Effect of Body Weight on Postnatal Development of the Proximal Small Intestine of the Rabbit

Self Cite

The role of gastrin and cholecystokinin (CCK) in postnatal development of the small intestine was examined in infant rabbits. Experimental animals received daily intraperitoneal injections of pentagastrin, 500 μg/kg, or CCK-octapeptide, 40 μg/kg, starting on day 3 of life. The animals were sacrificed at age 17–18 days. Weight and histologic sections of pancreas, stomach, duodenum, proximal jejunum, and ileum were obtained and mucosal lactase and sucrase activities determined in the intestinal segments. No differences were seen in any of the parameters assessed in pentagastrin-treated animals compared to saline-injected littermate controls. Body weight, weight and morphology of pancreas, stomach and intestinal segments, and enzyme activities did not differ significantly. Na+ transport in proximal jejunum under short-circuited conditions was not altered by pentagastrin. CCK-octapeptide also had no effect on weight or morphology of pancreas, stomach, and duodenum, but did lead to a significant increase in weight of proximal jejunum and ileum. Mucosal enzyme activities and morphometric measurements of villus height and mucosal thickness, however, did not differ significantly between CCK-octapeptide-treated animals and saline-injected littermate controls. The increase in weight of jejunal and ileal segments was reflected by an increase in thickness of the muscle layer. The findings indicate that neither gastrin nor CCK plays a role in the ontogenic development of the small intestine.

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 87%

Role of Gastrin and Cholecystokinin in the Ontogenic Development of the Gastrointestinal Tract

Zahavi¹,

Kelly²,

Dg³

1984

Self Cite

“…The increased villus height may reflect increased cell proliferation and an advanced degree of intestinal maturity with more mature mucosal barrier function. In addition, increased enteral nutrient intake and accelerated weight gain also led to precocious maturation of the small intestinal epithelium, suggesting that the volume of food ingested and body weight also trigger maturation of the gastrointestinal tract [207].…”

Section: Protein Undernutrition and Nutritionally Regulated Hormonal mentioning

confidence: 99%

Nutritionally Regulated Hormonal Factors in Prolonged Postnatal Growth Retardation and Its Associated Adverse Neurodevelopmental Outcome in Extreme Prematurity

Yeung¹,

Smyth²

2003

Recent published data show that at hospital discharge, most infants born at <30 weeks of gestation would not achieve the median birth weight of the reference fetus at the same postconceptional age, and many would be less than the 10th centile. Estimating from the current recommendations of calorie and protein intakes, these infants accrue large deficits in intakes of protein and calorie during the first weeks of life. Postnatal growth retardation over a prolonged period of time is related to neurodevelopmental delays. While a total energy intake of 120 kcal/kg/day has generally been considered adequate, protein requirement in low gestation infants remains a matter for debate. Increasing the dietary protein:calorie ratio has previously been proposed as a strategy to enhance growth and to achieve a body composition similar to that of the reference fetus. Previous study data reveal that serum insulin-like growth factor I (IGF-I) concentration is positively correlated with protein intake, and nitrogen retention, in turn, is positively correlated with serum IGF-I concentration. Remarkably, elevated serum growth hormone but low serum IGF-I concentrations have been reported in low gestation infants and in infants with intrauterine growth retardation, suggesting IGF-I being a nutritionally regulated hormonal factor in the postnatal growth retardation. As neurodevelopment in extreme prematurity is likely affected by multiple factors, we hypothesize that a combined strategy of the previously proposed hormonal supplement with hydrocortisone and tri-iodothyronine together with increased dietary protein intake (progressively increasing from 1.5 g/kg/day intravenously administered amino acids immediately after birth, then 3.6 g/100 kcal at ≈125 kcal/kg/day when enterally fed till the infant reaches a body weight of ≧1.8 kg and at ≧50th centile weight of the reference fetus at the same postconceptional age) would likely be synergistic and more effective in improving neurodevelopmental outcome.

“…The physiologic mechanisms that control postnatal develop ment are not well understood, but nutrition appears to play an important role. In a pre vious study, we demonstrated that increased oral nutrient intake and accelerated weight gain induced precocious ontogénie develop ment of the intestine [6], The effect of thera peutic nutritional manipulations, which may have important consequences on the imma ture gastrointestinal tract, has not been ex tensively studied. Total parenteral nutrition (TPN) and intragastric infusion of synthetic formulae are frequently employed in the managment of young infants.…”

Section: Introductionmentioning

confidence: 96%

Effects of Parenteral and Enteral Nutrition on Postnatal Development of the Small Intestine and Pancreas in the Rabbit

Gall¹,

Chung²,

O’Loughlin³

et al. 1987

Although TPN is used frequently in young infants, little information is available regarding its effect on postnatal development of the gut. The effect of total parenteral nutrition (TPN) and intragastric (IG) alimentation on ontogeny of the small intestine was examined in infant rabbits starting at 10–12 days. Animals were killed at 17–19 days. Body weight, organ weight and weight of segments of proximal, mid and distal small intestine were measured. Intestinal mucosa was scraped, weighed and homogenized for estimation of protein, DNA and disaccharidases. Na⁺ transport was examined in short-circuited jejunum. Weight gain was similar in controls, sham-treated and TPN animals, but was significantly reduced in IG animals. TPN induced precocious development of sucrase and maltase activity and glucose-stimulated Na⁺ transport, despite causing a significant decrease in mucosal weight and DNA and pancreatic amylase. IG alimentation also induced precocious development of sucrase, maltase and glucose-stimulated Na⁺ transport. Thus TPN, despite producing mucosal atrophy and decreased pancreatic exocrine development, stimulates accelerated postnatal maturation of the small intestine.