Modulation of gastrointestinal barrier and nutrient transport function in farm animals by natural plant bioactive compounds - A comprehensive review.

The use of antibiotics in diets has been restricted in several countries as a precautionary measure to avoid development of antibiotic resistance among pathogenic microorganisms. This regulation promoted the exploration of natural plant bioactive compounds (PBCs) as feed additives to improve productivity, welfare and health of livestock and poultry. Along with several beneficial attributes of PBCs, including antimicrobial, antioxidant and various pharmacological effects, they also improve barrier function and nutrient transport in the gastrointestinal (GI) tract. This comprehensive review discusses the effects of different PBCs on the integrity, nutrient transport and permeability of GI epithelia and their mechanism of actions. Dietary PBCs influence the maintenance and enhancement of GI integrity via a number of mechanisms including altered signaling pathways and expression of several tight junction proteins (claudins, occludin, and zonula occludens proteins), altered expression of various cytokines, chemokines, complement components and their transcription factors, goblet cell abundance and mucin gene expression, and the modulation of the cellular immune system. They also affect nutrient transporter gene expression and active absorption of nutrients, minerals and ammonia. One intriguing perspective is to select an effective dose at which a specific PBC could improve GI barrier function and nutrient absorption. The effective doses and clear-cut molecular mechanisms for PBCs are yet to be elucidated to understand discrepant observations among different studies and to improve the targeted biotechnological and pharmaceutical uses of PBCs in farm animals. The latter will also enable a more successful use of such PBCs in humans.

Ureases in the gastrointestinal tracts of ruminant and monogastric animals and their implication in urea-N/ammonia metabolism: A review.

Urea in diets of ruminants has been investigated to substitute expensive animal and vegetable protein sources for more than a century, and has been widely incorporated in diets of ruminants for many years. Urea is also recycled to the fermentative parts of the gastrointestinal (GI) tracts through saliva or direct secretory flux from blood depending upon the dietary situations. Within the GI tracts, urea is hydrolyzed to ammonia by urease enzymes produced by GI microorganisms and subsequent ammonia utilization serves the synthesis of microbial protein. In ruminants, excessive urease activity in the rumen may lead to urea/ammonia toxicity when high amounts of urea are fed to animals; and in non-ruminants, ammonia concentrations in the GI content and milieu may cause damage to the GI mucosa, resulting in impaired nutrient absorption, futile energy and protein spillage and decreased growth performance. Relatively little attention has been directed to this area by researchers. Therefore, the present review intends to discuss current knowledge in ureolytic bacterial populations, urease activities and factors affecting them, urea metabolism by microorganisms, and the application of inhibitors of urease activity in livestock animals. The information related to the ureolytic bacteria and urease activity could be useful for improving protein utilization efficiency in ruminants and for the reduction of the ammonia concentration in GI tracts of monogastric animals. Application of recent molecular methods can be expected to provide rationales for improved strategies to modulate urease and urea dynamics in the GI tract. This would lead to improved GI health, production performance and environmental compatibility of livestock production.

SLC41A1 is the only magnesium responsive gene significantly overexpressed in placentas of preeclamptic women.

OBJECTIVE: To examine expression profile of magnesium responsive genes (MRGs) in placentas of normoevolutive and preeclamptic women. METHODS: The expression profiles of MRGs were determined in placentas of normoevolutive (N=26) and preeclamptic (N=25) women by RT-qPCR. RESULTS: Among all tested MRGs (9) only SLC41A1 (encoding for Na(+)/Mg(2+) exchanger) was significantly overexpressed in ~54.2% of preeclamptic (n=24) and in ~9.5% of normoevolutive (n=21) specimens. On average, SLC41A1 was overexpressed sixfold in the preeclamptic group. Presence of SLC41A1 in placentas was confirmed by Western blot analysis. CONCLUSION. SLC41A1 is significantly overexpressed in nearly 55% of preeclamptic placentas. This may indicate a direct contribution of changed Mg homeostasis in the development of preeclampsia.

A high amount of dietary zinc changes the expression of zinc transporters and metallothionein in jejunal epithelial cells in vitro and in vivo but does not prevent zinc accumulation in jejunal tissue of piglets.

High dietary zinc concentrations are used to prevent or treat diarrhea in piglets and humans, but long-term adaptation to high zinc supply has yet not been assessed. Intestinal zinc uptake is facilitated through members of zinc transporter families SLC30 (ZnT) and SLC39 (ZIP). Whereas in rodents, regulation of zinc homeostasis at low or adequate zinc supply has been described, such mechanisms are unclear in piglets. A total of 54 piglets were fed diets containing 57 [low dietary zinc (LZn)], 164 [normal dietary zinc (NZn)], or 2425 [high dietary zinc (HZn)] mg/kg dry matter zinc. After 4 wk, 10 piglets/group were killed and jejunal tissues taken for analysis of zinc transporters SLC30A1 (ZnT1), SLC30A2 (ZnT2), SLC30A5 (ZnT5), SLC39A4 (ZIP4), divalent metal transporter 1 (DMT1), and metallothionein-1 (MT). Weight gain was higher (P < 0.05) in pigs fed HZn than in the LZn and NZn groups during the first 2 wk. Food intake did not differ between groups. The digesta and jejunal tissue zinc concentrations were higher (P < 0.05) in the HZn pigs than in NZn and LZn pigs. Expression of ZnT1 was higher (P < 0.05) and ZIP4 lower (P < 0.05) in HZn pigs than in the 2 other groups, whereas expression of ZnT5 and DMT1 did not differ between treatments. Expression of ZnT2 was lower (P < 0.05) in the LZn group than in the HZn and NZn groups. The mRNA expression and protein abundance of MT was higher (P < 0.05) in the HZn group than in the NZn and LZn groups. Studies with intestinal porcine cell line intestinal epithelial cell-J2 confirmed the dose-dependent downregulation of ZIP4 and upregulation of ZnT1 and MT (P < 0.05) with increasing zinc concentration within 24 h. In conclusion, high dietary zinc concentrations increase intracellular zinc, promote increased zinc export from intestinal tissues into extracellular compartments, and decrease zinc uptake from the gut lumen. The adaptive process appears to be established within 24 h; however, it does not prevent tissue zinc accumulation.