Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Technological advances in the intensive care of low birth weight (LBW) infants have resulted in major increases in their survival. New challenges in meeting their nutritional needs have emerged. Very low birth (VLBW) weight infants have very little body fat or glycogen reserves at birth, making them susceptible to starvation. If fed enterally, they require at least 120 calories/kg per day for growth. Numerous immaturities in the gastrointestinal tract and liver limit protein digestion, absorption, and metabolism. Several amino acids not considered essential to the older child or adult are essential to the VLBW infant. Supplying a high protein load with an inappropriate amino acid composition may lead to metabolic imbalances. The digestion and absorption of fats differs from the older child or adult. Lingual and gastric lipases are important, and the lack of bile acids limits fat absorption. Lipoprotein lipase deficiency causes problems when too much fat or fat of incorrect composition is provided. There are controversies regarding the most appropriate carbohydrate source, but research shows that lactose remains an important carbohydrate source for most of these infants. Calcium, magnesium, and phosphorus requirements pose questions in both enterally and parenterally nourished infants. Studies of iron usage suggest that VLBW infants fed either human milk or formula should receive iron supplements. Vitamin E may be helpful in preventing oxygen toxicity. Vitamin D deficiency contributes to bone demineralization and rickets. Controversy exists regarding the correlation between vitamin A nutrition and development of chronic lung disease. Guidelines have been developed for recommended intakes, but much needs to be learned to provide a sound scientific basis upon which to provide optimal nourishment for the high risk, LBW infant.
 ...
PMID:Scientifically-based strategies for nutrition of the high-risk low birth weight infant. 212 45

Vitamin D deficiency was induced in lactating rats and their pups by placing female rats on a vitamin D-deficient diet immediately after mating. Evidence of vitamin D deficiency included undetectable plasma levels of 25-hydroxyvitamin D3 in the dams, maternal hypocalcemia, the lack of pup growth, and pup hypocalcemia following starvation. This method of producing vitamin D-deficient pups was then used to determine whether the failure of vitamin D-deficient pups to grow properly results from a maternal or neonatal defect. Vitamin D-deficient dams and pups were injected with either vitamin D3 or the ethanol vehicle, and pup growth was monitored over the subsequent 6 days. Providing vitamin D3 to the pups directly had no effect on their growth, but administering vitamin D3 to the dams resulted in a tripling of the pup growth rate. The failure of vitamin D3 to promote pup growth when given directly to the pups was not the result of their inability to metabolize the vitamin because these pups converted [3H]-vitamin D3 to 25(OH)D3, 24,25(OH)2D3, and 1,25(OH)2D3 as determined by comigration with standards on both straight and reverse phase high-performance liquid chromatography systems. These results demonstrate that a maternal defect is responsible for the growth failure observed in vitamin D-deficient rat pups.
 ...
PMID:A maternal defect is responsible for growth failure in vitamin D-deficient rat pups. 670 50