable degree under hypometabolic states, such as starvation, estivation, or hibernation, as sources of glucose precursors and as direct energy sources. In addition to C02 and H20, amino acid catabolism of course releases ammonia, which in hibernation or in estivation creates added metabolic problems. The amount of regulatory and metabolic machinery that organisms have invested in order to deal with ammonia indicates how serious ammonia-associated problems actually are thus it is important to examine this metabolic end product in some detail. 

Yoshino A., Hovda D. A., Kawamata T., Katayama Y., and Becker D. P. (1991) Dynamic changes in local cerebral glucose utilization following cerebral conclusion in rats evidence of a hyper- and subsequent hypometabolic state. Brain Res. 561, 106-119. 

Phosphocreatine can supply phosphate to convert the breakdown product ADP back to ATP. Therefore, Cr is increased in hypometabolic states and decreased in hyper-metabolic states (Castillo et ai, 1996). In normal spectra, Cr is located to the immediate right of Cho and is the third-highest peak. Because this peak at 3.0 ppm remains fairly constant at 6-12 mM in normal brain and even in diseased states, it may be used as concentration reference. 

Taking this information together with the imaging data (MRI-CBV) maps demonstrating a hypermetabolic phase in very young AD and Down-syndrome mice and a later age-dependent hypometabolism (Moreno et al., 2006, 2007), it seems plausible to propose that this series of events leads to a biphasic neuronal disconnection syndrome, with an initial hyperactive state followed by subsequent synaptic failure phase (Fig. 12). 

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