The major metabolic defects apparent in the newborn pig are: (1) low level of phosphorylase potentially decreasing the rate of production of glucose from glycogen stores, although this may not be of particular physiological importance since the enzyme activity can be readily increased (e.g., by starvation, catecholamine injection or decapitation); (2) defective gluconeogenic capacity which limits the supply of glucose available for those animals exposed to any stressful situation, e.g., starvation, weakness or cold, and takes 1 to 2 days to be remedied; (3) a deficient hepatic mitochondrial number which limits the use of carbohydrate as well as fatty acid for energy production and presumably as a result of reduced ATP synthesis many biosynthetic processes as well; (4) a small amount of body fat, only gradually increased, mostly by dietary intake, which impairs both thermoinsulation and the quantitative contribution of a major energy store, (5) although not investigated in swine, a number of defects in amino acid metabolism which in other species impair transformation into carbon skeletons and, consequently, limit a source of substrate for gluconeogenesis. Other questions of protein and amino acid metabolism are even less well known. The newborn piglet is essentially dependent on large carbohydrate stores, extremely limited lipid stores and dietary intake. For the weak pig, these metabolic defects may be disastrous.
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H. J. Mersmann (1974) studied this question.