The effects of dietary protein deficiency on dynamic aspects of protein metabolism in pregnant rats

Abstract

Effects of a protein deficient diet on several aspects of protein metabolism in pregnant rats have been investigated. The groups of rats investigated were normal pregnant, protein deficient pregnant, protein deficient virgin controls and virgin controls treated with progesterone or an oestrogen. Measurements include: body weight and food intake; tissue composition of protein, free amino nitrogen, RNA and DNA; amino acid oxidation; whole body protein turnover; rates of protein synthesis in skeletal muscle, liver, foetus and placenta; activity of cathepsin D, calcium-activated protease, alkaline protease(s) in skeletal muscle; serum levels of progesterone, oestradiol, insulin and corticosterone. 

The results indicate that muscle protein metabolism was more influenced by pregnancy than by the diet. Muscle protein synthesis showed anabolic and catabolic responses during pregnancy. The diet only modified the biphasic pattern towards a lower rate of synthesis during the catabolic phase. Proteolytic enzymes examined, do not seem to regulate the reduction in muscle protein mass observed during the catabolic phase. 

When administered to virgin rats, progesterone produced anabolic and oestrogen catabolic effects on muscle protein metabolism. However, serum levels of oestradiol showed a positive correlation with muscle protein mass in the catabolic phase of both normal and protein deficient pregnancy. The same-was true for corticosterone. Muscle protein content is probably regulated by serum level of amino acids, progesterone and insulin. 

Liver protein metabolism was more affected by the diet than by pregnancy. No biphasic pattern was observed in liver protein metabolism. It is postulated that this is because in pregnancy, liver, unlike muscle, is not primarily a protein reservoir and its size and protein composition depend on the quantity of nutrients and metabolites it has to process. Thus, reduced amino acid oxidation, may contribute to protein economy in protein deficient pregnancy but not in normal pregnancy.

The size of both placenta and foetus were reduced by the diet to 60% and 80% of the control values respectively. However, they both have a normal composition. Also, their rates of protein synthesis increased with the protein deficient diet. It is postulated that foetal weight loss was due to the combination of low protein and high carbohydrate content of the diet and foetal amino acid supply was reduced only while the effect of the meal on maternal circulation persisted. Whole body protein turnover was increased in normal pregnancy particularly in the catabolic phase. The diet suppressed this increase. 

It was clear that all organs in the pregnant body were affected by the diet including the foetus. Nevertheless, pregnancy in general is an anabolic state with particular adaptations which at times of stress (of the type studied in the, present thesis) can operate with remarkable efficiency to protect primarily the foetus against any severe effects such as death or metabolic distortion. The maternal tissues also enjoy some degree of protection; but, while pregnancy lasts, the foetus has a minimum parasitic effect on maternal tissues regardless of the protein content of the diet.

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