angiotensinogen and Protein-Energy-Malnutrition

We tested the hypothesis that maternal protein deprivation during gestation results in changes in expression of the systemic renin-angiotensin system in fetal mice. Fetal weight was decreased significantly as a consequence of 50% maternal protein deprivation during second half of gestation. In fetal liver, angiotensinogen protein expression was reduced significantly despite a significant increase in messenger RNA (mRNA). In fetal kidneys, both mRNA and protein levels of renin were increased significantly. In the lungs, we observed a decrease in both angiotensin-converting enzyme I and II mRNA expression, whereas protein expression of both isoforms was increased significantly. The fetal heart showed significant increases in expression of angiotensin II type 1 (AT-1) and type 2 (AT-2) receptors mRNA. Protein expression of AT-1 receptors increased, while that of AT-2 receptors decreased. We conclude that maternal low-protein diet during gestation leads to significant changes in expression of the systemic renin-angiotensin system in fetal mice and may be important in the genesis of hypertension in the adult.

Topics: Adaptor Proteins, Signal Transducing; Angiotensin-Converting Enzyme 2; Angiotensinogen; Animals; Dietary Proteins; Female; Fetal Growth Retardation; Gene Expression Regulation, Developmental; Hypertension; Mice; Peptidyl-Dipeptidase A; Pregnancy; Pregnancy Complications; Protein-Energy Malnutrition; Receptor, Angiotensin, Type 2; Renin; Renin-Angiotensin System; RNA, Messenger

To investigate whether catch-up growth after maternal malnutrition would favor the development of obesity in adulthood.. Pregnant rats were submitted to protein or calorie restriction during the course of gestation. During lactation, pups were protein-restricted, normally fed, or overfed [reduced litter size, control (C) diet]. At weaning, rats were transferred to chow or to a hypercaloric diet (HCD) known to induce obesity. Body weight, food intake, blood parameters, glucose tolerance, adipocyte cellularity, and adipose factors contributing to cardiovascular disease development were measured.. Protein and calorie restriction during gestation led to growth retardation at birth. If malnutrition was prolonged throughout lactation, adult body weight was permanently reduced. However, growth-retarded offspring overfed during the suckling period underwent a rapid catch-up growth and became heavier than the normally fed Cs. Offspring of calorie-restricted rats gained more weight than those of dams fed protein-restricted diet. Feeding an HCD postnatally amplified the effect of calorie restriction, and offspring that underwent catch-up growth became more obese than Cs. The HCD was associated with hyperphagia, hyperglycemia, hyperinsulinemia, glucose intolerance, insulin resistance, and adipocyte hypertrophy. The magnitude of effects varied depending on the type and the timing of early malnutrition. The expression of genes encoding factors implicated in cardiovascular disease was also modulated differently by early malnutrition and adult obesity.. Catch-up growth immediately after early malnutrition should be a key point for the programming of obesity.

Topics: Adipocytes; Adiponectin; Adipose Tissue; Angiotensinogen; Animals; Animals, Newborn; Body Weight; Diet; Eating; Female; Leptin; Litter Size; Male; Obesity; Plasminogen Activator Inhibitor 1; Pregnancy; Prenatal Exposure Delayed Effects; Protein-Energy Malnutrition; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Time Factors; Triglycerides