Effect of Epidermal Growth Factor and Artificial Feeding in Suckling Rats

Moore, Mary Courtney; Greene, Harry L.; Said, Hamid M.; Orth, David N.

doi:10.1203/00006450-198612000-00012

Cited by 19 publications

(8 citation statements)

References 17 publications

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“…Sixty newborn male and female rat pups from nine litters were randomly assigned to one of two groups: in the first group, rats were fed adequate amounts of formula per gavage calculated to provide a daily energy intake of 500 kcal/kg as described previously in more detail (24,30). In the second group, rats suckled ad libitum by the dam and were sham intubated every 6 h. An additional group of 17 rat pups were studied immediately after delivery and served as newborn controls.…”

Section: Animalsmentioning

confidence: 99%

Gut-Derived Bone Infection in the Neonatal Rat

et al. 2001

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The risk of osteomyelitis is increased in the premature and critically ill neonate. Although potential sites of bacterial entry are present in many of these infants, the source of infection frequently cannot be established. This study was performed to assess the possible role of bacterial translocation from the intestine in the origin of bone infection using models of breast-fed and formula-fed rat pups. Newborn Sprague-Dawley rats suckled either ad libitum by the dam (n ϭ 30), or were fed a rat milk-simulated formula (n ϭ 30). After 3 d, the animals were killed, and the left femur, heart blood, mesenteric lymph nodes, liver, spleen, and terminal ileum were excised. Organs were analyzed for bacteria by standard microbiologic procedures. Bacterial translocation occurred in 23% of breast-fed rats; the bone was not infected in any of these animals. After feeding of formula diet, bacterial counts of the ileum were markedly elevated (p Ͻ 0.001), and the composition of the gut flora was disrupted. Bacterial translocation was noted in all formula-fed rats. Bone cultures were positive in 23 of 30 (77%) rats after formula-feeding (p Ͻ 0.001 versus breast-feeding). Organisms translocated to the bone included Enterococci, Proteus, Enterobacter, and Escherichia coli. Bacterial species cultured from the bone correlated with the individual colonization pattern of other extraintestinal organs and with the composition of the ileal flora. Members of the gut flora can escape the intestine and colonize the bone in formula-fed rats. The gut should be considered as a potential source for osteomyelitis in the neonate. Acute osteomyelitis in the neonate is a leading cause of destruction of the physis resulting in high rates of permanent handicaps (1-3). Because the major route of infection is via the bloodstream, opportunities for organisms to gain access to the circulation may favor the development of osteomyelitis. Premature and sick neonates represent the high-risk group, and in this population potential sites of bacterial entrance are frequently present. Many of these infants undergo vascular manipulation including insertion of central catheters for total parenteral nutrition or invasive monitoring, which have long been linked to the development of skeletal infection. In most cases, however, the origin of bacterial entry remains unknown (4). Therefore, alternative routes of infection should be considered.Among the organisms causing neonatal osteomyelitis, Staphylococcus aureus is most common, followed by group B streptococci and Gram-negative bacteria (1, 5-7). All of these organisms have the ability to colonize the neonatal gut. They may represent normal luminal residents, or members of an abnormal microflora, as frequently seen in hospitalized neonates (8). It is now widely accepted that organisms can escape from the gastrointestinal tract and invade extraintestinal organs, a process termed as bacterial translocation (9, 10). In normal adult individuals, translocation of bacteria from the gastrointestinal tract is limited by a n...

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Section: Animalsmentioning

confidence: 99%

Gut-Derived Bone Infection in the Neonatal Rat

et al. 2001

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“…To our knowledge, IGF-I is the only growth factor known to induce linear growth of the adult small bowel. While EGF injection has been reported to increase small intestinal length in suckling rats (Moore et al, 1986), a similar response has not been reported in normal or gut-resected adult rats. Our study did not identify the mechanism of IGFinduced linear growth of the small bowel.…”

Section: Discussionmentioning

confidence: 76%

Treatment with IGF-I Peptides Improves Function of the Remnant Gut Following Small Bowel Resection in Rats

et al. 1994

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The effects of 7 days' s.c. infusion of 111-700 micrograms/day IGF-I on gut growth and absorptive function were examined in growing rats following removal of 70 or 80% of the jejuno-ileum, and compared with the responses to the analogues, LR3IGF-I and des(1-3)IGF-I, which bind poorly to IGF binding proteins. Administration of 278 micrograms/day IGF-I, LR3IGF-I or des(1-3)IGF-I following 70% jejuno-ileal resection significantly attenuated malabsorption of fat and nitrogen. Responses in rats with 80% resection were less substantial, but a dose-responsive reduction in malabsorption was apparent with LR3IGF-I. Both IGF-I and LR3IGF-I were shown to increase body weight gain and food conversion efficiency in a dose-dependent manner following 80% jejuno-ileal resection. Total gut weight was increased by up to 21%, due predominantly to increased weight of the stomach and proximal small bowel, with the latter effect attributable at least in part to an increased bowel length. LR3IGF-I was more potent than IGF-I at stimulating body weight gain and food conversion efficiency, but its potency advantage on gut absorptive function and small intestinal re-growth was less marked. We conclude that administration of IGF-I peptides improves gastro-intestinal absorptive function following partial gut resection, most likely reflecting, at least in part, an increase in gut absorptive surface area.

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“…It is possible that one or more of these hormones is responsible for the effect colostrum has on intestinal growth and matu ration. Subcutaneous injections of EGF have been shown to increase the weight, protein, DNA and enzyme activities of the intestines in mice [11] and rats [ 12,13], and the stomach weight of rats [13]. The epithelial cells of the rat intestine possess receptors for EGF [14,15].…”

Section: Discussionmentioning

confidence: 99%

“…In the rat EGF has been shown to stimulate intestinal growth when injected subcutaneously [13], have no effect on intestinal growth when given orally in formula [13], but to alter the protein/DNA ratio of colon if given orally to artificially fed rats [18]. The majority of these studies have used rats of 3-7 days of age in which the initial neonatal gut growth has already started.…”

Section: Discussionmentioning

confidence: 99%

Oral Epidermal Growth Factor Is Trophic for the Stomach in the Neonatal Rat

Falconer

1987

Neonatology

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The stomach of the naturally suckled rat pup was shown to grow rapidly during the first 24 h following delivery. Both absolute weight (p < 0.001) and weight in proportion to body weight (p < 0.001) increased. The stomachs of pups fed formula containing epidermal growth factor (EGF) were larger than those of their control littermates (p < 0.05). These data support a role for milk EGF in the regulation of neonatal gut growth.

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Effect of Epidermal Growth Factor and Artificial Feeding in Suckling Rats

Cited by 19 publications

References 17 publications

Gut-Derived Bone Infection in the Neonatal Rat

Gut-Derived Bone Infection in the Neonatal Rat

Treatment with IGF-I Peptides Improves Function of the Remnant Gut Following Small Bowel Resection in Rats

Oral Epidermal Growth Factor Is Trophic for the Stomach in the Neonatal Rat

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