Effects of undernutrition and protein malnutrition on brain chemistry of rats.
The present study was undertaken to assess the effects of different degrees of nutritional restrictions during fetal life, suckling, and after weaning on the chemical composition of the brain. At 42 days of age, the rats were killed, and the brains were processed for analyses. The rats exposed to severe protein malnutrition after weaning had lower brain weights than those on controls. The brain seems to be resistant to the effects of moderate protein malnutrition imposed during suckling or after weaning. Thus, the brain is either resistant to the effects of mild nutritional deficiency imposed during suckling, or brain composition is very responsive to nutritional rehabilitation initiated after weaning. The effects of severe undernutrition during suckling were not, however, reversed when adequate nutrition was initiated after weaning. The suckling period seems to be critical during development, as the process of myelination was lowered and the levels of electrolytes were irreversibly disturbed. The brains of the rats born to the mothers protein malnourished during gestation were not significantly different from those of controls. The brain seems to be either preferentially protected from the effects of malnutrition imposed during fetal development, or the brain component are very responsive to nutritional rehabilitation initiated immediately after birth. It is suggested that the mother's nutritional status during gestation does not significantly affect the development of the brain. When the young were born to and nursed by protein-malnourished mothers, the growth and the maturation of the brain in such animals were similar to those in rats moderately undernourished during suckling. Growth and maturation of the brain are affected by a lowered level of protein in the diet. Moderate undernutrition imposed during suckling is not important, but the effect is maximum when undernutrition is severe during this period. The suckling period is therefore, comparatively more critical during development.
D000110:Acetylcholinesterase / Q000378:metabolism; D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D004044:Dietary Proteins; D005260:Female; D005333:Fetus / Q000378:metabolism; D007774:Lactation; D018377:Neurotransmitter Agents / Q000378:metabolism; D009748:Nutrition Disorders / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D011247:Pregnancy; D011248:Pregnancy Complications; D011488:Protein Deficiency / Q000378:metabolism*; D051381:Rats; D012964:Sodium / Q000378:metabolism
D004044:Dietary Proteins; D018377:Neurotransmitter Agents; D012964:Sodium; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D000110:Acetylcholinesterase; D011188:Potassium