Dietary carbohydrate effects on some plasma organic acids and aspects of glucose metabolism in turkey poults

Immune system dysfunction during exposure to poult enteritis and mortality syndrome agents

“…The etiological agent(s) for PEMS are currently not known. Several studies have suggested metabolic disorders (such as altered pancreatic function and carbohydrate assimilation) as a possible cause of poor weight gain and perhaps early poult mortality (Phelps et al, 1987a;Donaldson and Christensen, 1994). In these reports hematological changes, such as decreased leukocyte counts, were also found to be correlated with early poult mortality (Phelps et al, 1987b).…”

The effect of reproduction phase of breeder hens, poult hatch time, and fatty acid supplementation of the breeder hen diet on livability, growth characteristics, and yolk and liver fatty acid composition in posthatch poults

“…It is possible that the increased wt of the liver of poults from mature hens is not due only to protein accretion, or hypertrophy. Glycogen content of the liver has been shown to increase dramatically during the initial postfeeding period of poults (Rosebrough etal., 1979;Turner, 1991;Donaldson and Christensen, 1994).…”

“…A review by shows that avians rely greatly upon hepatic gluconeogenesis following their removal from the incubator and until given access to feedstuffs. In an attempt to maintain plasma glucose and cellular energy levels, the poult depends upon gluconeogenesis, thereby producing high circulating levels of ^-hydroxybutyric acid and uric acid as byproducts of lipid and protein catabolism, respectively (Donaldson and Chrlstensen, 1994).…”

“…Wallace and Newsholme (1967) reported that several hepatic metabolic intermediates of glycolysis (carbohydrate-based metabolism) remain at levels lower than normal for several days PH in avians. In an attempt to maintain plasma glucose and cellular energy levels after hatching, the poult depends on gluconeogenesis, thereby producing high circulating levels of ^-hydroxybutyric acid and uric acid as byproducts of lipid and protein c^atabolism, respectively (Donaldson and Christensen. 1994).…”

“…As lipid catabolism ovenvhelms the mitochondrial Kreb's cycle, ketone bodies (^-hydroxybutyric acid) prevail to transport excess cellular acetyl-CoA to various organs throughout the body. An increase in ketone bodies tends to parallel an increase in uric acid concentrations in the fasting poult (Donaldson and Christensen, 1994). Uric acid is a byproduct of amino acid catabolism, whether the amino acids emanate from muscle, organs, yolk proteins, or circulating amino acids.…”