Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.108 (lactase)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Milk growth factors are thought to contribute to postnatal gastrointestinal growth. The roles of epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I) in the neonatal piglet intestine were investigated. In the first study, piglets were infected with rotavirus on d 4 postpartum and received formula containing 0, 500 or 1000 micrograms/l of EGF for 8 days. A non-infected control group received no EGF. Infected piglets developed severe diarrhea and gained 60% less weight than controls. Rotaviral infection caused a 37% decrease in villus height and 40% decreases in intestinal enzyme activities compared to control. Oral EGF increased villus height and lactase activity in a linear dose-response fashion. Our results suggest that supplementation of formulas with high physiological levels of EGF may aid in small intestinal recovery. A second study investigated absorption of orally administered IGF-I. Newborn piglets were fitted with catheters via the umbilical artery and vein. Piglets were given formula containing 25 microCi of [125I]-IGF-I and blood samples were drawn for 24O min. Total radioactivity, protein bound counts, and counts immunoprecipitable with an antibody to IGF-I were determined in plasma. Radioactivity was detected in portal and arterial plasma within 15 min and rose throughout the study, however, protein bound counts were stable at 20-30% of total counts between 30 and 180 min postgavage. Approximately 10% of the counts were immunoprecipitable by a polyclonal antibody to IGF-I, suggesting that up to 10% of orally administered IGF-I may be absorbed intact.
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PMID:Use of the piglet to study the role of growth factors in neonatal intestinal development. 771 Dec 92

Insulin-like growth factor-I (IGF-I), a polypeptide growth factor found in milk, is hypothesized to play a functional role in the growth and development of neonates, particularly the gastrointestinal tract. Considerable evidence, based on direct tracer studies with 125I-labeled IGF-I and measurements of circulating IGF-I concentrations in neonatal animals fed a range of IGF-I doses, indicates that the intestinal absorption of IGF-I and the possible effect on metabolism and somatic growth are negligible. However, studies in neonatal animals indicate that oral administration of pharmacological doses of IGF-I increases small intestinal mucosal growth, whereas oral IGF-I provided within the physiological range may enhance the development of intestinal lactase. Therefore, clinical trials exploring the therapeutic use of oral IGF-I as an intervention for preterm neonates and those with compromised intestinal function seem warranted. However, milk-borne IGF-I may not be essential for normal healthy infants, perhaps because endogenous IGF-I provides a sufficient stimulus for maintenance of gastrointestinal structure and function. Future studies should explore the significance of endogenous IGF-I and whether milk-borne IGF-I may be important under pathological conditions in which the endogenous IGF-I production may be compromised.
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PMID:Is milk-borne insulin-like growth factor-I essential for neonatal development? 916 77

Infectious diarrheal diseases and protein-energy malnutrition (PEM) are major causes of child morbidity and mortality worldwide. In the present study, PEM was superimposed on rotavirus infection in neonatal pigs to simulate chronic small intestinal stress in malnourished infants with viral gastroenteritis. Two-day-old cesarean-derived pigs (n = 39) were allotted to three treatment groups: 1) noninfected, full-fed; 2) infected, full-fed; and 3) infected, malnourished. Two days postinfection, severe diarrhea and weight loss (11%) were accompanied by reductions in villus height (60%) and lactase activity (78%) and increased crypt depth (32%) in infected full-fed compared with noninfected pigs (P < 0.05). Malnutrition blunted (P < 0.05) increases in crypt depth elicited by rotavirus. By 9 d postinfection, body weight was 59% less, villus height and lactase activity remained lower (50%), and crypt depth remained greater (62%) in infected full-fed compared with noninfected pigs (P < 0.05). However, diarrhea began to clear in infected full-fed, but not in infected malnourished pigs. Plasma insulin-like growth factor-I (IGF-I) was reduced 68% and crypt depth was reduced 19% in infected-malnourished compared with infected full-fed pigs (P < 0.05). Sixteen days postinfection, full-fed pigs had recovered from rotaviral infection; however, in infected-malnourished pigs, diarrhea and growth stasis persisted, and plasma IGF-I, villus height and alkaline phosphatase activity remained reduced compared with infected full-fed pigs (P < 0.05). Overall, PEM prolonged diarrhea and delayed small-intestinal recovery, indicating that nutritional status during diarrhea is essential for recovery from rotaviral enteritis.
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PMID:Protein-energy malnutrition delays small-intestinal recovery in neonatal pigs infected with rotavirus. 918 26

Nutritional support of preterm infants by total parental nutrition (TPN) is common; however, TPN compromises intestinal structure and enzyme activity. Our goal was to develop a piglet model to assess the effect of limited enteral stimulation with formula and insulin-like growth factor-I (IGF-I) on intestinal morphology and enzyme activity. A nutritionally complete TPN solution was infused for 7 days and piglets were gavaged twice daily with 4 ml sterile water, formula, or formula containing 1,000 micrograms/l IGF-I. Litter mate piglets fed formula served as orally fed controls. On day 7, body weights and plasma hormone profiles of TPN and orally fed piglets were similar. However, intestinal weight, jejunal and ileal villus height and surface area, and mucosal lactase and sucrase activity of TPN piglets was reduced by approximately 50%. No effect of limited enteral stimulation or IGF-I was observed likely due to the small volume of formula administered enterally, which resulted in a low dose of IGF-I (4.3 micrograms IGF-I/kg/day).
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PMID:Delivery of total parenteral nutrition (TPN) via umbilical catheterization: development of a piglet model to investigate therapies to improve gastrointestinal structure and enzyme activity during TPN. 957 59

We tested the hypothesis that chronic ingestion of increased concentrations of milk-borne des(1-3) human insulin-like growth factor-I (hIGF-I) stimulates gastrointestinal growth and development in suckling mice. We used a transgenic mouse with targeted, lactation-dependent, overexpression of des(1-3) hIGF-I in the mammary gland (IGF). Pups were suckled (7 pups per litter) from birth by either IGF (n = 3-6 litters) or control (n = 3-5 litters) dams. In IGF and control pups, we measured the growth (protein and DNA content) and protein synthesis rate (3H-phenylalanine incorporation) of gastrointestinal and visceral organs in 4-, 8-, 12-, 16- and 29-d-old pups. Des(1-3) hIGF-I in milk from IGF dams was 40-200-fold higher than mouse IGF in either IGF or control dams, but was not detected in the plasma of pups suckling IGF dams. Small intestinal weight, protein and DNA content at 8 and 16 d were greater in pups suckling IGF dams than control dams; protein synthesis was also greater in IGF pups at 8 d. Total intestinal lactase activity at 8 and 12 d of age tended to be higher (P < 0.10) in IGF than in control pups. Hypersecretion of des(1-3) hIGF-I in milk ingested by suckling mice pups had limited effects on the growth and maturation of the gastrointestinal tract. Moreover, there was little evidence that milk-borne IGF-I is absorbed into the circulation and stimulates visceral organ growth. This study also demonstrates the feasibility of using mammary-specific transgenes to increase the concentration of milk-borne growth factors to examine whether they affect the growth and development of the suckling neonate.
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PMID:Transgenic hypersecretion of des(1-3) human insulin-like growth factor I in mouse milk has limited effects on the gastrointestinal tract in suckling pups. 991 75