Gastrointestinal Tract In Response Research Articles

In vivo imaging of vagal-induced myenteric plexus responses in gastrointestinal tract with an optical window

The vagus nerve (VN) extensively innervates the gastric enteric nervous system (ENS), but its influence on gastric ENS functionality and motility in vivo remains unclear due to technical challenges. Here we describe a method for stable, long-term observation of gastric ENS activity and muscle dynamics at cellular resolution, which can also be extended to intestinal applications. This method involves ENS-specific labeling and the implantation of an abdominal wall window for optical recording in male mice. In vivo calcium imaging reveals a linear relationship between vagal stimulation frequency and myenteric neuron activation in gastric antrum. Furthermore, the motility of gastric antrum is significantly enhanced and shows a positive correlation with the intensity and number of activated myenteric neurons. While vagal stimulation also activates proximal colonic myenteric neurons, this activation is not frequency-dependent and does not induce proximal colonic motility. The method and results provide important insights into VN-ENS interactions in vivo, advancing our understanding of gastrointestinal motility regulation.

Information on semaglutide and compounding

Semaglutide belongs to a class of medications known as glucagon‐like peptide‐1 (GLP‐1) receptor agonists. It mimics the GLP‐1 hormone that is released in the gastrointestinal tract in response to eating. One role of GLP‐1 is to prompt the body to produce more insulin, which reduces blood glucose (sugar). GLP‐1 in higher amounts also interacts with the parts of the brain that reduce appetite and signal a feeling of fullness.

Gut hormones and bone homeostasis: potential therapeutic implications.

Bone resorption follows a circadian rhythm, with a marked reduction in circulating markers of resorption (such as carboxy-terminal telopeptide region of collagen type I in serum) in the postprandial period. Several gut hormones, including glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide 1 (GLP1) and GLP2, have been linked to this effect in humans and rodent models. These hormones are secreted from enteroendocrine cells in the gastrointestinal tract in response to a variety of stimuli and effect a wide range of physiological processes within and outside the gut. Single GLP1, dual GLP1-GIP or GLP1-glucagon and triple GLP1-GIP-glucagon receptor agonists have been developed for the treatment of type 2 diabetes mellitus and obesity. In addition, single GIP, GLP1 and GLP2 analogues have been investigated in preclinical studies as novel therapeutics to improve bone strength in bone fragility disorders. Dual GIP-GLP2 analogues have been developed that show therapeutic promise for bone fragility in preclinical studies and seem to exert considerable activity at the bone material level. This Review summarizes the evidence of the action of gut hormones on bone homeostasis and physiology.

Therapeutic Potential of Palmitoylethanolamide in Gastrointestinal Disorders.

Palmitoylethanolamide (PEA) is an endocannabinoid-like bioactive lipid mediator belonging to the family of N-acylethanolamines, most abundantly found in peanuts and egg yolk. When the gastrointestinal (GI) effects of PEA are discussed, it must be pointed out that it affects intestinal motility but also modulates gut microbiota. This is due to anti-inflammatory, antioxidant, analgesic, antimicrobial, and immunomodulatory features. Additionally, PEA has shown beneficial effects in several GI diseases, particularly irritable bowel syndrome and inflammatory bowel diseases, as various studies have shown, and it is important to emphasize its relative lack of toxicity, even at high dosages. Unfortunately, there is not enough endogenous PEA to treat disturbed gut homeostasis, even though it is produced in the GI tract in response to inflammatory stimuli, so exogenous intake is mandatory to achieve homeostasis. Intake of PEA could be through animal and/or vegetable food, but bearing in mind that a high dosage is needed to achieve a therapeutic effect, it must be compensated through dietary supplements. There are still open questions pending to be answered, so further studies investigating PEA's effects and mechanisms of action, especially in humans, are crucial to implementing PEA in everyday clinical practice.

Sheep β-Defensin 2 Regulates Escherichia coli F17 Resistance via NF-κB and MAPK Signaling Pathways in Ovine Intestinal Epithelial Cells.

Simple SummaryThis study was conducted to explore the antibacterial ability of sheep β-defensin 2 (SBD-2) against E. coli F17 infection in ovine intestinal epithelial cells (OIECs). Our data revealed that E. coli F17 induces SBD-2 expression in OIECs in vitro, which appears to be mediated through the activation of the signaling pathways NF-κB and MAPK. Our results provide a novel insight for the functionality of SBD-2, which could be useful for developing anti-infective drugs and/or breeding for E. coli diarrhea disease-resistant sheep.Escherichia coli (E. coli) F17 is a member of enterotoxigenic Escherichia coli, which can cause massive diarrhea and high mortality in newborn lambs. β-defensin is mainly produced by the epithelial tissue of the gastrointestinal tract in response to microbial infection. However, the molecular mechanism of sheep β-defensin 2 (SBD-2) against E. coli F17 remains unclear. This study aims to reveal the antibacterial ability of SBD-2 against E. coli F17 infection in sheep. Firstly, we established the culture system of ovine intestinal epithelial cells (OIECs) in vitro, treated with different concentrations of E. coli F17 for an indicated time. Secondly, we performed RNA interference and overexpression to investigate the effect of SBD-2 expression on E. coli F17 adhesion to OIECs. Finally, inhibitors of NF-κB and MAPK pathways were pre-treated to explore the possible relationship involving in E. coli F17 infection regulating SBD-2 expression. The results showed that E. coli F17 markedly (p < 0.01) upregulated the expression levels of SBD-2 mRNA and protein in a concentration- and time-dependent manner. Overexpression of SBD-2 contributed to enhancing E. coli F17 resistance in OIECs, while silencing SBD-2 dramatically improved the adhesion of E. coli F17 to OIECs (p < 0.05 or p < 0.01). Furthermore, E. coli F17 stimulated SBD-2 expression was obviously decreased by pre-treatment with NF-κB inhibitor PDTC, p38 MAPK inhibitor SB202190 and ERK1/2 MAPK inhibitor PD98095 (p < 0.05 or p < 0.01). Interestingly, adhesion of E. coli F17 to OIECs were highly enhanced by pre-treated with PDTC, SB202190 and PD98095. Our data suggested that SBD-2 could inhibit E. coli F17 infection in OIECs, possibly through NF-κB and MAPK signaling pathways. Our results provide useful theoretical basis on developing anti-infective drug and breeding for E. coli diarrhea disease-resistant sheep.

Obesity-related gut hormones and cancer: novel insight into the pathophysiology.

The number of cancers attributed to obesity is increasing over time. The mechanisms classically implicated in cancer pathogenesis and progression in patients with obesity involve adiposity-related alteration of insulin, sex hormones, and adipokine pathways. However, they do not fully capture the complexity of the association between obesity-related nutritional imbalance and cancer. Gut hormones are secreted by enteroendocrine cells along the gastrointestinal tract in response to nutritional cues, and act as nutrient sensors, regulating eating behavior and energy homeostasis and playing a role in immune-modulation. The dysregulation of gastrointestinal hormone physiology has been implicated in obesity pathogenesis. For their peculiar function, at the cross-road between nutrients intake, energy homeostasis and inflammation, gut hormones might represent an important but still underestimated mechanism underling the obesity-related high incidence of cancer. In addition, cancer research has revealed the widespread expression of gut hormone receptors in neoplastic tissues, underscoring their implication in cell proliferation, migration, and invasion processes that characterize tumor growth and aggressiveness. In this review, we hypothesize that obesity-related alterations in gut hormones might be implicated in cancer pathogenesis, and provide evidence of the pathways potentially involved.

The fatty acid profile in new-onset paediatric Crohn's disease

Background and Aims: Crohn's disease (CD) is one of two most common forms of inflammatory bowel disease, children and adolescents accounting for a quarter of all new cases. The changing epidemiology of CD points at raising role of environmental factors including lipids and dysregulated inflammatory responses in gastrointestinal tract that are connected with fatty acid metabolism. In the present study, we explored the plasma profiles of n-3 and n-6 PUFA (polyunsaturated fatty acids) in treatment-naive paediatric patients with new-onset CD.

233 Efficacy of fat-embedded calcium gluconate on lactation performance in dairy cattle

Abstract Several beneficial effects have been observed in the gastrointestinal tract in response to the provision of short-chain fatty acids such as butyrate, including the improvement of gut barrier function, stimulation of epithelial cell proliferation and gastrointestinal homeostasis. By improving gut barrier integrity, it is possible that less energy would be spent mounting an immune response against infiltrating xenobiotic compounds, allowing for more energy to be partitioned towards productive activities, such as milk synthesis. Previous work has demonstrated that gluconic acid and its salts have a prebiotic effect in the lower gut in monogastric animals, where it acts as a substrate for butyrate synthesis, with new data suggesting a similar response in dairy cattle. The objective of this study was to evaluate the effects of supplementation of a fat-embedded calcium gluconate product on milk production in dairy cattle. Lactating heifers (n = 22) and cows (n = 53) were offered either a total mixed ration supplemented with 0.07% fat-embedded calcium gluconate or a negative control ration over the course of a full lactation. Milk production and dry matter intake were recorded daily, while milk composition was determined at regular intervals over the lactation. Cows receiving the supplement displayed significant (P ≤ 0.046) increases in milk and component yields, while consuming 1 kg DM/d more during lactation compared to control. Heifers receiving the supplement displayed decreased (P ≤ 0.044) yield of milk fat and fat-corrected milk, 0.09% increased milk protein content, and decreased feed efficiency. Overall, the results in multiparous animals are consistent with previous work examining calcium gluconate. Further work is needed to characterize the differential response in heifers.

Non-IgE-Mediated Gastrointestinal Food Allergies in Children: An Update.

Non-immunoglobulin E-mediated gastrointestinal food allergic disorders (non-IgE-GI-FA) include food protein-induced enterocolitis syndrome (FPIES), food protein-induced enteropathy (FPE) and food protein-induced allergic proctocolitis (FPIAP), which present with symptoms of variable severity, affecting the gastrointestinal tract in response to specific dietary antigens. The diagnosis of non-IgE-GI-FA is made clinically, and relies on a constellation of typical symptoms that improve upon removal of the culprit food. When possible, food reintroduction should be attempted, with the documentation of symptoms relapse to establish a conclusive diagnosis. Management includes dietary avoidance, nutritional counselling, and supportive measures in the case of accidental exposure. The prognosis is generally favorable, with the majority of cases resolved before school age. Serial follow-up to establish whether the acquisition of tolerance has occurred is therefore essential in order to avoid unnecessary food restriction and potential consequent nutritional deficiencies. The purpose of this review is to delineate the distinctive clinical features of non-IgE-mediated food allergies presenting with gastrointestinal symptomatology, to summarize our current understanding of the pathogenesis driving these diseases, to discuss recent findings, and to address currents gaps in the knowledge, to guide future management opportunities.

The pathogenic role of the GIP/GIPR axis in human endocrine tumors: emerging clinical mechanisms beyond diabetes.

The glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone produced in the gastrointestinal tract in response to nutrients. GIP has a variety of effects on different systems, including the potentiation of insulin secretion from pancreatic β-cells after food intake (i.e. incretin effect), which is probably the most important. GIP effects are mediated by the GIP receptor (GIPR), a G protein-coupled receptor expressed in several tissues, including islet β-cells, adipocytes, bone cells, and brain. As well as its involvement in metabolic disorders (e.g. it contributes to the impaired postprandial insulin secretion in type 2 diabetes (T2DM), and to the pathogenesis of obesity and associated insulin resistance), an inappropriate GIP/GIPR axis activation of potential diagnostic and prognostic value has been reported in several endocrine tumors in recent years. The ectopic GIPR expression seen in patients with overt Cushing syndrome and primary bilateral macronodular adrenal hyperplasia or unilateral cortisol-producing adenoma has been associated with an inverse rhythm of cortisol secretion, with low fasting morning plasma levels that increase after eating. On the other hand, most acromegalic patients with an unusual GH response to oral glucose suppression have GIPR-positive somatotropinomas, and a milder phenotype, and are more responsive to medical treatment. Neuroendocrine tumors are characterized by a strong GIPR expression that may correlate positively or inversely with the proliferative index MIB-1, and that seems an attractive target for developing novel radioligands. The main purpose of this review is to summarize the role of the GIP/GIPR axis in endocrine neoplasia, in the experimental and the clinical settings.

Histomorphology of gastrointestinal tract in bullfrog Rana ( Lithobates ) catesbeiana and evaluation of the changes induced by a soybean meal‐based diet

Two studies were carried out to (a) characterize the gastrointestinal (GI) tract of bullfrog Rana (Lithobates) catesbeiana and (b) to evaluate the effects of total replacement of fish meal (FM) with soybean meal (SBM) on GI tract health. For characterization of the GI tract, oesophagus, stomach and intestine sections were sampled from 20 bullfrogs (80 g) fed a FM-based diet. The results revealed that the GI tract of bullfrog is consisted of four tissue layers including mucosa, submucosa, muscularis and serosa, and that the intestine could be divided into duodenum, jejunum, ileum and rectum. Furthermore, the abundance and length of mucosal folds suggested that jejunum is the primary site of digestion and absorption of nutrients. In the second study, a diet containing 44% fish meal (FM) was formulated and used as a FM-based diet, and a SBM-based diet was prepared by entire substitution of FM with SBM. Sixty bullfrogs (35 ± 1 g) were divided into three replicates of the two groups and were fed the test diets to apparent satiation twice daily for 8 weeks. The changes in pH and morphology of GI tract in response to the shift in dietary protein source were evaluated. The results showed the enhancement of pH values in GI tract of the SBM group excluding cardia, jejunum and rectum. Also, SBM diet triggered significant decreases in the number, height and width of mucosal folds, while an opposite trend was observed for thickness of lamina propria. Moreover, the entire replacement of FM with SBM led to the separation of submucosa from muscularis and incidence of lesion in mucous epithelium. The findings in this study showed that jejunum is the main site of nutrients digestion and absorption. Also, it was demonstrated that entire replacement of FM with SBM adversely influenced the GI tract health in bullfrog.

144 Recovery of the gastrointestinal tract in response to nutritional challenges.

144 Recovery of the gastrointestinal tract in response to nutritional challenges.

Ginger and 6-shogaol protect intestinal tight junction and enteric dopaminergic neurons against 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine in mice

Objective: Ginger and its compound, 6-shogaol, have been known for improving gastrointestinal (GI) function and reducing inflammatory responses in GI tract. Recently, the treatment of GI dysfunction has been recognized as an important part of the management of neurodegenerative diseases, especially for Parkinson’s disease (PD). In this study, we investigated whether ginger and 6-shogaol attenuate disruptions induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on the intestinal barrier and the enteric dopaminergic neurons.Methods: C57BL/6J mice received MPTP (30 mg/kg) for 5 days to induce GI alterations. Ginger (30, 100, 300 mg/kg) and 6-shogaol (10 mg/kg) were treated by gavage feeding for 15 days including the period of MPTP injection.Results: Ginger and 6-shogaol protected intestinal tight junction proteins disrupted by MPTP in mouse colon. In addition, ginger and 6-shogaol suppressed the increase of inducible nitric oxide synthase, cyclooxygenase-2, TNF-α and IL-1β activated by macrophage. Moreover, ginger and 6-shogaol suppressed the MPTP-induced enteric dopaminergic neuronal damage via increasing the cell survival signaling pathway.Conclusion: These results indicate that ginger and 6-shogaol restore the disruption of intestinal integrity and enteric dopaminergic neurons in an MPTP-injected mouse PD model by inhibiting the processes of inflammation and apoptosis, suggesting that they may attenuate the GI dysfunction in PD patients.

Controlling lipid digestion profiles using mixtures of different types of microgel: Alginate beads and carrageenan beads

For certain applications, it is useful to control the rate and extent of lipid digestion in different regions of the gastrointestinal tract (GIT) e.g., to control bioavailability, satiety, or blood lipid levels. In the current study, lipid digestion was modulated by mixing two kinds of lipid-loaded biopolymer microgels (alginate beads and carrageenan beads) with different GIT responses. The microgels were formed by mixing lipid droplets with anionic polysaccharide solutions, and then injecting them into a calcium ion solution to cross-link the polysaccharides. Alginate beads remained intact throughout the GIT, leading to a relatively slow digestion rate, whereas carrageenan beads became deformed and dissociated, leading to faster digestion. Experiments using an in vitro GIT model indicated that the rate of lipid digestion could be controlled by mixing alginate microgels with carrageenan microgels. The rate of lipid digestion of the mixed system (1:1) was between that of the two individual systems. These mixed microgel systems may be useful in developing functional foods that modulate lipid blood levels, hormone release, and energy intake.

Gastrointestinal tract (gut) health in the young pig.

An optimally functioning gastrointestinal tract (GIT) clearly is of importance to the overall metabolism, physiology, disease status and performance of pigs of all stages of growth and development. Recently, the ‘health’ of the GIT (‘gut health’) has attracted much attention despite the lack of a clear definition to the term or its aetiology, although in broad terms, ‘gut health’ encompasses a number of physiological and functional features including nutrient digestion and absorption, host metabolism and energy generation, a stable and appropriate microbiota/microbiome, defence mechanisms including barrier function and mucosal immune mechanisms, and the interactions between these components. ‘Gut health’ in the newly-weaned (young) pig is of obvious interest due to changes in GIT structure and function associated with the post-weaning transition, and more recently to the upsurge in interest in different feed additives as dietary alternatives/replacements caused by bans/reductions in certain antimicrobial compounds being available in some parts of the world. In the presence of enteric disease(s) after weaning, a deterioration in ‘gut health’ may be synonymous to the overall health of the pig, and although some direct relationships can be drawn between pig performance and efficiency and a ‘healthy’ GIT, sometimes this connection is subtler and less obvious, especially in the absence of overt enteric disease(s). The factors and conditions involved in ‘gut health’ are multifactorial, complex, often poorly described and sometimes incorrectly interpreted, although it is evident that perturbations of the GIT can cause an imbalance and disturb the generalized homeostasis. In addition to any enteric diseases or conditions that might arise as a result of these disturbances, other influences will also impact such as the responses occurring in the GIT in the period immediately after weaning, any changes that might occur after a change in diet, and (or) disruptions to meal patterns and hence the flow of nutrients. Ultimately, ‘gut health’ represents the outcome of the GIT in response to its capacity and ability to respond and adapt to the insults and challenges it encounters.

Faecal lactoferrin and calprotectin in patients with Clostridium difficile infection: a case–control study

Calprotectin and lactoferrin are released by the gastrointestinal tract in response to infection and mucosal inflammation. Our objective was to assess the usefulness of quantifying faecal lactoferrin and calprotectin concentrations in Clostridium difficile infection (CDI) patients with or without free toxins in the stools. We conducted a single-centre 22-month case-control study. Patients with a positive CDI diagnosis were compared to two control groups: group 1=diarrhoeic patients negative for C. difficile and matched (1:1) to CDI cases on the ward location and age, and group 2=diarrhoeic patients colonised with a non-toxigenic strain of C. difficile. Faecal lactoferrin and calprotectin concentrations in faeces were determined for patients with CDI and controls. Of 135 patients with CDI, 87 (64.4%) had a positive stool cytotoxicity assay (free toxin) and 48 (35.6%) had a positive toxigenic culture without detectable toxins in the stools. The median lactoferrin values were 26.8μg/g, 8.0μg/g and 15.8μg/g in CDI patients and groups 1 and 2, respectively. The median calprotectin values were 218.0μg/g, 111.5μg/g and 111.3μg/g, respectively. Among patients with CDI, faecal lactoferrin and calprotectin levels were higher in those with free toxins in their stools (39.2 vs. 10.2μg/g, p=0.003 and 274.0 vs. 166.0μg/g, p=0.051, respectively). Both faecal calprotectin and lactoferrin were higher in patients with CDI, especially in those with detectable toxin in faeces, suggesting a correlation between intestinal inflammation and toxins in stools.

Glucagon-like peptide-1 inhibits vascular smooth muscle cell dedifferentiation through mitochondrial dynamics regulation

Glucagon-like peptide-1 (GLP-1) is a neuroendocrine hormone produced by gastrointestinal tract in response to food ingestion. GLP-1 plays a very important role in the glucose homeostasis by stimulating glucose-dependent insulin secretion, inhibiting glucagon secretion, inhibiting gastric emptying, reducing appetite and food intake. Because of these actions, the GLP-1 peptide-mimetic exenatide is one of the most promising new medicines for the treatment of type 2 diabetes. In vivo treatments with GLP-1 or exenatide prevent neo-intima layer formation in response to endothelial damage and atherosclerotic lesion formation in aortic tissue. Whether GLP-1 modulates vascular smooth muscle cell (VSMC) migration and proliferation by controlling mitochondrial dynamics is unknown. In this report, we showed that GLP-1 increased mitochondrial fusion and activity in a PKA-dependent manner in the VSMC cell line A7r5. GLP-1 induced a Ser-637 phosphorylation in the mitochondrial fission protein Drp1, and decreased Drp1 mitochondrial localization. GLP-1 inhibited PDGF-BB-induced VSMC migration and proliferation, actions inhibited by overexpressing wild type Drp1 and mimicked by the Drp1 inhibitor Mdivi-1 and by overexpressing dominant negative Drp1. These results show that GLP-1 stimulates mitochondrial fusion, increases mitochondrial activity and decreases PDGF-BB-induced VSMC dedifferentiation by a PKA/Drp1 signaling pathway. Our data suggest that GLP-1 inhibits vascular remodeling through a mitochondrial dynamics-dependent mechanism.

P-199 Lipocalin2 Affecting Bacterial Clearance in Activated Macrophages Contributes the Onset of Intestinal Inflammation

Lipocalin2 (Lcn2) is an extracellular transport protein expressed in neutrophil granules, activated macrophages, and epithelial cells of the respiratory and gastrointestinal tract in response to inflammatory signals. It is well known that Lcn2 exerts bacteriostatic effect by sequestrating iron-containing siderophores because iron is essential for the growth and virulence of most bacterial species. In this regards, Lcn2 is considered to be involved in innate immune response. However, little is known about the exact role of Lcn2 in the intestinal inflammation. The aim of this study is to investigate the role of Lcn2 in the intestinal inflammation using IL-10 knock out (KO) mice. (1) Time-dependent expression of Lcn2 in the colonic tissues of IL-10 KO mice was compared with that of C57BL/6 wild type (WT) mice by quantitative PCR (qPCR) and immunohistochemistry (IHC). (2) We compared intestinal inflammation between IL-10 KO and Lcn2/IL-10 double knock out (DKO) mice. Inflammation was quantified by histologic scores, TNF-alpha and IL-12p40 secretion from cultured colonic explants, and IFN-gamma and IL-17A secretion from unseparated mesenteric lymph node (MLN) cells stimulated with cecal bacterial lysate. (3) Thioglycollate-elicited peritoneal macrophages were obtained from IL-10 KO (IL-10 KO-derived TEPM) and Lcn2/IL-10 DKO mice (DKO-derived TEPM), and infected with Escherichia coli. We examined the bacteria-killing function of macrophages by gentamicin protection assay. Also, TNF-alpha secretion from infected macrophages was determined by enzyme-linked immune-sorbent assay (ELISA). (1) qPCR and IHC demonstrated that Lcn2 expression in the colonic tissues of IL-10 KO mice was apparently up-regulated compared to that of WT mice from early 4 weeks after birth, and further increased over time. (2) Histologic scores in DKO mice were significantly higher than those in IL-10 KO mice at 4 weeks after birth (DKO versus IL-10 KO mice, 15.0 ± 0.0 versus 0.6 ± 0.5). Gene expressions of IL-1beta, TNF-alpha, IFN-gamma, and IL-17A in the colonic tissues of DKO mice were significantly up-regulated compared to those in IL-10 KO mice. TNF-alpha and IL-12p40 secretion from colonic explants of DKO mice were significantly higher than those of IL-10 KO mice (DKO versus IL-10 KO mice, TNF-alpha; 6.5 ± 0.7 versus 3.6 ± 1.2 ng/mL, IL-12p40; 30.6 ± 9.2 versus 5.3 ± 1.9 ng/mL). IFN-gamma and IL-17A production from MLN cells of DKO mice were higher than those of IL-10 KO mice (DKO versus IL-10 KO mice, IFN-gamma; 28.6 ± 33.7 versus 21.3 ± 32.7, P = 0.29, IL-17A; 2.5 ± 3.8 versus 0.6 ± 0.8 ng/mL, P < 0.05). (3) Uptake of bacteria was significantly enhanced in DKO-derived TEPM compared to that in IL-10 KO-derived TEPM (colony forming unit (CFU) at 2 hours after infection; DKO versus IL-10 KO-derived TEPM, 1461.7 ± 201.0 versus 868.3 ± 300.0 cfu/mL). In addition, intracellular survival of phagocytosed bacteria in DKO-derived TEPM persisted compared to that in IL-10 KO-derived TEPM (CFU at 8 hours after infection; DKO versus IL-10 KO-derived TEPM, 30.0 ± 17.9 versus 8.3 ± 13.3 cfu/mL, P < 0.05). Consequently, TNF-alpha production from DKO-derived TEPM significantly increased compared to IL-10 KO-derived TEPM (DKO versus IL-10 KO-derived TEPM, 14.6 ± 1.2 versus 4.0 ± 0.9 pg/mL at 16 hours after infection). Lcn2 affecting bacterial clearance in activated macrophages contributes to the onset of intestinal inflammation.

Gastrointestinal tract response and growth performance of growing turkeys as influenced by the whole wheat content of diets in two feeding programmes

The objective of this study was to determine the physiological re- sponses and growth performance of turkeys fed 20% whole wheat (WW) in two feeding programmes, diets A and B, consistent with the NRC (1994) and B.U.T. (2012) recommendations, respectively. In diet B, in successive feeding periods (weeks 5-18), the soyabean meal content was increased by 2.89% to 5.13%, the wheat content was decreased by 5.29% to 8.18%, and the concentrations of L-lysine, DL-methionine and L-threonine were considerably increased. A total of 896 four-week-old Big-6 male turkeys with similar initial body weights were randomly assigned to four equal dietary treatment groups, with seven replicate pens per treatment. The birds had free access to water and pelleted diets that contained no WW or 20% WW. After 14 weeks of feeding, the body weight gains (BWG) of turkeys were similar in all dietary treatments. From week 13 to 18, WW contributed to a significant ( P = 0.040) increase in the feed conversion ratio (FCR), whereas the increase in FCR noted over the entire experiment was nearly significant ( P = 0.065). Dietary inclusion of WW had no effect on the weights of the gizzard, small intestine, or caecum, and it enhanced fermentation in the caecum, including increasing α-glucosidase activity and the concentra- tions of total short-chain fatty acids, and decreasing the pH of caecal digesta (all P = 0.001). No significant differences were noted in the parameters of gastroin - testinal function and BWG between turkeys fed diets A and B. Diet B did, how- ever, significantly (P = 0.045) improve FCR over the entire experiment.

Cytokines and Hormones That Contribute to the Positive Association between Fat and Bone.

The positive association between body weight and bone density has been established in numerous laboratory and clinical studies. Apart from the direct effect of soft tissue mass on bone through skeletal loading, a number of cytokines and hormones contribute to the positive association between adipose and bone tissue, acting either locally in sites where cells of the two tissues are adjacent to each other or systemically through the circulation. The current review describes the effects of such local and systemic factors on bone physiology. One class of factors are the adipocyte-secreted peptides (adipokines), which affect bone turnover through a combination of direct effects in bone cells and indirect mechanisms mediated by the central nervous system. Another source of hormones that contribute to the coupling between fat and bone tissue are beta cells of the pancreas. Insulin, amylin, and preptin are co-secreted from pancreatic beta cells in response to increased glucose levels after feeding, and are also found in high circulating levels in obesity. A number of peptide hormones secreted from the gastrointestinal tract in response to feeding affect both fat and bone cells and thus can also act as mediators of the association between the two tissues. The current review focuses on results of laboratory studies investigating possible mechanism involved in the positive association between fat mass and bone mass.