scholarly journals PSIV-22 Supplemental effects of dietary lysophospholipids in lactation diets on sow performance, milk composition, and intestinal health of piglets

2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 174-175
Author(s):  
Kibeom Jang ◽  
Jerry Purvis ◽  
Sung Woo Kim
Keyword(s):  
Cell Proliferation ◽  
Block Design ◽  
Nutrient Utilization ◽  
Proliferation Rate ◽  
Crypt Cell ◽  
Intestinal Cell ◽  
Intestinal Health ◽  
Cell Proliferation Rate ◽  
Crypt Cell Proliferation ◽  
Supplemental Effects

Abstract Dietary lysophospholipids could enhance nutrient utilization through a structural change of enterocyte membrane with increasing permeability. The objective of this study was to determine supplemental effects of dietary lysophospholipids in lactation diets on sow performance, milk characteristics, and intestinal health of piglets. The 52 pregnant sows were allotted to 2 treatments in randomized complete block design with parity and BW as blocks at d 110 of pregnancy. The treatments were CON (no added lysophospholipids) and LPL (at 0.05% lysophospholipids; Lipidol-Ultra, Pathway Intermediates, Shrewsbury, UK). The lactation diets were formulated to meet or exceed nutrient requirements suggested by NRC (2012). Milk samples from 12 sows per treatment were collected to measure gross energy, protein, fat, fatty acid profile, and immunoglobulins (IgG and IgA) on d 1 and d 18 of lactation. Twelve piglets per treatment were euthanized on d 18 to collect tissues to measure tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), malondialdehyde, protein carbonyl, IgA, microbiota in jejunal and colonic mucosa, morphology and crypt cell proliferation rate in the jejunum. Data were analyzed using the MIXED procedure of SAS. Sows fed LPL tended to increase (P = 0.084) litter size (11.9 vs. 12.6) on d 18 of lactation and decrease (P = 0.079) ADFI (8.72 vs. 8.02 kg) during d 9 to d 18 of lactation. Sows fed LPL tended to increase (P = 0.092) IgG (1.14 vs. 1.94 g/L) in the milk. Sows fed LPL increased (P < 0.05) crypt cell proliferation rate (39.38 vs. 40.94%) in the jejunum. Supplementation of lysophospholipids in lactation diet did not affect proinflammatory cytokines, oxidative stress markers, and microbiota in jejunum and colon of piglets on d 18 of lactation. In conclusion, supplementation of dietary lysophopholipids improved productive performance and the intestinal cell proliferation of piglets with enhancing IgG concentration in the milk.

scholarly journals Supplemental effects of dietary lysophospholipids in lactation diets on sow performance, milk composition, gut health, and gut-associated microbiome of offspring

2020 ◽  
Vol 98 (8) ◽  
Author(s):  
Ki Beom Jang ◽  
Jerry M Purvis ◽  
Sung Woo Kim
Keyword(s):  
Cell Proliferation ◽  
Block Design ◽  
Milk Composition ◽  
Proliferation Rate ◽  
Crypt Cell ◽  
Gut Health ◽  
Intestinal Health ◽  
Cell Proliferation Rate ◽  
Crypt Cell Proliferation ◽  
Lactating Sows

Abstract Dietary lysophospholipids (LPL) would influence milk composition of sows, thus positively affect intestinal health of offspring. The objective of this study was to determine effects of dietary LPL fed to lactating sows on performance, milk characteristics, gut health, and gut-associated microbiome of offspring. Sixty pregnant sows were allotted to 2 treatments in a randomized complete block design with parity and BW as blocks on day 110 of gestation. Treatments were CON (no added LPL) and LPL (0.05% LPL; Lipidol-Ultra, Pathway Intermediates, Shrewsbury, UK). Sows were fed 2 kg/d from day 110 of gestation until farrowing and ad libitum after farrowing. Diets were formulated to meet NRC requirement for lactating sows. Colostrum and milk samples from 12 sows per treatment were collected to measure nutrients and immunoglobulins on days 1 and 18 of lactation, respectively. Twelve piglets per treatment (1 piglet per litter) were euthanized on day 18 to collect tissues to measure tumor necrosis factor-α, interleukin-8 (IL-8), malondialdehyde, protein carbonyl, IgA, histomorphology, crypt cell proliferation rate, and microbiota in the jejunum and colon. Data were analyzed using the MIXED procedure of SAS, and the mortality was analyzed using the GLIMMIX procedure of SAS. There was no difference in sow BW, parity, and litter size between treatments on day 0 of lactation. Sows fed LPL had increased (P < 0.05) litter BW gain (53.9 vs. 59.4 kg) and decreased piglet mortality (13.9% vs. 10.6%) on day 18 of lactation. Sows fed LPL had increased (P < 0.05) omega-6:omega-3 (22.1 vs. 23.7) and unsaturated:saturated (1.4 vs. 1.6) fatty acids ratios with increased oleic acid (29.1% vs. 31.4%) and tended to have increased (P = 0.092) IgG (1.14 vs. 1.94 g/L) and linoleic acid (17.7% vs. 18.7%) in the milk on day 18 of lactation. Piglets from sows fed LPL had increased (P < 0.05) IL-8 (184 vs. 245 pg/mg) and crypt cell proliferation rate (39.4% vs. 40.9%) and tended to have increased (P = 0.095) Firmicutes:Bacteroidetes ratio (1.0 vs. 3.5) in the jejunum. In conclusion, sows fed with LPL had milk with increased IgG, oleic acids, and linoleic acids without changes in BW and backfat during lactation. These changes could contribute to improved survivability and intestinal health of piglets by increasing IL-8 concentration, enhancing balance among gut-associated microbiome, and increasing enterocyte proliferation in the jejunum.

scholarly journals 143 Supplemental effects of whey permeate on growth performance and gut health of nursery pigs

2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 81-82
Author(s):  
Ki Beom Jang ◽  
Jerry M Purvis ◽  
Sung Woo Kim
Keyword(s):  
Cell Proliferation ◽  
Growth Performance ◽  
Proliferation Rate ◽  
Crypt Cell ◽  
Gut Health ◽  
Whey Permeate ◽  
Nursery Pigs ◽  
Cell Proliferation Rate ◽  
Crypt Cell Proliferation ◽  
Line Analysis

Abstract Lactose or milk oligosaccharides in milk products may enhance gut health and thus growth of nursery pigs. This study aimed to evaluate supplemental effects of increasing levels of whey permeate on growth performance and gut health in nursery pigs during 7 to 11 kg BW. 1,200 pigs at 7.5 kg BW were allotted to 6 treatments based on a randomized complete block design using BW of pen as blocks. Treatment diets were formulated to meet NRC nutrient requirements with 6 levels of whey permeate (0, 3.75, 7.50, 11.25, 15.00, and 18.75%) and fed to pigs for 11 d. Feed intake and BW were measured during 11 d, and 1 pig per pen were euthanized to collect the jejunum to evaluate TNF-α, IL-8, morphology, digestive enzyme activity, crypt cell proliferation rate, and microbiota. Data were analyzed using contrasts in the MIXED procedure and a broken-line analysis in NLIN procedure of SAS. Increasing whey permeate linearly increased (P < 0.05) ADG (349 to 414 g/d) and G:F (0.783 to 0.851), tended to linearly increase (P = 0.062) ADFI (442 to 484 g/d), linearly increased (P < 0.05) crypt cell proliferation rate (27.8 to 37.0%), linearly decreased (P < 0.05) lactase activity (15.84 to 6.60 U/mg), and tended to linearly decrease (P = 0.082) crypt depth (268 to 251 μm). Using a broken line analysis, the optimum supplementation level of whey permeate was 13.60% for G:F. Supplementation of whey permeate increased (P < 0.05) IL-8 (170 to 209 pg/mg) and decreased (P < 0.05) Firmicutes to Bacteroidetes ratio (6.24 to 3.24) in the jejunum. In conclusion, supplementation of whey permeate enhanced growth performance and also positively affected gut health by modulating inflammatory response and microbiota in the jejunum of nursery pigs from 7 to 11 kg BW.

scholarly journals Supplemental effects of dietary nucleotides on intestinal health and growth performance of newly weaned pigs

2019 ◽  
Vol 97 (12) ◽  
pp. 4875-4882 ◽  
Author(s):  
Ki Beom Jang ◽  
Sung Woo Kim
Keyword(s):  
Cell Proliferation ◽  
Growth Performance ◽  
Phase 1 ◽  
Proliferation Rate ◽  
Crypt Cell ◽  
Intestinal Health ◽  
Weaned Pigs ◽  
Dietary Nucleotides ◽  
Crypt Cell Proliferation ◽  
Tnf Α

Abstract Intestinal challenges upon weaning would increase the needs of nucleotides for enterocyte proliferation, whereas de novo synthesis maybe insufficient. This study aimed to evaluate supplemental effects of dietary nucleotides on intestinal health and growth performance in newly weaned pigs. Fifty newly weaned pigs (19-d-old, 25 barrows and 25 gilts, 4.76 ± 0.42 kg BW) were individually housed and allotted to 5 treatments with increasing nucleotide supplementation (0, 50, 150, 250, and 500 mg/kg) based on a randomized complete block design with the initial BW and sex as blocks. Dietary nucleotides were provided from YT500 (Hinabiotech, Guangzhou, China). Pigs were fed for 21 d based on 2 phases (phase 1: 11 d and phase 2: 10 d) and experimental diets were formulated to meet or exceed nutrient requirements suggested by NRC (2012). Feed intake and BW were recorded. Titanium oxide (0.4%) was added as an indigestible marker from day 17. Plasma collected on day 18 was used to measure tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and malondialdehyde (MDA). Pigs were euthanized on day 21 to collect tissues to evaluate TNF-α, IL-6, MDA, morphology, and crypt cell proliferation rate in the jejunum. Ileal digesta were collected to measure ileal nutrient digestibility. Data were analyzed using contrasts in the MIXED procedure of SAS. Nucleotide supplementation increased (P &lt; 0.05) ADFI in phase 1. Nucleotide supplementation at 50 and 150 mg/kg increased (P &lt; 0.05) ADG in phase 1, whereas increased (P &lt; 0.05) ADFI and tended to increase (P = 0.082) ADG in overall. Increasing nucleotide supplementation changed (quadratic, P &lt; 0.05) villus height-crypt ratio (at 247 mg/kg) and decreased (linear, P &lt; 0.05) crypt cell proliferation rate in the jejunum. Increasing nucleotide supplementation reduced (P &lt; 0.05) jejunal IL-6 (at 50 and 150 mg/kg) and tended to change (quadratic, P = 0.074) plasma MDA (at 231 mg/kg). Nucleotide supplementation at 50 and 150 mg/kg increased (P &lt; 0.05) ileal digestibility of energy and ether extract. In conclusion, nucleotide supplementation at a range of 50 to 250 mg/kg in the diets seems to be beneficial to newly weaned pigs by enhancing growth performance possibly due to reduced intestinal inflammation and oxidative stress as well as improved intestinal villi structure and energy digestibility.

PSXVI-7 Supplemental effects of Lactobacillus extract postbiotics in prevention of post-weaning diarrhea caused by enterotoxigenic F18+ Escherichia coli in nursery pigs

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 416-416
Author(s):  
Xiangyi Xu ◽  
Marcos E Duarte ◽  
Sung Woo Kim
Keyword(s):  
Escherichia Coli ◽  
Cell Proliferation ◽  
Growth Performance ◽  
Protein Carbonyl ◽  
Crypt Cell ◽  
Intestinal Health ◽  
Nursery Pigs ◽  
Crypt Cell Proliferation ◽  
Dietary Treatments ◽  
Supplemental Effects

Abstract This study determined the supplemental effects of Lactobacillus extract (LBE) postbiotics on intestinal health and prevention of postweaning diarrhea caused by F18+ Escherichia coli (ETEC) in nursery pigs. Sixty-four weaned pigs (6.6 ± 0.7 kg BW) were allotted in a RCBD to 4 dietary treatments (NC: no-challenge; PC: challenge/no-treat; BMD: challenge/bacitracin; LBE: challenge/LBE 0.2%) and fed diets for 28 d. At d 7, challenged groups were orally inoculated with ETEC (2.4 x 1010 CFU) and NC group received sterile solution. Growth performance was analyzed weekly and pigs were euthanized on d 28 to measure intestinal health. Data were analyzed using the SAS 9.4. During post-challenge period, PC tended to decrease (P = 0.067) ADG (373 to 284 g/d), whereas BMD increased (P &lt; 0.05) ADG (284 to 408 g/d); LBE tended to increase (P = 0.081) ADG (284 to 370 g/d). PC increased fecal score (P &lt; 0.05, 3.4 to 3.9) on d 14, whereas BMD decreased it (P &lt; 0.05, 3.9 to 3.5) on d 21. PC increased (P &lt; 0.05) protein carbonyl (0.76 to 1.12 nmol/mg protein), crypt cell proliferation (28 to 36%), and Helicobacter rodentium (0.4 to 3.7%). However, BMD decreased (P &lt; 0.05) crypt cell proliferation (36 to 32%) and Helicobacter spp. (15.0 to 1.4%); and increased (P &lt; 0.05) villus height (309 to 377 µm), Bifidobacterium boum (0.04 to 2.0%), Pelomonas spp. (1.5 to 8.5%), and Microbacterium ginsengisoli (0.5 to 3.0%). LBE reduced (P &lt; 0.05) crypt cell proliferation (36 to 27%) and Helicobacter rodentium (3.7 to 0.04%); and increased (P &lt; 0.05) Lactobacillus salivarius (0.3 to 4.1%) and Propionibacterium acnes (0.4 to 7.4%). Collectively, ETEC reduced growth performance by adversely affecting microbiota and intestinal health. BMD and LBE improved growth performance by enhancing intestinal health and increasing beneficial microbiota in ETEC challenged pigs.

scholarly journals Evidence for a Negative Correlation between Human Reactive Enamine-Imine Intermediate Deaminase A (RIDA) Activity and Cell Proliferation Rate: Role of Lysine Succinylation of RIDA

2021 ◽  
Vol 22 (8) ◽  
pp. 3804
Author(s):  
Luisa Siculella ◽  
Laura Giannotti ◽  
Benedetta Di Chiara Stanca ◽  
Matteo Calcagnile ◽  
Alessio Rochira ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Negative Correlation ◽  
Cancer Biology ◽  
Human Tumor ◽  
In Silico Analysis ◽  
Proliferation Rate ◽  
Reactive Intermediate ◽  
Cell Proliferation Rate

Reactive intermediate deaminase (Rid) proteins are enzymes conserved in all domains of life. UK114, a mammalian member of RidA subfamily, has been firstly identified as a component of liver perchloric acid-soluble proteins (L-PSP). Although still poorly defined, several functions have been attributed to the mammalian protein UK114/RIDA, including the reactive intermediate deamination activity. The expression of UK114/RIDA has been observed in some tumors, arousing interest in this protein as an evaluable tumor marker. However, other studies reported a negative correlation between UK114/RIDA expression, tumor differentiation degree and cell proliferation. This work addressed the question of UK114/RIDA expression in human non-tumor HEK293 cell lines and in some human tumor cell lines. Here we reported that human RIDA (hRIDA) was expressed in all the analyzed cell line and subjected to lysine (K-)succinylation. In HEK293, hRIDA K-succinylation was negatively correlated to the cell proliferation rate and was under the control of SIRT5. Moreover, K-succinylation clearly altered hRIDA quantification by immunoblotting, explaining, at least in part, some discrepancies about RIDA expression reported in previous studies. We found that hRIDA was able to deaminate reactive enamine-imine intermediates and that K-succinylation drastically reduced deaminase activity. As predicted by in silico analysis, the observed reduction of deaminase activity has been related to the drastic alterations of hRIDA structure inferred by K-succinylation. The role of hRIDA and the importance of its K-succinylation in cell metabolism, especially in cancer biology, have been discussed.

Reduction of mucosal crypt cell proliferation in patients with colorectal adenomatous polyps by dietary calcium supplementation

1992 ◽  
Vol 79 (6) ◽  
pp. 581-583 ◽  
Author(s):  
G. H. Barsoum ◽  
C. Hendrickse ◽  
M. C. Winslet ◽  
D. Youngs ◽  
I. A. Donovan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Calcium Supplementation ◽  
Dietary Calcium ◽  
Crypt Cell ◽  
Adenomatous Polyps ◽  
Crypt Cell Proliferation

scholarly journals Glucagon-Like Peptide-2 Activates β-Catenin Signaling in the Mouse Intestinal Crypt: Role of Insulin-Like Growth Factor-I

Endocrinology ◽  
2007 ◽  
Vol 149 (1) ◽  
pp. 291-301 ◽  
Author(s):  
Philip E. Dubé ◽  
Katherine J. Rowland ◽  
Patricia L. Brubaker
Keyword(s):  
Cell Proliferation ◽  
Nuclear Translocation ◽  
Glycogen Synthase ◽  
Crypt Cell ◽  
Acute Administration ◽  
Intestinal Crypt ◽  
Crypt Cell Proliferation ◽  
Igf I ◽  
Glucagon Like Peptide ◽  
Crypt Cells

Chronic administration of glucagon-like peptide-2 (GLP-2) induces intestinal growth and crypt cell proliferation through an indirect mechanism requiring IGF-I. However, the intracellular pathways through which IGF-I mediates GLP-2-induced epithelial tropic signaling remain undefined. Because β-catenin and Akt are important regulators of crypt cell proliferation, we hypothesized that GLP-2 activates these signaling pathways through an IGF-I-dependent mechanism. In this study, fasted mice were administered Gly2-GLP-2 or LR3-IGF-I (positive control) for 0.5–4 h. Nuclear translocation of β-catenin in non-Paneth crypt cells was assessed by immunohistochemistry and expression of its downstream proliferative markers, c-myc and Sox9, by quantitative RT-PCR. Akt phosphorylation and activation of its targets, glycogen synthase kinase-3β and caspase-3, were determined by Western blot. IGF-I receptor (IGF-IR) and IGF-I signaling were blocked by preadministration of NVP-AEW541 and through the use of IGF-I knockout mice, respectively. We found that GLP-2 increased β-catenin nuclear translocation in non-Paneth crypt cells by 72 ± 17% (P &lt; 0.05) and increased mucosal c-myc and Sox9 mRNA expression by 90 ± 20 and 376 ± 170%, respectively (P &lt; 0.05–0.01), with similar results observed with IGF-I. This effect of GLP-2 was prevented by blocking the IGF-IR as well as ablation of IGF-I signaling. GLP-2 also produced a time- and dose-dependent activation of Akt in the intestinal mucosa (P &lt; 0.01), most notably in the epithelium. This action was reduced by IGF-IR inhibition but not IGF-I knockout. We concluded that acute administration of GLP-2 activates β-catenin and proliferative signaling in non-Paneth murine intestinal crypt cells as well as Akt signaling in the mucosa. However, IGF-I is required only for the GLP-2-induced alterations in β-catenin.

Vitamin A deficiency inhibits intestinal adaptation by modulating apoptosis, proliferation, and enterocyte migration

2003 ◽  
Vol 285 (2) ◽  
pp. G424-G432 ◽  
Author(s):  
Deborah A. Swartz-Basile ◽  
Lihua Wang ◽  
Yuzhu Tang ◽  
Henry A. Pitt ◽  
Deborah C. Rubin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Small Bowel ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Intestinal Adaptation ◽  
Collagen Iv ◽  
Crypt Cell ◽  
Migration Rates ◽  
Crypt Cell Proliferation ◽  
Extracellular Matrix Components

In a prior study, vitamin A-deficient rats subjected to submassive small bowel resections did not mount a normal intestinal adaptive response by 10 days postoperatively, although adaptive increases in crypt cell proliferation were not attenuated and there were no differences in apoptotic indexes. The present study was designed to address the mechanisms by which vitamin A status effects adaptation by analyzing proliferation, apoptosis, and enterocyte migration in the early postoperative period (16 and 48 h) in vitamin A-sufficient, -deficient, and partially replenished sham-resected and resected rats. At 16 h postresection, apoptosis was significantly greater in the remnant ileum of resected vitamin A-deficient rats compared with the sufficient controls. Crypt cell proliferation was increased by resection in all dietary groups at both timepoints. However, at 48 h postresection, proliferation was significantly decreased in the vitamin A-deficient and partially replenished rats. By 48 h after resection, vitamin A deficiency also reduced enterocyte migration rates by 44%. This occurred in conjunction with decreased immunoreactive collagen IV at 48 h and 10 days postoperation. Laminin expression was also reduced by deficiency at 10 days postresection, whereas fibronectin and pancadherin were unchanged at 48 h and 10 days. These studies indicate that vitamin A deficiency inhibits intestinal adaptation following partial small bowel resection by reducing crypt cell proliferation, by enhancing early crypt cell apoptosis, and by markedly reducing enterocyte migration rates, which may be related to changes in the expression of collagen IV and other extracellular matrix components.

Cell proliferation rate and nuclear morphometry in Roberts syndrome

2008 ◽  
Vol 54 (6) ◽  
pp. 512-516 ◽  
Author(s):  
Petros M Pavlopoulos ◽  
Anastasia E Konstantinidou ◽  
Emmanuel Agapitos ◽  
Panagiotis Davaris
Keyword(s):  
Cell Proliferation ◽  
Proliferation Rate ◽  
Roberts Syndrome ◽  
Nuclear Morphometry ◽  
Cell Proliferation Rate
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