scholarly journals 92 Postnatal growth retardation impairs intestinal mucosal barrier in piglets

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 78-78
Author(s):  
Ming Qi ◽  
B I E Tan ◽  
Yulong Yin ◽  
Simeng Liao ◽  
Jianjun Li ◽  
...  
Keyword(s):  
Small Intestine ◽  
P38 Mapk ◽  
Growth Retardation ◽  
Postnatal Growth ◽  
Mucosal Barrier ◽  
Jejunal Mucosa ◽  
Ileal Mucosa ◽  
Intestinal Mucosal Barrier ◽  
Postnatal Growth Retardation ◽  
Villous Height

Abstract The piglets with postnatal growth retardation (PGR) have high mortality and morbidity during their growth and development. Abnormal development of small intestine is casually implicated in impaired growth, but the exact mechanism still remains poorly understood. Thus, the present study investigated the immune profiles related to intestinal mucosal barrier in PGR and healthy piglets. The plasma sample, middle segments of small intestine, and the intestinal mucosa were obtained from healthy and PGR piglets at 42d of age. Compared to healthy piglets, higher plasma concentrations of diamine oxidase and D-lactate were observed in PGR piglets (P < 0.05). Decreased villous height, ratio of villous height to crypt depth, as well as sparse villi, jagged microvilli were also found in jejunum and ileum of PGR piglets. PGR also decreased the percentage of proliferating cell nuclear antigen (PCNA)-positive cells, as well as abundance of Zonula occludens-1, Occludin, Claudin-1, and E-cadherin mRNA and protein in jejunal and ileal mucosa (P < 0.05). The lower concentration of sIgA in jejunal mucosa, and lysozyme in both jejunal and ileal mucosa, but higher level of β-defensins in the ileal mucosa were observed in PGR piglets as compared to healthy piglets (P < 0.05). The percentage of CD68-positive cells were significantly increased, but the levels of P-glycoprotein were decreased in jejunum and ileum from PGR piglets (P < 0.01). Moreover, the expression of proteins involved in p38 MAPK/NF-kB pathway was significantly upregulated in jejunal and ileal mucosa from PGR piglets (P < 0.05). Collectively, these results indicated that the PGR piglets exhibited impaired intestinal integrity, and decreased capacity of mucosal immune function, which may result in severe inflammatory response via the activation of p38 MAPK/NF-kB pathway. Our findings may have important implications in the prevention and treatment of the intestinal mucosal barrier dysfunction in piglets.

scholarly journals Small intestinal transcriptome analysis revealed changes of genes involved in nutrition metabolism and immune responses in growth retardation piglets1

2019 ◽  
Vol 97 (9) ◽  
pp. 3795-3808 ◽  
Author(s):  
Ming Qi ◽  
Bie Tan ◽  
Jing Wang ◽  
Jianjun Li ◽  
Simeng Liao ◽  
...  
Keyword(s):  
Small Intestine ◽  
Immune Responses ◽  
Growth Retardation ◽  
Abnormal Development ◽  
Mucosal Barrier ◽  
Jejunal Mucosa ◽  
Rna Seq ◽  
Nutrient Metabolism ◽  
Oxidoreductase Activity ◽  
Mucosal Barrier Function

Abstract Postnatal growth retardation (PGR) is common in piglets. Abnormal development in small intestine was casually implicated in impaired growth, but the exact mechanism is still implausible. The present study unveiled transcriptome profile of jejunal mucosa, the major site of nutrient absorption, in PGR and healthy piglets using RNA-sequencing (RNA-seq). The middle segments of jejunum and ileum, and jejunal mucosa were obtained from healthy and PGR piglets at 42 d of age. Total RNA samples extracted from jejunal mucosa of healthy and PGR piglets were submitted for RNA-seq. Lower villus height was observed in both jejunum and ileum from PGR piglets suggesting structural impairment in small intestine (P < 0.05). RNA-seq libraries were constructed and sequenced, and produced average 4.8 × 107 clean reads. Analysis revealed a total of 499 differently expressed genes (DEGs), of which 320 DEGs were downregulated in PGR piglets as compared to healthy piglets. The functional annotation based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) highlighted that most DEGs were involved in nutrient metabolism and immune responses. Our results further indicated decreased gene expression associated with glucose, lipid, protein, mineral, and vitamin metabolic process, detoxication ability, oxidoreductase activity, and mucosal barrier function; as well as the increased insulin resistance and inflammatory response in the jejunal mucosa of PGR piglets. These results characterized the transcriptomic profile of the jejunal mucosa in PGR piglets, and could provide valuable information with respect to better understanding the nutrition metabolism and immune responses in the small intestine of piglets.

Absence of Na+–H+ barrier function in mucosa of canine small bowel

1978 ◽  
Vol 56 (4) ◽  
pp. 617-623 ◽  
Author(s):  
Darlene G. Kelly ◽  
Charles F. Code
Keyword(s):  
Small Intestine ◽  
Small Bowel ◽  
Barrier Function ◽  
Hexanoic Acid ◽  
Water Soluble ◽  
Mucosal Barrier ◽  
Jejunal Mucosa ◽  
Gastric Corpus ◽  
Gastric Mucosal Barrier ◽  
Made In

The study was designed to determine whether the special Na+–H+ barrier function or the gastric mucosa is present in the mucosa of the small bowel and whether a gastric mucosal barrier breaker (hexanoic acid) would accelerate the fluxes of sodium in duodenum–jejunum and ileum as in the stomach. The observations were made in healthy conscious dogs with Thiry-Vella fistulae of the small bowel or Heidenhain pouches of the gastric corpus. These barrier characteristics of the stomach were completely absent in the small intestine where bidirectional Na fluxes were 5–10 times greater than in the stomach and were not accelerated by hexanoic acid as they were in the stomach.A comparison was made between the rates of absorption of hexanoic acid, sodium hexanoate, and HCl from the pouches and fistulae. The lipid-soluble fatty acid was transported at all sites more rapidly than its water-soluble sodium salt. In the stomach and ileum the H+ of HCl and sodium hexanoate were absorbed at similar slow rates. The duodenal–jejunal mucosa, however, transported H+ at rates nearly identical to those of hexanoic acid. In our tests HCl was not neutralized in duodenal contents while large quantities were neutralized in the contents of ileum.

Novel missense mutation in the IGF-I receptor L2 domain results in intrauterine and postnatal growth retardation

2012 ◽  
Vol 77 (2) ◽  
pp. 246-254 ◽  
Author(s):  
Yuki Kawashima ◽  
Katsumi Higaki ◽  
Toshiaki Fukushima ◽  
Fumihiko Hakuno ◽  
Jun-ichi Nagaishi ◽  
...  
Keyword(s):  
Missense Mutation ◽  
Growth Retardation ◽  
Postnatal Growth ◽  
Postnatal Growth Retardation ◽  
Igf I

PRENATAL AND POSTNATAL DEVELOPMENTAL CONSEQUENCES OF MATERNAL PHENYLKETONURIA

PEDIATRICS ◽  
1966 ◽  
Vol 37 (6) ◽  
pp. 979-986
Author(s):  
Robert O. Fisch ◽  
William A. Walker ◽  
John A. Anderson
Keyword(s):  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Detrimental Effect ◽  
Postnatal Growth ◽  
Maternal Phenylketonuria ◽  
Phenylalanine Level ◽  
Postnatal Growth Retardation ◽  
Intrauterine Growth ◽  
Prenatal Growth ◽  
Abnormal Metabolism

Two children, one homozygous and the other heterozygous for phenylketonuria, born of an untreated phenylketonuric mother were found to exhibit intrauterine growth retardation and persistent postnatal growth retardation. Microcephaly was present in both children at birth. Microcephaly, mental retardation, and growth retardation were present in the heterozygous child at 5 years of age and in the untreated homozygous child at 2 years of age. The possibility that the comparatively high phenylalanine level in the mother's blood and the concomitant abnormal metabolism had a detrimental effect on the child's prenatal growth and predetermined the rate of their postnatal physical as well as mental development, was discussed.

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