Selenium deficiency causes apoptosis through endoplasmic reticulum stress in swine small intestine.

Selenium (Se) plays a crucial role in intestinal health. However, the specific mechanism by which deficiency of Se causes intestinal damage remains unclear. This study was to explore whether Se deficiency can cause ER stress and induce apoptosis in swine small intestine. We established the Se deficiency swine model in vivo and the intestinal epithelial (IPEC-J2) cell Se deficiency model in vitro. The results of morphological observation showed that Se deficiency caused structural damage in intestinal villi and the decrease of goblet cell structure. The apoptotic characteristics such as nucleolar condensation, mitochondrial swelling, and apoptotic bodies were observed in the IPEC-J2 cells. The results of acridine orange/ethidium bromide and mitochondrial membrane potential fluorescence staining in vitro showed that there were more apoptotic cells in the Se-deficiency group than that in the control group. The protein and/or mRNA expression levels of Bax, Bcl-2, caspase 3, caspase 8, caspase 9, cytc, PERK, ATF6, IRE, XBP1, CHOP, GRP78, which are related to ER stress-apoptosis pathway, were significantly increased in the Se-deficient group which compared with the control group in vivo and in vitro were consistent. These results indicated that Se deficiency induced ER stress and increased the apoptosis in swine small intestine and IPEC-J2 cells and then caused the damage in swine small intestinal tissue. Besides, the results of gene expressions in our experiment proved that ER stress induced by Se deficiency promoted apoptosis. These results filled the blank in the mechanism of Se deficiency-induced intestinal injury in swine.

Nutritional and pharmacological strategy in children with short bowel syndrome.

Short bowel syndrome in neonates is a severe and life-threatening disease after a major loss of small bowel with or without large bowel. Intestinal adaptation, by which the organism tries to restore digestive and absorptive capacities, is entirely dependent on stimulation of the active enterocytes by enteral nutrition. This review summarizes recent knowledge about the pathophysiologic consequences after the loss of different intestinal parts and outlines the options for enteral nutrition and pharmacological therapies to support the adaptation process.

Poria ameliorates the side effects of rhubarb in pair treatment.

To investigate the effect of Poria and effective constituents on gastrointestinal injury animals in the area of the side effects which caused by Rhubarb. Mice were administered i.g. with Rhubarb until the induction of diarrhea followed by gastrointestinal injury. The gastrointestinal injured mice were treated with high, medium and low doses of poria water extract and it's subfractions for 5 days. All indexes were determined to evaluate the action of poria in the pair treatment. The results showed that the higher dose of poria water decoction was discovered to be the most effective dose to treat gastrointestinal injury induced by rhubarb. Body weight, thymus and spleen indexes, the small intestinal propulsion rate and D-xylose absorption in mice with diarrhea and intestinal injury were analyzed to reveal the significant difference with the model group (P<0.01). EAF (Ethyl Acetate Fraction), PEF (Petroleum Ether Fraction) and CPF (Crude Polysaccharide Fraction) not only increase the levels of AMS, GAS and VIP significantly but also ameliorate diarrhea and intestinal injury situation compared with the model group (P<0.01). EAF, PEF and CPF were the most effective components to alleviate diarrhea and gastrointestinal injury induced by rhubarb.

Probiotics, Nutrition, and the Small Intestine.

PURPOSE OF REVIEW: Probiotics are promising remedial treatments for symptoms of small intestine (SI) diseases and promoters of overall good health. Probiotics play an important role in supporting a healthy SI microbiome (eubiosis), and in preventing establishment of unhealthy microbiota. SI eubiosis promotes optimal nutrient uptake, and optimal nutritional status maintains a healthy SI, reducing the likelihood of SI diseases. It is important to understand the advantages and limitations of probiotic therapies. RECENT FINDINGS: Microbial dysbiosis decreases the capacity of the small bowel to utilize and absorb dietary compounds. In some studies, probiotic supplements containing lactic acid bacteria and Bifidobacterium have been demonstrated effective in supporting beneficial microbes in the SI while improving barrier integrity and reducing nutrient malabsorption and SI disease-related pathology. Strain-specific probiotic therapy may be a natural and effective approach to restoring SI barrier integrity and eubiosis, resulting in improved nutrient absorption and better health, including reducing the incidence of and severity of SI diseases.

The Traditional Medicine Banhasasim-Tang Depolarizes Pacemaker Potentials of Cultured Interstitial Cells of Cajal through M3 Muscarinic and 5-HT3 Receptors in Murine Small Intestine.

BACKGROUND: Banhasasim-tang (BHSST) is a classic herbal formulation in traditional Chinese medicine widely used for gastrointestinal (GI) tract motility disorder. We investigated the effects of BHSST on the pacemaker potentials of cultured interstitial cells of Cajal (ICCs) in small intestine in vitro and its effects on GI motor functions in vivo. METHODS: We isolated ICCs from the small intestines and recorded pacemaker potentials in cultured ICCs with the whole-cell patch-clamp configuration in vitro. Intestinal transit rates (ITR%) were investigated in normal mice and GI motility dysfunction (GMD) mouse models in vivo. RESULTS: BHSST (20-50 mg/mL) depolarized pacemaker potentials and decreased their amplitudes in a concentration-dependent manner. Pretreatment with methoctramine (a muscarinic M2 receptor antagonist) did not inhibit BHSST-induced pacemaker potential depolarization. However, when we applied 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4-DAMP; a muscarinic M3 receptor antagonist), BHSST-induced effects were blocked. Pretreatment with Y25130 (a 5-HT3 receptor antagonist) blocked BHSST-induced effects in ICCs. In addition, when we applied 4-DAMP and Y25130 together, BHSST-induced effects were completely blocked. Pretreatment with Ca2+-free solution or thapsigargin inhibited BHSST-induced effects. Moreover, BHSST blocked both the transient receptor potential melastatin (TRPM) 7 and voltage-sensitive calcium-activated chloride (anoctamin-1, ANO1) channels. In normal mice, ITR% values were significantly increased by BHSST in a dose-dependent manner. The ITR% of GMD mice was significantly reduced relative to those of normal mice, which were significantly reversed by BHSST in a dose-dependent manner. CONCLUSION: These results suggested that BHSST depolarizes the pacemaker potentials of ICCs in a dose-dependent manner through the M3 and 5-HT3 receptors via internal and external Ca2+-dependent and TRPM7- and ANO1-independent pathways in vitro. Moreover, BHSST increased ITR% in vivo in normal mice and GMD mouse models. Taken together, the results of this study showed that BHSST had the potential for development as a prokinetic agent in GI motility function.

Controversy in Nutrition Recommendations for Short Bowel Syndrome: How Type of SBS Impacts Response.

PURPOSE OF REVIEW: This review examines the current recommendations for dietary management of patients living with short bowel syndrome (SBS) and outlines the need for future research to provide optimal care for this unique group of patients. RECENT FINDINGS: Providers caring for patients with SBS lack sufficient data to help guide recommendations regarding diet. The majority of studies are conducted at a single medical institution on a small number of anatomically diverse patients. Multi-center studies would allow for inclusion of a larger number of patients and may lead to more individualized dietary recommendations. Patients with short bowel syndrome should be evaluated on an individual basis by a multidisciplinary team including physicians, dieticians, pharmacists, and nurses specializing in the care of these complex patients. Tailoring both medical and nutritional therapy will help realize the overarching goal for these patients of maintaining adequate nutrition with diet and medications, and achieving independence from parenteral support.

Drug-Induced Small Bowel Injury: a Challenging and Often Forgotten Clinical Condition.

PURPOSE OF REVIEW: Most drugs are given by the oral route. Oral intake allows direct contact between the drug and the entire GI tract mucosa, exposing it to potential topical damage until absorption. Medication-induced GI symptoms and lesions are therefore commonly encountered in clinical practice. This review will examine the most common drugs or classes of drugs affecting small bowel function and/or structure. RECENT FINDINGS: Since non-steroidal anti-inflammatory drugs (NSAIDs) are among the most widely used medicines, NSAID enteropathy is highly prevalent and brings about considerable morbidity. Antimicrobials and proton-pump inhibitors profoundly modify intestinal microbiota, affecting gut sensory and motor functions, while other drugs (like iron and gold derivatives) impair intestinal permeability. Olmesartan (and likely ACE inhibitors) induce villous atrophy and consequent malabsorption. Mycophenolate mofetil, cancer chemotherapeutic agents, and immune checkpoint inhibitors cause intestinal inflammation, abdominal pain, and diarrhea. Potassium chloride supplements may induce small bowel ulceration, stenosis, and perforation while the cotraceptive pill and anticoagulants are associated with intestinal ischemia and spontaneous intramural hematoma, respectively. In clinical practice, a deep knowledge of clinical pharmacology and toxicology and a high degree of suspicion of drug-related adverse events are mandatory. Only then, the practicing physician will be able to diagnose medication-induced small bowel lesions correctly and will implement the best strategies to treat them.

Zinc Deficiency and Long-Term Outcome in Cases After Isolated Intestinal Transplantation in Taiwan.

OBJECTIVES: The small intestine is the primary site for absorption of dietary zinc. Intestinal transplant recipients are at high risk for zinc deficiency because of the long process of posttransplant adaptation. We initiated an intestinal transplant program in Taiwan in 2007. In this study, we aimed to retrospectively investigate the incidence of zinc deficiency in recipients after intestinal transplantation. METHODS: Twenty-one isolated intestinal transplants were performed in 20 patients with 1 retransplantation. The level of serum zinc was monitored periodically, and zinc supplements were administered when zinc level was below 700 ng/mL. Twelve patients with graft above 1-year survival and with available related data were enrolled for the analysis of zinc deficiency. The levels of serum zinc were tracked, and the protocol of zinc supplementation is discussed herein. RESULTS: The survival rates of 20 transplant recipients for 1 year, 3 years, and 5 years were 85%, 75%, and 65%, respectively. In the 12 grafts that survived longer than 1 year, we found that zinc deficiency was highest during the third (41.7%) to sixth (50%) month after transplantation. Sustained supplementation of zinc was required for over 70% of patients throughout the 3-year period to maintain their zinc level around the lower normal limit. CONCLUSION: The outcome of isolated small bowel transplantation is promising. Periodical monitoring and sufficient dosing of zinc supplements should be considered into the posttransplant protocol to prevent zinc deficiency after intestinal transplantation.

Antidiarrhoeal properties of Syzygium guineense leaf extract and identification of chemical constituents in its active column fractions.

Background Syzygium guineense (Myrtaceae) has been used in traditional medicine against various ailments, including diarrhoea. This study was conducted to scientifically evaluate the antidiarrheal effects of S. guineense extract and fractions. Methods An ethanol extract of S. guineense leaves was prepared and tested for its effect on small intestinal propulsion in mice and castor oil-induced fluid accumulation in rats. The extract was also evaluated for its effect on itopride-induced small intestine propulsion in mice. Column fractions were also investigated in rats and sub-fractions were tested for activity on spontaneous contractions of isolated rabbit jejunum. Results The results showed that the extract significantly (p<0.05) inhibited intrinsic small intestinal propulsion and itopride-induced propulsive activity, similar to atropine (0.3 mg/kg) although its inhibitory effect against castor oil-induced intestinal fluid accumulation and diarrhoea was statistically insignificant (p>0.05). Column separation yielded 14 fractions, with three fractions producing significant (p<0.001) inhibition of small intestinal propulsion. Sub-fractions 1, 7 and 16 obtained from an active column fraction also exhibited relaxant effects on isolated rabbit jejunum. Spectral analysis (proton, 13C NMR) of sub-fractions 7 and 16 revealed the presence of betulinic acid, ursolic acid, oleanolic acid in 7 and a mixture of luteolin and friedelane-type triterpenes in 16. Conclusions These findings provide scientific evidence that S. guineense leaf extract possess antidiarrhoeal activity and may be potentially beneficial in treatment diarrhoeal disease. The identified compounds may also be implicated in its antidiarrhoeal effects.

Lactobacillus plantarum YS-3 Prevents Activated Carbon-Induced Constipation in Mice.

The aim of this study was to determine the effects of Lactobacillus plantarum YS-3 (LP-YS3) on activated carbon-induced constipation in Kunming mice. The results of the experiment show that the antigastric acid activity and bile salt tolerance of LP-YS3 were stronger than those of Lactobacillus bulgaricus (LB). LP-YS3 inhibited loss of body weight caused by constipation and further reductions in fecal weight, particle number, and water content in mice. Moreover, LP-YS3 elevated the gastrointestinal transit rate and reduced the time required for initial black stool defecation. LP-YS3 also elevated motilin (MTL), endothelin (ET), acetylcholinesterase (AChE), substance P (SP), and VIP serum levels and reduced somatostatin (SS) levels in constipated mice. Hematoxylin-eosin (H&E) staining revealed that high concentration of LP-YS3 reduced the incidence of injuries to small intestine villi and the intestinal wall compared to carbon-induced constipation groups. Reverse transcription-polymerase chain reaction and western blot experiments demonstrated that LP-YS3 upregulated c-Kit, stem cell factor, and glial cell line-derived neurotrophic factor mRNA and protein expression and downregulated transient receptor potential vanilloid 1 and nitric oxide synthase expression in small intestine tissue from constipated mice. In conclusion, high concentrations of LP-YS3 had stronger and more beneficial effects than LB. Based on these results, we conclude that LP-YS3 can effectively inhibit constipation.

No Gut No Gain! Enteral Bile Acid Treatment Preserves Gut Growth but Not Parenteral Nutrition-Associated Liver Injury in a Novel Extensive Short Bowel Animal Model.

BACKGROUND: Parenteral nutrition (PN) provides nutrition intravenously; however, this life-saving therapy is associated with significant liver disease. Recent evidence indicates improvement in PN-associated injury in animals with intact gut treated with enteral bile acid (BA), chenodeoxycholic acid (CDCA), and a gut farnesoid X receptor (FXR) agonist, which drives the gut-liver cross talk (GLCT). We hypothesized that similar improvement could be translated in animals with short bowel syndrome (SBS). METHODS: Using piglets, we developed a novel 90% gut-resected SBS model. Fifteen SBS piglets receiving PN were given CDCA or control (vehicle control) for 2 weeks. Tissue and serum were analyzed posteuthanasia. RESULTS: CDCA increased gut FXR (quantitative polymerase chain reaction; P = .008), but not downstream FXR targets. No difference in gut fibroblast growth factor 19 (FGF19; P = .28) or hepatic FXR (P = .75), FGF19 (P = .86), FGFR4 (P = .53), or Cholesterol 7 α-hydroxylase (P = .61) was noted. PN resulted in cholestasis; however, no improvement was noted with CDCA. Hepatic fibrosis or immunostaining for Ki67, CD3, or Cytokeratin 7 was not different with CDCA. PN resulted in gut atrophy. CDCA preserved (P = .04 vs control) gut mass and villous/crypt ratio. The median (interquartile range) for gut mass for control was 0.28 (0.17-0.34) and for CDCA was 0.33 (0.26-0.46). CONCLUSIONS: We note that, unlike in animals with intact gut, in an SBS animal model there is inadequate CDCA-induced activation of gut-derived signaling to cause liver improvement. Thus, it appears that activation of GLCT is critically dependent on the presence of adequate gut. This is clinically relevant because it suggests that BA therapy may not be as effective for patients with SBS.

Cellular Composition of the B- and T-Cell-Dependent Areas in the Small Intestine during the Post-Stress Period (Experimental Study).

A quantitative study of lymphoid cells in the B- and T-cell-dependent areas of intestinal lymphoid nodules and mesenteric lymph nodes in behaviorally passive and active rats was performed at various periods after acute stress on the model of 1-h immobilization with simultaneous electrocutaneous stimulation. Stress exposure is accompanied by a decrease in the number of lymphoid cells in immunogenic structures of the gastrointestinal tract. Post-stress changes in the cytoarchitectonics of B- and T-cell-dependent areas in mesenteric lymph nodes of animals are less pronounced than in lymphoid nodules. Quantitative changes in lymphoid cells of B-cell-dependent areas in the small intestine of rats are greater than in T-cell-dependent areas. Changes in the cellular composition of immunogenic structures in the digestive system are most significant at the early stages of the post-stress period (1st week). Passive rats are characterized by significant changes in the cytoarchitectonics of B- and Tcell-dependent areas in the small intestine after extreme exposure, which illustrates functional exhaustion of the lymphoid tissue in stress-predisposed specimens.

Nutritional Therapy in Adult Short Bowel Syndrome Patients with Chronic Intestinal Failure.

Intestinal failure (IF) is the reduction of gut function below the minimum necessary for the absorption of macronutrients and/or water and electrolytes, such that parenteral support (PS) is required to maintain health and/or growth. This article critically revises the gaps in and evidence for providing general nutritional therapy recommendations in the Short Bowel Syndrome-IF population. It addresses the need for an individualized approach, aiming to reduce or even eliminate the need for PS, and emphasizes a need to focus on effects of dietary interventions on the quality of life of these patients.

[Primary intestinal lymphangiectasia (Waldmann's disease)]. / Lymphangiectasies intestinales primitives (maladie de Waldmann).

Primary intestinal lymphangiectasia (PIL), Waldmann's disease, is a rare disorder of unknown etiology characterized by dilated intestinal lacteals leading to lymph leakage into the small-bowel lumen and responsible for protein-losing enteropathy leading to lymphopenia, hypoalbuminemia and hypogammaglobulinemia. PIL is generally diagnosed before 3 years of age but may be diagnosed in older patients. The main symptom is bilateral lower limb edema. Edema may be moderate to severe including pleural effusion, pericarditis or ascites. Protein-losing enteropathy is confirmed by the elevated 24-h stool α1-antitrypsin clearance and diagnosis by endoscopic observation of intestinal lymphangiectasia with the corresponding histology of biopsies. Videocapsule endoscopy may be useful when endoscopic findings are not contributive. Several B-cell lymphomas of the gastrointestinal tract or with extra-intestinal localizations were reported in PIL patients. A long-term strictly low-fat diet associated with medium-chain triglyceride and liposoluble vitamin supplementation is the cornerstone of PIL medical management. Octreotide, a somatostatin analog, have been proposed with an inconsistent efficacy in association with diet. Surgical small-bowel resection is useful in the rare cases with segmental and localized intestinal lymphangiectasia. A prolonged clinical and biological follow-up is recommended.

Specific protein supplementation using soya, casein or whey differentially affects regional gut growth and luminal growth factor bioactivity in rats; implications for the treatment of gut injury and stimulating repair.

Modulation of regional growth within specific segments of the bowel may have clinical value for several gastrointestinal conditions. We therefore examined the effects of different dietary protein sources on regional gut growth and luminal growth factor bioactivity as potential therapies. Rats were fed for 14 days on isonitrogenous and isocaloric diets comprising elemental diet (ED) alone (which is known to cause gut atrophy), ED supplemented with casein or whey or a soya protein-rich feed. Effects on regional gut growth and intraluminal growth factor activity were then determined. Despite calorie intake being similar in all groups, soya rich feed caused 20% extra total body weight gain. Stomach weight was highest on soya and casein diets. Soya enhanced diet caused greatest increase in small intestinal weight and preserved luminal growth factor activity at levels sufficient to increase proliferation in vitro. Regional small intestinal proliferation was highest in proximal segment in ED fed animals whereas distal small intestine proliferation was greater in soya fed animals. Colonic weight and proliferation throughout the colon was higher in animals receiving soya or whey supplemented feeds. We conclude that specific protein supplementation with either soya, casein or whey may be beneficial to rest or increase growth in different regions of the bowel through mechanisms that include differentially affecting luminal growth factor bioactivity. These results have implications for targeting specific regions of the bowel for conditions such as Crohn's disease and chemotherapy.

Randomized controlled trial of 3 days fasting and oral senna, combined with mannitol and simethicone, before capsule endoscopy.

BACKGROUND AND STUDY AIMS: The approach to small bowel preparation before capsule endoscopy (CE) is still suboptimal. PATIENTS AND METHODS: One hundred eighty patients were randomly allocated to 3 groups. Patients in Group A took 250 mL 20% mannitol and 1 L 0.9% saline orally at 05:00 hours on the day of the procedure. In Group B the same preparation was taken at 20:00 on the day before, and at 05:00 on the day of CE; in addition, 20 mL oral simethicone was taken 30 minutes before CE. Group C was treated identically to Group B, except that the patients fasted for 3 days and took 3 g senna orally 3 times daily before CE. The length of bowel containing green luminal contents was assessed by ImageJ software and bowel cleanliness was evaluated by computed assessment of the cleansing score. RESULTS: Cleansing of the whole small bowel and the distal small bowel were significantly different between the 3 groups (χ = 22.470, P = .000; χ = 17.029, P = .000, respectively). There were also significant differences between the 3 groups in the length of small bowel and specifically the length of the distal small bowel containing green luminal contents (χ = 12.390, P = .000, χ = 15.141, P = .000, respectively), but not with regard to the proximal small bowel (χ = 0.678, P = .509). CONCLUSIONS: Three days fasting and oral senna, combined with 20% mannitol and simethicone, before CE, can reduce the effects of bile on the small bowel and improve small bowel cleansing, especially in the distal small intestine.

N-Acetylcysteine improves intestinal function in lipopolysaccharides-challenged piglets through multiple signaling pathways.

This study determined whether N-acetylcysteine (NAC) could improve intestinal function through phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), epithelial growth factor receptor (EGFR), toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB), adenosine 5'-monophosphate-activated protein kinase (AMPK), and type I interferon (IFN) signaling pathways in a piglet model of lipopolysaccharides (LPS) challenge. Thirty-two piglets (24-day-old) were randomly allocated to one of four treatments, with eight replicates per treatment and one piglet per replicate. The experiment consisted of four treatments in a 2 × 2 factorial arrangement with two diets (supplemented with 0 or 500 mg NAC/kg diet) and saline or LPS administration. On day 20 of the trial, piglets in the LPS and LPS + NAC groups were intraperitoneally injected with 0 (saline) or 100 µg LPS/kg BW. Blood samples were obtained at 3 h and intestinal mucosae were collected at 6 h post LPS or saline injection. The growth performance was not affected by dietary NAC. LPS induced intestinal dysfunction, as indicated by: (1) reductions in the small-intestinal glutathione concentrations and plasma D-xylose levels; (2) elevations in plasma diamine oxidase activity, mucosal MMP3 mRNA levels and caspase-3 protein abundance; (3) reduced the activities of the small-intestinal mucosal maltase, sucrase and lactase. The adverse effects of LPS on porcine intestinal function and redox status were mitigated by NAC supplementation through the activation of multiple signaling pathways involving PI3K/Akt/mTOR, EGFR, TLR4/NF-κB, AMPK, and type I IFN. Our findings provide novel mechanisms for beneficial effects of NAC in protecting the intestine from inflammation in animals.

N-Acetylcysteine supplementation alleviates intestinal injury in piglets infected by porcine epidemic diarrhea virus.

Porcine epidemic diarrhea virus (PEDV) infects the intestine of young pigs, but effective measures for prevention and treatment are lacking. N-Acetylcysteine (NAC) has been shown to reduce endotoxin-induced intestinal dysfunction. This study was conducted with the PEDV-infected neonatal piglet model to determine the effect of NAC supplementation on intestinal function. Thirty-two 7-day-old piglets were randomly allocated to one of four treatments in a 2 × 2 factorial design consisting of two liquid diets (0 or 50 mg/kg BW NAC supplementation) and oral administration of 0 or 104.5 TCID50 (50% tissue culture infectious dose) PEDV. On day 7 of the trial, half of the pigs (n = 8) in each dietary treatment received either sterile saline or PEDV (Yunnan province strain) solution at 104.5 TCID50 per pig. On day 10 of the trial, D-xylose (0.1 g/kg BW) was orally administrated to all pigs. One hour later, jugular vein blood samples were collected, and then all pigs were killed to obtain the small intestine. PEDV infection increased diarrhea incidence, while reducing ADG. PEDV infection also decreased plasma D-xylose concentration, small intestinal villus height, mucosal I-FABP and villin mRNA levels but increased mucosal MX1 and GCNT3 mRNA levels (P < 0.05). Dietary NAC supplementation ameliorated the PEDV-induced abnormal changes in all the measured variables. Moreover, NAC reduced oxidative stress, as indicated by decreases in plasma and mucosal H2O2 levels. Collectively, these novel results indicate that dietary supplementation with NAC alleviates intestinal mucosal damage and improves the absorptive function of the small intestine in PEDV-infected piglets.

Definitions of intestinal failure and the short bowel syndrome.

The European Society for Clinical Nutrition and Metabolism defined intestinal failure (IF) as "the reduction of gut function below the minimum necessary for the absorption of macronutrients and/or water and electrolytes, such that intravenous supplementation is required to maintain health and/or growth". IF is classified as type 1-acute, type 2-prolonged acute and type 3-chronic IF. A short bowel syndrome (SBS) due to the intestinal malabsorption associated with a functional small intestine length of less than 200 cm is the most frequent mechanism of IF. SBS is a difficult and multifaced disease. Complications due to SBS itself and to treatments, such as long term home parenteral nutrition, can adversely affect the patient outcome. The care of SBS requires complex technologies and multidisciplinary and multiprofessional activity and expertise. Patient outcome is strongly dependent on care and support from an expert specialist team. This paper focuses on the aspects of the pathophysiology and on the complications of SBS, which are most relevant in the clinical practice, such as intestinal failure associated liver disease, renal failure, biliary and renal stones, dehydration and electrolyte depletion, magnesium deficiency and D-lactic acidosis.

Anti-diarrhoeal Activity.

Diarrhoea is characterized by an increase in the frequency of bowel movements, wet stool and abdominal pains. It is the world's third highest killer disease, contributing substantially to paediatric morbidity and mortality, especially in the malnourished. Antibiotics used as anti-diarrhoeal drugs sometimes provoke adverse effects and microorganisms tend to develop resistance towards them. Therefore, the search for safe and more effective agents from plant origin using standard protocols of charcoal meal-induced diarrhoea has been defined in this chapter.