| Popis: |
Colostrum and milk contain a variety of hormones and peptides which are known to stimulate cellular growth and differentiation both in vivo and in vitro.1,2 The marked enhancement of porcine neonatal intestinal growth and development upon ingestion of milk or colostrum3,4 has led to the speculation that milkborne hormones and growth factors may be at least partially responsible for this effect.1,2 Widdowson et al.3 observed a 61% increase in intestinal mass in piglets which had suckled colostrum for 24 hr compared to piglets fed water. Although a portion of the intestinal mass increase can be attributed to macromolecular absorption of colostral immunoglobulin (IgG),4 increases in intestinal length and DNA content suggested cellular proliferation also was occurring.3 Recently, these early observations were validated and extended upon in a series of studies by Burrin et al.4–6 Piglets fed colostrum or milk for 6 hr postpartum showed a 300% increase in jejunal protein synthesis rate compared to water fed controls. A potential role for nonnutritive components in colostrum was demonstrated in a subsequent study in which piglets were fed either colostrum or a milk replacer with comparable macronutrient composition.5 In that study, skeletal muscle and jejunal protein synthesis rates were higher in piglets fed colostrum, indicating that colostral components themselves, or endogenous factors which are released in response to colostrum intake, may mediate growth not only of the intestine but of tissues outside the gastrointestinal tract as well. The rapid small intestinal growth observed by Widdowson et al.3 was associated with functional development in that total small intestinal lactase and acid phosphatase activities were increased in suckled piglets. Burrin et al.6 observed changes in lactase isoform abundance in newborn pigs fed milk or colostrum for 6 hr compared to water fed controls, which suggests the increase in intestinal lactase activity may arise from alterations in posttranslational processing of lactase in response to feeding. |
