SEVERE PROTEIN-DEFICIENCY AND REPLETION ALTER BODY AND BRAIN COMPOSITION AND ORGAN WEIGHTS IN INFANT PIGS

Citation
Wg. Pond et al., SEVERE PROTEIN-DEFICIENCY AND REPLETION ALTER BODY AND BRAIN COMPOSITION AND ORGAN WEIGHTS IN INFANT PIGS, The Journal of nutrition, 126(1), 1996, pp. 290-302
Citations number
29
Categorie Soggetti
Nutrition & Dietetics
Journal title
ISSN journal
00223166
Volume
126
Issue
1
Year of publication
1996
Pages
290 - 302
Database
ISI
SICI code
0022-3166(1996)126:1<290:SPARAB>2.0.ZU;2-0
Abstract
Three-wk-old genetically lean or obese pigs were used in two experimen ts to determine the changes in body composition, visceral organs and b rain in response to severe protein deficiency. In Experiment 1, 16 obe se pigs were fed an adequate (A, 21% protein, 3% fat) or a protein-def icient (D, 5% protein, 23% fat) diet for 7 wk, One-half of each group was killed at 7 wk, and the remainder of each group was fed the A diet for an additional 8 wk. At 7 wk, pigs fed D contained a higher percen tage of fat than those fed A (P < 0.01); after 8-wk of repletion, body composition of the two groups was similar. Duodenum, jejunum, and ile um of the protein-deficient pigs had severely atrophic villi, submucos al edema, and atrophic muscle layers; after 8 wk of repletion, however , microscopic architecture of the gastrointestinal tract was restored to normal. Absolute cerebrum weight at 7 wk, but not after 8 wk replet ion, in the pigs fed D were significantly less than in pigs fed A, ind icating reduced brain cellularity after 7 wk of protein restriction, b ut not after 8 wk repletion. In Experiment 2, genetically obese (O, n = 8) and lean (L, n = 8) pigs consumed the A or D diet ad libitum for 10 wk. L and O pigs responded similarly to protein deficiency; D pigs were fatter than A pigs and plasma constituents, bone mineral content, bone mineral density and most organ weights revealed no interactions between diet and genotype. The pig model system used in these experime nts enabled the isolation of protein deficiency from infectious diseas e, parasites and social environmental stimulation that may confound in terpretation of human infant malnutrition experiments. The data sugges t that genetically controlled body fatness is not a major determinant in the response of the infant pig to severe protein deficiency.