Expression Of Nutrient Transporters Research Articles

Assessing the expression of placental nutrient transporters following teratogenic valproic acid exposure in CD-1 mice.

Assessing the expression of placental nutrient transporters following teratogenic valproic acid exposure in CD-1 mice.

Dietary supplementation of microencapsulated botanicals and organic acids enhances the expression and function of intestine epithelial digestive enzymes and nutrient transporters in broiler chickens

Organic acids and botanicals have shown protective effects on gut barrier and against inflammation in broilers. However, their effects on intestinal digestive enzymes and nutrients transporters expression and functions have not been fully studied. The objective of this study was to understand how a microencapsulated blend of botanicals and organic acids affected intestinal enzyme activities and nutrient transporters expression and functions in broilers. A total of 288 birds were assigned to a commercial control diet or diet supplemented with 500 g/MT (metric ton) of the microencapsulated additive. Growth performance was recorded weekly. At d 21 and d 42, jejunum and ileum were isolated for enzyme (maltase, sucrase, and aminopeptidase) and transporter (SGLT1, GLUT2, GLUT1, EAAT3, B0AT1, and PepT1) analyses. Jejunum specific nutrients (glucose, alanine, and glutamate) transport activities were evaluated by Ussing chamber. Protein expression of nutrient transporters in small intestine were measured in mucosa and brush-border membrane (BBM) samples by western blot. Intestinal gene expression of the transporters was determined by RT-PCR. Statistical analysis was performed using Student's t-test comparing the supplemented diet to the control. The feed efficiency was significantly improved through the study period in the supplemented group (P ≤ 0.05). Significant changes of intestinal histology were shown in both jejunum (P ≤ 0.10) and ileum (P ≤ 0.05) after 21 d of treatment. At d21, jejunal maltase activity was upregulated (P ≤ 0.10). The Ussing chamber transport of glucose and alanine was increased, which was in line with increased gene expression (GLUT2, GLUT1, EAAT3, and B0AT1) (P ≤ 0.10 and P ≤ 0.05, respectively) and BBMV protein levels (B0AT1, P < 0.10). At d21, ileal sucrase and maltase activities were upregulated (P ≤ 0.05). Increased expressions of GLUT1, EAAT3, and B0AT1 were observed in both mRNA and protein levels (P ≤ 0.05). Similar pattern of changes was also shown at d42 of age. Our results suggest that feeding microencapsulated additives improves intestinal nutrient digestion and transporter expression and function in broilers, thereby enhancing feed efficiency.

Neurotrophic factor Neuritin modulates T cell electrical and metabolic state for the balance of tolerance and immunity.

The adaptive T cell response is accompanied by continuous rewiring of the T cell's electric and metabolic state. Ion channels and nutrient transporters integrate bioelectric and biochemical signals from the environment, setting cellular electric and metabolic states. Divergent electric and metabolic states contribute to T cell immunity or tolerance. Here, we report that neuritin (Nrn1) contributes to tolerance development by modulating regulatory and effector T cell function. Nrn1 expression in regulatory T cells promotes its expansion and suppression function, while expression in the T effector cell dampens its inflammatory response. Nrn1 deficiency causes dysregulation of ion channel and nutrient transporter expression in Treg and effector T cells, resulting in divergent metabolic outcomes and impacting autoimmune disease progression and recovery. These findings identify a novel immune function of the neurotrophic factor Nrn1 in regulating the T cell metabolic state in a cell context-dependent manner and modulating the outcome of an immune response.

Increased expression of nutrient transporters in gestational diabetes

Increased expression of nutrient transporters in gestational diabetes

Sex differences in gene expression of nutrient transporters in the placenta of rats subjected to high-intensity resistance training associated with an obesogenic diet

Sex differences in gene expression of nutrient transporters in the placenta of rats subjected to high-intensity resistance training associated with an obesogenic diet

Root and rhizosphere traits for enhanced water and nutrients uptake efficiency in dynamic environments.

Modern agriculture's goal of improving crop resource acquisition efficiency relies on the intricate relationship between the root system and the soil. Root and rhizosphere traits play a critical role in the efficient use of nutrients and water, especially under dynamic environments. This review emphasizes a holistic perspective, challenging the conventional separation of nutrient and water uptake processes and the necessity for an integrated approach. Anticipating climate change-induced increase in the likelihood of extreme weather events that result in fluctuations in soil moisture and nutrient availability, the study explores the adaptive potential of root and rhizosphere traits to mitigate stress. We emphasize the significance of root and rhizosphere characteristics that enable crops to rapidly respond to varying resource availabilities (i.e. the presence of water and mobile nutrients in the root zone) and their accessibility (i.e. the possibility to transport resources to the root surface). These traits encompass for example root hairs, mucilage and extracellular polymeric substance (EPS) exudation, rhizosheath formation and the expression of nutrient and water transporters. Moreover, we recognize the challenge of balancing carbon investments, especially under stress, where optimized traits must consider carbon-efficient strategies. To advance our understanding, the review calls for well-designed field experiments, recognizing the limitations of controlled environments. Non-destructive methods such as mini rhizotron assessments and in-situ stable isotope techniques, in combination with destructive approaches such as root exudation analysis, are proposed for assessing root and rhizosphere traits. The integration of modeling, experimentation, and plant breeding is essential for developing resilient crop genotypes capable of adapting to evolving resource limitation.

Physically active pregnancies: Insights from the placenta.

Physical activity (PA) positively influences pregnancy, a critical period for health promotion, and affects placental structure and function in ways previously overlooked. Here, we summarize the current body of literature examining the association between PA, placenta biology, and physiology while also highlighting areas where gaps in knowledge exist. PA during pregnancy induces metabolic changes, influencing nutrient availability and transporter expression in the placenta. Hormones and cytokines secreted during PA contribute to health benefits, with intricate interactions in pro- and anti-inflammatory markers. Extracellular vesicles and placental "-omics" data suggest that gestational PA can shape placental biology, affecting gene expression, DNA methylation, metabolite profiles, and protein regulation. However, whether cytokines that respond to PA alter placental proteomic profiles during pregnancy remains to be elucidated. The limited research on placenta mitochondria of physically active gestational parents (gesP), has shown improvements in mitochondrial DNA and antioxidant capacity, but the relationship between PA, placental mitochondrial dynamics, and lipid metabolism remains unexplored. Additionally, PA influences the placenta-immune microenvironment, angiogenesis, and may confer positive effects on neurodevelopment and mental health through placental changes, vascularization, and modulation of brain-derived neurotrophic factor. Ongoing exploration is crucial for unraveling the multifaceted impact of PA on the intricate placental environment.

Autolyzed yeast and sodium butyrate supplemented alone to diets promoted improvements in performance, intestinal health and nutrient transporter in weaned piglets

This study investigated the effects of supplemental nucleotides, autolyzed yeast (Saccharomyces cerevisiae), and sodium butyrate in diets for nursery pigs on growth performance, diarrhea incidence, blood profile, intestinal morphology, mRNA expression of nutrient transporters, inflammatory markers, antioxidant profile, and tight junction proteins in the small intestine. One hundred eighty 21-day-old pigs (5.17 ± 0.57 kg) were assigned in a randomized block design to 1 of 4 dietary treatments: (1) CON: control, basal diet, (2) NUC: CON + nucleotides, (3) YSC: CON + lysed yeast S. cerevisiae, (4) ASB: CON + acidifier sodium butyrate. Pigs were fed for 24 days, phase 1 (21–32 days) and 2 (32–45 days). During phase 1, YSC and ASB improved average daily gain (ADG) and feed conversion (FC) compared with CON. At the overall period, ASB improved ADG and YSC improved FC compared with CON. The NUC diet did not affect growth performance. The ASB increased ileal villus height compared to CON. The YSC and ASB reduced the number of Peyer’s patches in the ileum compared with CON. The YSC increased mRNA expression of nutrient transporters (SMCT2, MCT1, and PepT1), tight junction proteins (OCL and ZO-1), antioxidants (GPX), and IL1-β in the jejunum compared with CON. The ASB increased mRNA expression of nutrient transporters (SGLT1 and MCT1), tight junction proteins (OCL and ZO-1), and antioxidants (GPX and SOD) compared with CON. In conclusion, autolyzed yeast and sodium butyrate promoted growth performance by improving the integrity of the intestinal barrier, the mRNA expression of nutrient transporters, and antioxidant enzymes in the jejunum of nursery pigs whereas supplementation of nucleotides did not show such effects.

The type of fatty acid dictates their impact on gut permeability and nutrient absorption

We showed that short- and long-term (3 to 12 weeks) high-fat diet (HFD) feeding reduced protein expression of nutrient transporters in the proximal jejunum of mice. The most abundant fatty acids (FA) in HFD were oleic (OA), palmitic (PA) and stearic (EA) acid. Because PA and EA are generally regarded as pro-inflammatory, we hypothesize that dietary PA and EA alter gut permeability and absorption via inflammatory activation. To test this hypothesis, we orally administered HFD-matched doses of OA, PA, and EA to male C57BL/6 mice, fed on purified diet control (LFD), for 3 weeks. Food intake and body weight were monitored, and composition were also evaluated. We next qPCR-assessed the mRNA expression of cytokines ( TNF-α, IL-6, IL-1β, IFN-γ, IL-10) and inflammatory signaling transducers ( MD-2 and Myd88) as well as the protein content of nutrient transporters (Glut2, Pept1, Fat/cd36 and Npc1l1) and cell-cell adhesion proteins (Occludin) in the gut. Small intestinal permeability was assessed ex vivo and gut morphology was histologically determined. In addition, Caco-2 enterocytes were used to assess the impact of specific cytokines on nutrient transport and gut barrier integrity. All dietary FA reduced food intake without affecting lean or fat mass. In the jejunum, OA increased TNF-α gene expression whereas PA upregulated IFN-γ and MD-2 gene expression. Furthermore, OA reduced the nutrient transporters Glut2, Pept1, and Fat/cd36 without affecting Npc1l1, whereas PA and EA reduced Occludin protein content. PA, but not OA and EA, increased jejunum paracellular permeability ex vivo and increased villus length. In Caco-2 cells, while Tnf-α did not affect Glut2, Pept1 and Fat/cd36 or Npc1l1 content, Ifn-γ downregulated Occludin protein content. We conclude that OA and, more potently, PA exert inflammatory effects which contribute to damage gut barrier integrity and downregulate nutrient absorption. Our data point to IFN-γ as a main player coupling dietary stress from PA to altered gut homeostasis. Funding: FAPESP (grants number: 2014/12871-9, 2019/05086-7, 2020/12201-4, and 2022/14545). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Differentiation of intestinal stem cells toward goblet cells under systemic iron overload stress are associated with inhibition of Notch signaling pathway and ferroptosis

Iron overload can lead to oxidative stress and intestinal damage and happens frequently during blood transfusions and iron supplementation. However, how iron overload influences intestinal mucosa remains unknown. Here, the aim of current study was to investigate the effects of iron overload on the proliferation and differentiation of intestinal stem cells (ISCs). An iron overload mouse model was established by intraperitoneal injection of 120 mg/kg body weight iron dextran once a fortnight for a duration of 12 weeks, and an iron overload enteroid model was produced by treatment with 3 mM or 10 mM of ferric ammonium citrate for 24 h. We found that iron overload caused damage to intestinal morphology with a 64 % reduction in villus height/crypt depth ratio, and microvilli injury in the duodenum. Iron overload mediated epithelial function by inhibiting the expression of nutrient transporters and enhancing the expression of secretory factors in the duodenum. Meanwhile, iron overload inhibited the proliferation of ISCs and regulated their differentiation into secretory mature cells, such as goblet cells, through inhibiting Notch signaling pathway both in mice and enteroid. Furthermore, iron overload caused oxidative stress and ferroptosis in intestinal epithelial cells. In addition, ferroptosis could also inhibit Notch signaling pathway, and affected the proliferation and differentiation of ISCs. These findings reveal the regulatory role of iron overload on the proliferation and differentiation of ISCs, providing a new insight into the internal mechanism of iron overload affecting intestinal health, and offering important theoretical basis for the scientific application of iron nutrition regulation.

Effects of the kinetic pattern of dietary glucose release on nitrogen utilization, the portal amino acid profile, and nutrient transporter expression in intestinal enterocytes in piglets

BackgroundPromoting the synchronization of glucose and amino acid release in the digestive tract of pigs could effectively improve dietary nitrogen utilization. The rational allocation of dietary starch sources and the exploration of appropriate dietary glucose release kinetics may promote the dynamic balance of dietary glucose and amino acid supplies. However, research on the effects of diets with different glucose release kinetic profiles on amino acid absorption and portal amino acid appearance in piglets is limited. This study aimed to investigate the effects of the kinetic pattern of dietary glucose release on nitrogen utilization, the portal amino acid profile, and nutrient transporter expression in intestinal enterocytes in piglets.MethodsSixty-four barrows (15.00 ± 1.12 kg) were randomly allotted to 4 groups and fed diets formulated with starch from corn, corn/barley, corn/sorghum, or corn/cassava combinations (diets were coded A, B, C, or D respectively). Protein retention, the concentrations of portal amino acid and glucose, and the relative expression of amino acid and glucose transporter mRNAs were investigated. In vitro digestion was used to compare the dietary glucose release profiles.ResultsFour piglet diets with different glucose release kinetics were constructed by adjusting starch sources. The in vivo appearance dynamics of portal glucose were consistent with those of in vitro dietary glucose release kinetics. Total nitrogen excretion was reduced in the piglets in group B, while apparent nitrogen digestibility and nitrogen retention increased (P < 0.05). Regardless of the time (2 h or 4 h after morning feeding), the portal total free amino acids content and contents of some individual amino acids (Thr, Glu, Gly, Ala, and Ile) of the piglets in group B were significantly higher than those in groups A, C, and D (P < 0.05). Cluster analysis showed that different glucose release kinetic patterns resulted in different portal amino acid patterns in piglets, which decreased gradually with the extension of feeding time. The portal His/Phe, Pro/Glu, Leu/Val, Lys/Met, Tyr/Ile and Ala/Gly appeared higher similarity among the diet treatments. In the anterior jejunum, the glucose transporter SGLT1 was significantly positively correlated with the amino acid transporters B0AT1, EAAC1, and CAT1.ConclusionsRational allocation of starch resources could regulate dietary glucose release kinetics. In the present study, group B (corn/barley) diet exhibited a better glucose release kinetic pattern than the other groups, which could affect the portal amino acid contents and patterns by regulating the expression of amino acid transporters in the small intestine, thereby promoting nitrogen deposition in the body, and improving the utilization efficiency of dietary nitrogen.

Shifts in microbiota and gene expression of nutrient transporters, mucin and interleukins in the gut of fast-growing and slow-growing chickens infected by Salmonella Enteritidis.

Slow-growing breeds are more resistant to Salmonella infection compared to fast-growing broilers. However, it is unclear whether that is associated with innate resistance or rather rely on differences in Salmonella-induced gut responses. We investigated the microbial composition and gene expression of nutrient transporters, mucin, and interleukin in the gut of a fast-growing (Cobb500) and a slow-growing naked neck (NN) chicken breeds challenged with Salmonella Enteritidis. Hatchlings were inoculated at two days of age using sterile broth (sham) or Salmonella Enteritidis (SE) and distributed according to a completely randomized design into four treatments: Cobb-sham; Cobb-SE; NN-sham; and NN-SE. Cecal SE counting and microbial composition by 16S rRNA sequencing were determined at 24-, 96-, and 168-hours post-inoculation (hpi). Gene expression of amino acid (Asct1) and peptide transporters (PepT1), glucose transporters (Sglt1, Glut2 and Glut5) and mucin (Muc2) in the jejunum and expression of interleukins (IL1 beta, IL8, IL17 and IL22) in the cecum was assessed by qPCR at 24 and 168 hpi. NN birds were colonized by SE just as Cobb birds but showed innate upregulation of Muc2, IL8 and IL17 in comparison to Cobb. While nutrient transporter mRNA expression was impaired in SE-challenged Cobb birds, the opposite was observed in NN. There were no differences in microbial diversity at different sampling times for Cobb-SE, whereas the other groups had higher diversity and lower dominance at 24 hpi compared with 96 hpi and 168 hpi. NN birds apparently develop earlier gut microbial stability, have higher basal level of mucin gene expression as well as differential nutrient transporter and interleukin gene expression in the presence of SE which might mitigate the effects of SE infection compared to Cobb birds.

Cannabidiol Exposure During Rat Pregnancy Leads to Labyrinth-Specific Vascular Defects in the Placenta and Reduced Fetal Growth.

Introduction: Cannabis use is increasing among pregnant people, and cannabidiol (CBD), a constituent of cannabis, is often perceived as "natural" and "safe" as it is non-intoxicating. In utero, cannabis exposure is associated with negative health outcomes, including fetal growth restriction (FGR). The placenta supplies oxygen and nutrients to the fetus, and alterations in placental development can lead to FGR. While there has been some investigation into the effects of Δ9-THC, there has been limited investigation into the impacts of in utero gestational CBD exposure on the placenta. Methods: This study used histological and transcriptomic analysis of embryonic day (E)19.5 rat placentas from vehicle and CBD (3 mg/kg intraperitoneal injection) exposed pregnancies (E6.5-18.5). Results: The study revealed that pups from CBD-exposed pregnancies were 10% smaller, with the placentae displaying a decreased fetal blood space perimeter-to-area ratio. The transcriptomic analysis supported compromised angiogenesis and blood vessel formation with downregulated biological processes, including tube morphogenesis, angiogenesis, blood vessel morphogenesis, blood vessel development and vasculature development. Further, the CBD-exposed placentas displayed changed expression of glucose transporters (decreased GLUT1 and GR expression and increased GLUT3 expression). Transcriptomic analysis further revealed upregulated biological processes associated with metabolism. Finally, histological and transcriptomic analysis revealed altered cell populations within the placenta, specifically to syncytiotrophoblast layer II and endothelial cells. Conclusion: Together these results suggest that the structural changes in CDB-exposed placentae, including the altered expression of nutrient transporters and the changes to the placental fetal vasculature, may underlie the reduced fetal growth.

In-Ovo Glutamine Administration Enhances Intestinal Development and Functions in Broiler Chickens: Insights from Enteroid Models

BackgroundEarly life events play significant roles in tissue development and animal health in their later life. Early nutrition, through in-ovo delivery, has shown beneficial effects on improving intestinal health in broiler chickens. However, the underlying mechanism is not fully investigated. A recently developed enteroid culture technique allows investigations on intestinal epithelial functions that are close to physiologic conditions. ObjectivesIn this study, we evaluated the short- and long-term effects of in-ovo administration of glutamine (Gln) on intestinal epithelial development and functions by using intestinal enteroid culture and tissue electrophysiologic analysis. MethodsA hundred eggs of commercial Cobb500 broilers were in-ovo injected with 0.2 mL of either phosphate-buffered saline (PBS) or 3% Gln at embryonic day 18 (E18). Chicks were killed on the day of hatch, and at 3- and 14-d posthatch. Enteroids were generated from the small intestine. After 4 d of culture, enteroids were harvested for 5-ethynyl-2′-deoxyuridine proliferation, fluorescein isothiocyanate-4 kDa dextran permeability, and glucose absorption assays. At day 3 (d3) and day 14 (d14), intestinal barrier and nutrient transport functions were measured by the Ussing chamber. The gene expression of epithelial cell markers, nutrient transporters, and tight-junction proteins were analyzed in both intestinal tissues and enteroids. ResultsIn comparison with the PBS control group, in-ovo Gln increased intestinal villus morphology, epithelial cell proliferation, and differentiation, and altered epithelial cell population toward increased number of enteroendocrine and goblet cells while decreasing Paneth cells. Enteroids gene expression of nutrient transporters (B0AT1, SGLT1, and EAAT3), tight junction (ZO2), glucose absorption, and barrier functions were enhanced on the day of hatch. Long-term increases of intestinal di-peptide and alanine transport were observed at day 14 posthatch. ConclusionsTogether our results suggested that the in-ovo injection of Gln stimulated intestinal epithelium proliferation and programmed the epithelial cell differentiation toward absorptive cells.

Overexpression of Human sFLT1 in the Spongiotrophoblast Is Sufficient to Induce Placental Dysfunction and Fetal Growth Restriction in Transgenic Mice.

Preeclampsia (PE) is characterized by maternal hypertension and placental dysfunction, often leading to fetal growth restriction (FGR). It is associated with an overexpression of the anti-angiogenic sFLT1 protein, which originates from the placenta and serves as a clinical biomarker to predict PE. To analyze the impact of sFLT1 on placental function and fetal growth, we generated transgenic mice with placenta-specific human sFLT1 (hsFLT1) overexpression. Immunohistochemical, morphometrical, and molecular analyses of the placentas on 14.5 dpc and 18.5 dpc were performed with a focus on angiogenesis, nutrient transport, and inflammation. Additionally, fetal development upon placental hsFLT1 overexpression was investigated. Dams exhibited a mild increase in serum hsFLT1 levels upon placental hsFLT1 expression and revealed growth restriction of the fetuses in a sex-specific manner. Male FGR fetuses expressed higher amounts of placental hsFLT1 mRNA compared to females. FGR placentas displayed an altered morphology, hallmarked by an increase in the spongiotrophoblast layer and changes in labyrinthine vascularization. Further, FGR placentas showed a significant reduction in placental glycogen storage and nutrient transporter expression. Moreover, signs of hypoxia and inflammation were observed in FGR placentas. The transgenic spongiotrophoblast-specific hsFLT1 mouse line demonstrates that low hsFLT1 serum levels are sufficient to induce significant alterations in fetal and placental development in a sex-specific manner.

141 Adrenomedullin upregulates mRNA expression of nutrient transporters in human trophoblast cell line: implications for GDM

141 Adrenomedullin upregulates mRNA expression of nutrient transporters in human trophoblast cell line: implications for GDM

Rotavirus-mediated DGAT1 degradation: A pathophysiological mechanism of viral-induced malabsorptive diarrhea.

Gastroenteritis is among the leading causes of mortality globally in infants and young children, with rotavirus (RV) causing ~258 million episodes of diarrhea and ~128,000 deaths annually in infants and children. RV-induced mechanisms that result in diarrhea are not completely understood, but malabsorption is a contributing factor. RV alters cellular lipid metabolism by inducing lipid droplet (LD) formation as a platform for replication factories named viroplasms. A link between LD formation and gastroenteritis has not been identified. We found that diacylglycerol O-acyltransferase 1 (DGAT1), the terminal step in triacylglycerol synthesis required for LD biogenesis, is degraded in RV-infected cells by a proteasome-mediated mechanism. RV-infected DGAT1-silenced cells show earlier and increased numbers of LD-associated viroplasms per cell that translate into a fourfold-to-fivefold increase in viral yield (P < 0.05). Interestingly, DGAT1 deficiency in children is associated with diarrhea due to altered trafficking of key ion transporters to the apical brush border of enterocytes. Confocal microscopy and immunoblot analyses of RV-infected cells and DGAT1-/- human intestinal enteroids (HIEs) show a decrease in expression of nutrient transporters, ion transporters, tight junctional proteins, and cytoskeletal proteins. Increased phospho-eIF2α (eukaryotic initiation factor 2 alpha) in DGAT1-/- HIEs, and RV-infected cells, indicates a mechanism for malabsorptive diarrhea, namely inhibition of translation of cellular proteins critical for nutrient digestion and intestinal absorption. Our study elucidates a pathophysiological mechanism of RV-induced DGAT1 deficiency by protein degradation that mediates malabsorptive diarrhea, as well as a role for lipid metabolism, in the pathogenesis of gastroenteritis.

Superiority of Intestinal Adaptation by Hepatocyte Growth Factor in the Jejunum: An Experimental Study in a Short-Bowel Rat Model

BackgroundWe evaluated the effect of recombinant human hepatocyte growth factor (rh-HGF) on intestinal adaptation in a rat model of short-bowel syndrome (SBS). MethodsSprague–Dawley rats underwent jugular vein catheterization for continuous total parenteral nutrition (TPN) and 90 % small bowel resection. The animals were divided into 3 groups: TPN/SBS (control group, n = 7), TPN/SBS/intravenous recombinant human hepatocyte growth factor (HGF) (0.3 mg/kg/day) (HGF group, n = 7), and TPN/SBS/intravenous c-Met inhibitor (0.3 mg/kg/day) (anti-HGF group, n = 5). On day 7, rats were euthanized and histologically evaluated. Serum diamine oxidase (S-DAO) levels were evaluated using an enzyme-linked immunosorbent assay. The nutrient transporter and glucagon-like peptide-2 (GLP-2) receptor expression were evaluated using real-time polymerase chain reaction. ResultsThe jejunal and ileal villus heights were higher and the S-DAO concentrations significantly higher (p = 0.04) in the HGF group than in the control and anti-HGF groups. The sodium-dependent glucose transporter 1 expression in the HGF group was significantly higher than in the control group and significantly suppressed in the anti-HGF group (p < 0.01). The peptide transporter 1 expression in the jejunum was higher in the HGF group than in the other groups and significantly suppressed in the anti-HGF group (p < 0.01). The GLP-2 receptor expression in the jejunum was higher in the HGF group than the other groups, and it was significantly suppressed in the anti-HGF group (p < 0.01). These jejunal results regarding nutrient transporter an GLP-2 receptor were not found in the ileum. ConclusionsThe administration of rh-HGF appears to be more effective in the jejunum than in the ileum. Type of StudyExperimental Research. Level of EvidenceN/A.

Effect of Phytobiotics and Antibiotic on Growth Performance, Intestinal Morphology and Nutrients Transporters Expression of Broiler Chickens

This study investigated the effect of Phytobiotics (PB) and Antibiotic Growth Promoter (AGP) on performance, intestinal morphology and nutrients transporters mRNA gene expression of broiler chickens. One hundred eighty unsexed one-day-old Ross strains with an average initial body weight (BW) of 45 ± 0.5 g were randomly assigned into three treatments with six replications of 10 chicks in each pen. (1) Control group (CON), basal diets only; (2) antibiotic group, Antibiotic Growth promoter (AGP), basal diet supplemented with 5 mg/kg tetramycin; (3) Phytobiotics (PB), basal diet supplemented with 0.5g/kg, phytobiotics the research lasted for 42 days. Average Daily Feed Intake (ADFI), Average Daily Gain (ADG) and Feed Conversion Ratio (FCR) were calculated weekly, and intestinal morphology of Villus Height (VH), Crypt Depth (CD), and Villus Height to crypt depth ratio (VH: CD) from the duodenum, jejunum, and ileum, nutrients transporters qRT-PCR mRNA expression of GLUT1, SGLT4, GLUT5, PEPT2, CAT1, and LAT1 were evaluated at day 42. Chicks fed PB had significantly (P=0.0413) higher ADG at 1-42 days, PB and AGP significantly had lower FCR (P=0.0001) and (P=0.0001) at 22-42 d and 1-42 days, respectively, in duodenum the villus height was significantly (P=0.0001) longer in PB fed chickens and the lowest was recorded in CON, while the CD and VH: CD were significantly longer in AGP and PB fed chickens, in jejunum VH and CD were significant (P=0.0001) longer in PB and AGP than the CON fed chickens, in ileum PB fed birds had significant higher VH and CD than the AGP and CON fed groups, in duodenum and ileum GLUT1, SGLT4 and GLUT5 expression were highly expressed in AGP and PB fed chickens similar results was obtained in jejunum and ileum by PEPT2 and CAT1. These findings suggest that supplementing phytobiotics in broiler diets improves growth performance and intestinal morphology and up-regulated the expression of nutrient transporters' genes. However, the underlying detailed biological mechanisms and dose standardisation for inclusion in broiler diets need to be further studied.

Fetoplacental Disposition and Toxicity of Cadmium in Mice Lacking the Bcrp Transporter.

The environmental toxicant cadmium (Cd) impairs the growth of rodents and humans in utero which in turn heightens susceptibility to diseases later in life. We previously demonstrated that the maternal-facing efflux transporter, breast cancer resistance protein (human BCRP/ABCG2, mouse Bcrp/Abcg2) confers resistance against Cd toxicity in human trophoblasts. In the current study, we sought to determine whether the absence of Bcrp alters the fetoplacental disposition and toxicity of Cd in mice. Pregnant female wild-type (WT) and Bcrp-null mice (n = 9-10/group) were administered a single injection of saline (5 ml/kg) or CdCl2 (5 mg/kg) on gestational day (GD) 9. Following Cd treatment, Bcrp-null offspring were shorter and accumulated more Cd in their placentas on GD 17 compared to WT mice. Because Cd can adversely impact placentation and transplacental nutrient delivery in mice, multiple pathways were assessed using morphometrics and immunohistochemistry including placenta zonation, vasculature development, and nutrient transporter expression. Most notably, the placentas of Bcrp-null mice had reduced immunostaining of the cell adhesion marker, β-catenin, and the trophoblast marker, cytokeratin, as well as decreased expression of divalent metal nutrient transporters (Dmt1, Zip14, and ZnT1) following Cd treatment. In summary, the absence of Bcrp expression increased placental concentrations of Cd which was associated with shorter fetal size that may be related to differential changes in molecular patterns of placental development and nutrition.