Current opinion in clinical nutrition and metabolic care
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Brain nutrient sensing allows a fine regulation of different physiological functions, such as food intake and blood glucose, related to energy homeostasis. Glucose sensing is the most studied function and a parallel has been made between the cellular mechanisms involved in pancreatic beta cells and neurons. ⋯ Recent observations in brain nutrient sensing indicate subtle mechanisms, with different cellular and molecular mechanisms involved. This fact would explain the discrepancies reported in the expression of different proteins (glucose transporters, hexokinases, channels). Astrocytes may be involved in one type of response, thus adding a new level of complexity.
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The current review focuses on recent studies, both clinical and from basic sciences, which approach possible pathomechanisms of critical illness myopathy in order to better derive potential clinical strategies for a preventive or curative clinical setting. Trends and concepts of clinical diagnosis and handling will be evaluated and their implications for muscle physiology and nutritional/metabolic intervention discussed. ⋯ The search for pathomechanisms is an important task for both clinical and basic sciences. Targets for treatment or prevention of critical illness myopathy include systemic inflammatory response, increased proteolysis and reduced antioxidative capacitance in critically ill patients.
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Curr Opin Clin Nutr Metab Care · May 2006
ReviewGlutamine: the first clinically relevant pharmacological regulator of heat shock protein expression?
It is well known that enhanced heat shock protein expression protects organisms against morbidity and mortality following experimental injury/illness. Presently, chemical/gene therapy based laboratory methods of enhancing heat shock protein expression are impractical for clinical application. Our laboratory has shown glutamine enhances heat shock protein expression following models of experimental illness/injury. The purpose of this review is to examine recent data supporting the use of glutamine as a clinically relevant enhancer of heat shock protein expression. ⋯ Currently, extensive data support glutamine as a gene level regulator of heat shock protein expression. Glutamine depletion, following critical illness/injury, is likely to lead to a state in which organisms are unable to induce heat shock proteins appropriately. Further, pharmacologic supplementation of glutamine potentiates the heat shock protein response prior to and following a stress. Pharmacologic trials utilizing glutamine to enhance heat shock proteins in humans are indicated.