Biomedical subjects

S M Donovan

Publications and source records attributed to S M Donovan.

58 records · Page 4Linked to original sources

PubMedDate not supplied

Neither intact nor hydrolyzed soy proteins elicit intestinal inflammation in neonatal piglets.

BACKGROUND: Efficacy of feeding hydrolyzed soy proteins to infants intolerant to cow milk proteins has not been determined fully. This study compared growth and intestinal responses of neonatal piglets fed formulas with hydrolyzed soy protein to piglets fed formulas with intact soy or cow milk (casein-whey) proteins. METHODS: Piglets (n = 40, day 2 postpartum) were fed commercial milk replacer until day 7 postpartum (designated day 0) and then were assigned randomly to casein-whey (CW) or soy (intact, SI; hydrolyzed SH) formulas to evaluate intestinal responses on days 0, 2, 5, and 10. RESULTS: Average daily gain was higher for CW (121 g/d; p < .05) compared with SI piglets 85 g/d); SH pig weight gain was intermediate (109 g/d). Villus height-to-crypt depth ratio in proximal jejunum was lower (p < .05) on day 2 than day 0 in soy-fed pigs and lower (p < .05) on day 5 than day 0 in CW pigs. Mucosal mast cells were generally higher in CW pigs compared with soy-fed pigs. Villus goblet cell numbers in the midjejunum of SH-fed piglets were lower (p < .05) on day 5 compared with day 0. On day 5, crypt goblet cell numbers were higher (p < .05) in the midjejunum of CW-fed piglets compared with SH-fed piglets with numbers intermediate for SI-fed piglets. Intestinal differences were not detected among dietary treatments for major histocompatibility complex class I and II gene expression, tissue concentrations of prostaglandin E2, or CD8+ T-cell numbers. CONCLUSIONS: Hydrolyzed soy proteins do not elicit intestinal inflammatory responses in piglets and may be viable alternatives to milk and intact soy proteins for feeding infants.

Animal Nutritional Physiological Phenomena↗

PubMedDate not supplied

Total parenteral nutrition alters molecular and cellular indices of intestinal inflammation in neonatal piglets.

BACKGROUND: The adverse effects of TPN on systemic immunity are well-documented; however, the impact of IV feeding on neonatal intestinal immunity is unknown. METHODS: A piglet TPN model was used to compare immune cell composition within the intestinal epithelium and lamina propria of parenterally and orally fed piglets. RESULTS: Small intestinal weight of piglets maintained intravenously was reduced 50% after 7 days. Intestinal atrophy in piglets fed parenterally was evidenced by decreased width of intestinal villi and colon cuffs and reduced intestinal crypt depth. The numbers of CD4+ and CD8+ T lymphocytes were threefold greater within the lamina propria of jejunal and ileal villi of piglets supported intravenously. Inverse correlations were observed between villus height or width and T-lymphocyte numbers (r = -.80; p < .05). Major histocompatibility complex class II mRNA expression, an indicator of localized inflammation, was increased in the ileum and colon of piglets receiving parenteral nutrition. Goblet cell numbers were two-fold greater in jejunal and ileal villi, and mast cells were more abundant in the colon of piglets fed parenterally. Furthermore, jejunal T-lymphocyte numbers were correlated with goblet cell numbers (r = .80; p = .01). CONCLUSIONS: These data identify molecular and cellular indices of intestinal inflammation that are responsive to IV feeding in neonates and provide a novel framework to investigate mechanisms underlying gut atrophy during TPN.

Animals↗

PubMedDate not supplied

Nutritional aspects of manganese from experimental studies.

In experimental animals, dietary manganese deficiency can result in numerous biochemical and structural abnormalities. Deficient animals can be characterized by impaired insulin production, alterations in lipoprotein metabolism, an impaired oxidant defense system, and perturbations in growth factor metabolism. If the deficiency occurs during early development, there can be pronounced skeletal abnormalities and an irreversible ataxia. Several lines of evidence suggest that manganese deficiency may be a problem in some human populations. Manganese toxicity can also pose a significant health risk. In experimental animals, acute manganese toxicity can result in numerous biochemical pathologies. However, the above occurs typically when the manganese is given via injection; most animals show considerable resistance to dietary manganese toxicosis. Similarly, confirmed cases of manganese toxicity in humans are currently restricted to cases of exposure to high levels of airborne manganese, and to cases when manganese excretory pathways are compromised.

Animal Nutritional Physiological Phenomena↗

PubMedDate not supplied

Response of the IGF-I system to prolonged undernutrition and its involvement in somatic and skeletal muscle growth retardation in rats.

We examined the response of the IGF-I system to prolonged undernutrition and its involvement in somatic and skeletal muscle growth retardation. Male rats were food-restricted to 50% of freely-fed controls (C) from birth to 120 days postpartum. Serum and tissues were collected at d 50 and d 120 postpartum. Somatic growth of food-restricted animals (R) was proportional to food intake while organ and tissue growth was disproportionate. Skeletal muscle DNA content and synthesis rates were depressed by undernutrition and DNA synthesis decreased with age. Food-restriction abated serum IGF-I concentrations, serum IGFBP-3 expression and hepatic IGF-I mRNA levels at d 50. Conversely, at d 120, hepatic IGF-I mRNA levels in R were similar to C despite decreased serum IGF-I concentrations and serum IGFBP-3 expression. Hepatic IGFBP-1 and -2 mRNA expression in R was increased at both d 50 and 120, and hepatic IGFBP-4 mRNA expression was elevated on d 120 compared to C. Gastrocnemius IGF-I mRNA levels in R were not different from C at either d 50 or 120. These results suggest that hepatic IGF-I sensitivity to undernutrition decreases with increasing age, and endocrine regulation of IGF-I following adaptation to chronic undernutrition occurs post-transcriptionally. Further, local production of IGF-I in skeletal muscle does not appear to be responsible for the marked decline in muscle DNA synthesis, for skeletal muscle IGF-I mRNA expression was not altered by undernutrition.

Aging↗