Brain alterations, energy metabolism

Phosphorus MRS studies of depressed subjects strongly indicate that this disorder arises from altered brain energy metabolism 944 Hydrogen MRS has revealed unique and consistent metabolic characteristics in the brains of patients with probable AD 944 Hydrogen and phosphorus MRS have proven to be useful tools in the characterization of several epilepsies 944... 

Pettegrew, J. W., Keshavan, M. S., Panchalingam, K. et al. Alterations in brain high-energy phosphate and membrane phospholipid metabolism in first-episode, drug-naive schizophrenics. A pilot study of the dorsal prefrontal cortex by in vivo phosphorus 31 nuclear magnetic resonance spectroscopy. Arch. Gen. Psychiat. 48 563-568,1991. 

Another important difficulty in the evaluation of the correct activity values for enzymes involved in energy metabolism in neurons resides in the fact that opposite processes may occur simultaneously, like the reduction of neuronal metabolism and compensatory enhancement in glial activity. The altered activities of some glycolytic enzymes in brain homogenates represent a net-effect, and it is unclear how the energy state (ATP level) of the neurons is perturbed if the metabolic activation is... 

The motion of the body-mass set point had led scientists to postulate that there must be a homeostatic signal from the fuel stores of the body to the brain. This has been referred to as a lipostat which can communicate the level of fuel stores to the brain to alter the appetite and metabolic rate control centers in the brain. In 1995, the hormone leptin was discovered. It is secreted by white adipose tissue at a rate that is proportional to the size of the fat reserves. The hypothalamus in the brain influences energy intake and expenditure, and it possesses receptors for leptin. Binding of leptin reduces food intake and increases whole body BMR. 

Alteration in mental status occurring in patients with systanic sepsis always carries a serious prognosis. The mechanisms of impaired brain function are poorly understood and are probably multifactorial. Considerations include hypoxia, ischemia, mitochondrial dysfunction and anaerobic cerebral energy metabolism, blood-brain barrier dysfunction or impaired transporter function, cerebral edema, toxins like ammonia or endotoxins, and last but not least, clinical use of cerebral depressants and sedatives in severely ill patients. In patients with multi-organ failure, clearance of common short-acting sedatives can become prolonged, resulting in severe and protracted alteration of mentation. 

Altered glycolysis via inhibition of pyruvate kinase and other enzymes involved in brain energy metabolism [36]... 

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