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Amino adds gluconeogenesis

Figure 8.13 The central role of transdeamination in metabolism of amino adds and further metabolism of the oxoacids in the liver. The box contains the reactions for conversion of the amino acids to their respective oxoacids. Processes are as follows (1) digestion of protein in the intestine and absorption of resultant amino acids, (2) degradation of endogenous protein to amino acids (primarily but not exclusively muscle protein), (3) protein synthesis, (4) conversion of amino acid to other nitrogen-containing compounds (see Table 8.4), (5) oxidation to CO2, (6) conversion to glucose via gluconeogenesis, (7) conversion to fat. Figure 8.13 The central role of transdeamination in metabolism of amino adds and further metabolism of the oxoacids in the liver. The box contains the reactions for conversion of the amino acids to their respective oxoacids. Processes are as follows (1) digestion of protein in the intestine and absorption of resultant amino acids, (2) degradation of endogenous protein to amino acids (primarily but not exclusively muscle protein), (3) protein synthesis, (4) conversion of amino acid to other nitrogen-containing compounds (see Table 8.4), (5) oxidation to CO2, (6) conversion to glucose via gluconeogenesis, (7) conversion to fat.
Protein degradation and amino acid metabolism are highly elevated in the diabetic, because the stimulatory effect of insulin on protein synthesis is nonexistent and the relative excess of glucagon and glucocorticoids causes protein breakdown to continue. Indeed, muscle wasting is a cardinal symptom of the untreated diabetic. Insulin also inhibits amino add release into the bloodstream, and this may be a reason a moderate rise in plasma amino add levels is observed in the diabetic. Such increased amino adds are largely of the branched-chain type, and alanine levels are in fact lower than normal. Nevertheless, alanine uptake by the liver is twice that of the normal individual, and it continues to be a major actor in the gluconeogenesis process. [Pg.589]

The energy supply required by cirrhotic patients is achieved by mobihzing fats the patient s fatty tissue is reduced and body weight decreases the continuing energy requirement is met by the breakdown of muscle proteins with the result that amino adds are formed, which in turn are used for gluconeogenesis in the liver. Catabolism increases and leads to muscular atrophy, which is known as wasting syndrome. (29, 32, 62, 86, 104, 116, 117, 126)... [Pg.728]

A. When insulin is low and glucagon is high, the carbon skeletons of amino adds derived from muscle protein are converted to glucose in the liver by gluconeogenesis. The amino add... [Pg.318]

Figure 5.20 The entry of amino add carbon skeletons into the citric acid cycle for gluconeogenesis. Figure 5.20 The entry of amino add carbon skeletons into the citric acid cycle for gluconeogenesis.
Pyridoxine is involved as a co-factor coenzyme in about 100 enzyme systems. Thus, in addition to the reactions mentioned above, it is required for glycogen phosphoryl-ase, which catalyses the release of glucose from stored glycogen, haemoglobin biosynthesis, the generation of glucose from amino acids (gluconeogenesis), the biosynthesis of niacin from tryptophan and nucleic add biosynthesis. [Pg.531]


See other pages where Amino adds gluconeogenesis is mentioned: [Pg.155]    [Pg.322]    [Pg.597]    [Pg.729]    [Pg.208]    [Pg.423]    [Pg.444]    [Pg.754]    [Pg.231]    [Pg.331]    [Pg.34]    [Pg.364]    [Pg.1777]    [Pg.31]    [Pg.763]    [Pg.308]    [Pg.553]   
See also in sourсe #XX -- [ Pg.208 ]




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