The capacity of foetal and neonatal liver to oxidize short-, medium- and long-chain fatty acids was studied in the guinea pig. Liver mitochondria from foetal and newborn animals were unable to synthesize ketone bodies from octanoate, but octanoylcarnitine and palmitoylcarnitine were readily ketogenic. The ketogenic capacity at 24 h after birth was as high as in adult animals. Hepatocytes isolated from term animals were unable to oxidize fatty acids, but at 6 h after birth production of 14CO2, acid-soluble products and acetoacetate from 1-14C-labelled fatty acids was 40-50% of the rates at 24 h. At 12 h of age these rates had already reached the 24 h values and did not change during suckling in the first week of life. The activities of hepatic fatty acyl-CoA synthetases, which were minimal in the foetus or at term, increased to maximal values in 12-24 h. The data show that the capacity for beta-oxidation and ketogenesis develops maximally in this species during the first 6-12 h after birth, and appears to be partly dependent on the development of fatty acid-activating enzyme.

No abstract

Studies were carried out to identify the minimum levels of protein (casein) needed in the diet in order to prevent or reverse the deficits in brain enzymes previously found with protein deficiency. Groups of weanling albino rats were fed diets containing variable amounts of protein (5, 8, 10. 15 or 20 per cent in experiment I, and 5, 6,7, 8 or 20 per cent in experiment 11) for 5 or 10 weeks. Deficits in brain wt and brain glutamate dehydrogenase and decarboxylase were found to be prevented by a diet containing 8 per cent or more of protein, although for optimum growth 15 per cent protein in the diet was found to be necessary. Groups of rats were fed a 5 or 20% protein diet for 10 weeks after which the 5% protein animals were either continued on the diet for another 10 weeks or changed to one containing 8, 10, 15 or 20% protein. The brain enzyme deficits found with the 5% protein diet were found to be fully reversed by feeding a 10% protein diet during rehabilitation.

A tobacco leaf protein concentrate (TLPC) from bidi tobacco leaves was prepared by a heat coagulation method which contained 52% protein and was free from nicotine and polyphenols. When TLPC was fed to weanling wistar albino rats to supplement 25% of the dietary protein, the growth of the animals was found to be comparable to control animals. Reproductive performance of male and female rats fed the TLPC supplemented diet was normal and no histopathological changes were seen in their tissues.

Gluconeogenesis from (U-¹⁴C)-lactate occurred in hepatocytes prepared from term fetuses which lack cytosolic phosphoenolpyruvate carboxykinase and was almost completely inhibited by 3-mercaptopicolinate but was relatively insensitive to amino-oxyacetate. 12 h after birth when up to 32% of the total hepatic phosphoenolpyruvate carboxykinase activity was detectable in the cytosol, glucose synthesis was increased 4.4-fold in hepatocytes from fasted neonates and was partially (37%) sensitive to amino-oxyacetate. In livers of fasted 24-hour-old neonates total phosphoenolpyruvate carboxykinase activity was distributed between the mitochondria and the cytosol in the ratio of 60:40. In hepatocytes prepared from such animals, amino-oxyacetate inhibited glucose synthesis by about 56%, suggesting that up to half of the carbon flow from lactate to glucose was via the formation of phosphoenolpyruvate in the mitochondria. These studies indicate an important role for mitochondrial phosphoenolpyruvate carboxykinase in neonatal gluconeogenesis.