QUANTITATIVE ASPECTS OF GLUCOSE AND GLUTAMINE-METABOLISM BY INTESTINAL-CELLS

Gut fuel utilisation has several unique features. Arterial and luminal fuels provide nutrition for the enterocyte, the former being of more importance. This factor, and the heterogeneity of cell types within th e gut makes it difficult to define its fuel utilisation. Metabolic con trol logic suggests that modulation of the maximal activity of any pat hway resides in those enzymes that operate in vivo at rates far below their maximal capacity and that catalyse non-equilibrium reactions. On this basis, although enterocyte hexokinase activity is much higher th an in other 'glycolytic' cells (for example, brain), potentially high rates of glucose utilisation are modulated by substrate cycling of glu cose 6-phosphate back to glucose through glucose 6-phosphatase. Glutam ine metabolism proceeds by glutaminase to produce glutamate, which may then be transaminated (aspartate-aminotransferase and alanine-amino t ransferase) to produce alpha-ketoglutarate, alanine, and aspartate. Th e end products of glutamine metabolism by incubated gut preparations i n vitro (mainly alanine), suggests that enterocytes, not immune cells, are responsible for most gut glutamine metabolism. High flux rates of glucose and glutamine metabolism in the enterocyte may result from th e need for de novo synthesis of purines and pyrimidines and ribose sug ars for nucleic acid synthesis. Sepsis reduces rates of glucose and gl utamine metabolism, perhaps to preserve the increased consumption of t hese fuels by activated lymphocytes and macrophages in the gut wall.