Impaired Fat Absorption Research Articles

Impaired Fat Absorption from Intestinal Tract in High-Fat Diet Fed Male Mice Deficient in Proglucagon-Derived Peptides.

(1) Background: Proglucagon-derived peptides (PDGPs) including glucagon (Gcg), GLP-1, and GLP-2 regulate lipid metabolism in the liver, adipocytes, and intestine. However, the mechanism by which PGDPs participate in alterations in lipid metabolism induced by high-fat diet (HFD) feeding has not been elucidated. (2) Methods: Mice deficient in PGDP (GCGKO) and control mice were fed HFD for 7 days and analyzed, and differences in lipid metabolism in the liver, adipose tissue, and duodenum were investigated. (3) Results: GCGKO mice under HFD showed lower expression levels of the genes involved in free fatty acid (FFA) oxidation such as Hsl, Atgl, Cpt1a, Acox1 (p < 0.05), and Pparα (p = 0.05) mRNA in the liver than in control mice, and both FFA and triglycerides content in liver and adipose tissue weight were lower in the GCGKO mice. On the other hand, phosphorylation of hormone-sensitive lipase (HSL) in white adipose tissue did not differ between the two groups. GCGKO mice under HFD exhibited lower expression levels of Pparα and Cd36 mRNA in the duodenum as well as increased fecal cholesterol contents compared to HFD-controls. (4) Conclusions: GCGKO mice fed HFD exhibit a lesser increase in hepatic FFA and triglyceride contents and adipose tissue weight, despite reduced β-oxidation in the liver, than in control mice. Thus, the absence of PGDP prevents dietary-induced fatty liver development due to decreased lipid uptake in the intestinal tract.

Dietary intervention for a growing Australian Kelpie with intestinal lipid malabsorption

AbstractA 12‐week‐old male Australian Kelpie was referred for nutritional consultation after being diagnosed with autosomal recessively inherited intestinal lipid malabsorption (ILM). At the timepoint of referral, the dog's bodyweight was below the ideal growth curve, the faecal quality was poor and the patient received a pancreatic enzyme supplement. The patient's diet at referral was based on a commercial dry food for all age groups and contained approximately 20% fat in dry matter (DM). We formulated a highly digestible homemade diet with a low‐fat content (10% DM) while meeting the recommendations for linoleic acid, α‐linolenic acid, eicosapentaenoic acid and docosahexaenoic acid, which supported the nutritional requirements of a growing dog with impaired fat absorption. The diet was adapted according to the different growth phases.To our knowledge, this is the first case report highlighting the nutritional management of an Australian Kelpie with ILM. After diet adaptation, the patient reached his growth potential.

Factors contributing to nonalcoholic fatty liver disease (NAFLD) and fat deposition after pancreaticoduodenectomy: A retrospective analysis.

Nonalcoholic fatty liver disease (NAFLD) can occur due to various reasons after pancreaticoduodenectomy (PD). This study examined the risk and perioperative determinants of NAFLD and fat deposition after PD. A total of 101 patients who had undergone computed tomography 6 months after PD were included. We compared perioperative factors between patients who developed NAFLD and those who developed fatty deposits after PD. In the NAFLD group, pancreatic cancer was significantly more prevalent among patients who developed postoperative NAFLD (p = 0.024) and had a lower postoperative body mass index (BMI; p = 0.008). Multivariate analysis revealed that pancreatic carcinoma (hazard ratio [HR] 4.42, 95% confidence interval [CI] 1.118-17.442, p = 0.034) and lower postoperative BMI (HR 0.51, 95% CI 0.274-0.954, p = 0.0355) were risk factors for fatty liver. Pancreatic leakage (p = 0.024) and postoperative BMI (p = 0.002) were significantly lower in the fat deposition group than those in the NAFLD group. Multivariate analysis also revealed that a lower postoperative BMI was a risk factor for fat deposition (HR 0.56, 95% CI 0.523-0.982, p = 0.042). Moreover, multivariate analysis revealed that the fat deposition group had significantly lower pancreatic leakage than the NAFLD group (HR 7.944, 95% CI 1.993-63.562, p = 0.049). The findings of this study suggest that postoperative BMI and pancreatic cancer are associated with a higher risk of NAFLD after PD, possibly because of pancreatic exocrine insufficiency and impaired fat absorption.

Surf4 (Surfeit Locus Protein 4) Deficiency Reduces Intestinal Lipid Absorption and Secretion and Decreases Metabolism in Mice.

Postprandial dyslipidemia is a causative risk factor for cardiovascular disease. The majority of absorbed dietary lipids are packaged into chylomicron and then delivered to circulation. Previous studies showed that Surf4 (surfeit locus protein 4) mediates very low-density lipoprotein secretion from hepatocytes. Silencing hepatic Surf4 markedly reduces the development of atherosclerosis in different mouse models of atherosclerosis without causing hepatic steatosis. However, the role of Surf4 in chylomicron secretion is unknown. We developed inducible intestinal-specific Surf4 knockdown mice (Surf4IKO) using Vil1Cre-ERT2 and Surf4flox mice. Metabolic cages were used to monitor mouse metabolism. Enzymatic kits were employed to measure serum and tissue lipid levels. The expression of target genes was detected by qRT-PCR and Western Blot. Transmission electron microscopy and radiolabeled oleic acid were used to assess the structure of enterocytes and intestinal lipid absorption and secretion, respectively. Proteomics was performed to determine changes in protein expression in serum and jejunum. Surf4IKO mice, especially male Surf4IKO mice, displayed significant body weight loss, increased mortality, and reduced metabolism. Surf4IKO mice exhibited lipid accumulation in enterocytes and impaired fat absorption and secretion. Lipid droplets and small lipid vacuoles were accumulated in the cytosol and the endoplasmic reticulum lumen of the enterocytes of Surf4IKO mice, respectively. Surf4 colocalized with apoB and co-immunoprecipitated with apoB48 in differentiated Caco-2 cells. Intestinal Surf4 deficiency also significantly reduced serum triglyceride, cholesterol, and free fatty acid levels in mice. Proteomics data revealed that diverse pathways were altered in Surf4IKO mice. In addition, Surf4IKO mice had mild liver damage, decreased liver size and weight, and reduced hepatic triglyceride levels. Our findings demonstrate that intestinal Surf4 plays an essential role in lipid absorption and chylomicron secretion and suggest that the therapeutic use of Surf4 inhibition requires highly cell/tissue-specific targeting.

Excess Growth Hormone Alters the Male Mouse Gut Microbiome in an Age-dependent Manner.

The gut microbiome has an important role in host development, metabolism, growth, and aging. Recent research points toward potential crosstalk between the gut microbiota and the growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis. Our laboratory previously showed that GH excess and deficiency are associated with an altered gut microbial composition in adult mice. Yet, no study to date has examined the influence of GH on the gut microbiome over time. Our study thus tracked the effect of excess GH action on the longitudinal changes in the gut microbial profile (ie, abundance, diversity/maturity, predictive metabolic function, and short-chain fatty acid [SCFA] levels) of bovine GH (bGH) transgenic mice at age 3, 6, and 12 months compared to littermate controls in the context of metabolism, intestinal phenotype, and premature aging. The bGH mice displayed age-dependent changes in microbial abundance, richness, and evenness. Microbial maturity was significantly explained by genotype and age. Moreover, several bacteria (ie, Lactobacillus, Lachnospiraceae, Bifidobacterium, and Faecalibaculum), predictive metabolic pathways (such as SCFA, vitamin B12, folate, menaquinol, peptidoglycan, and heme B biosynthesis), and SCFA levels (acetate, butyrate, lactate, and propionate) were consistently altered across all 3 time points, differentiating the longitudinal bGH microbiome from controls. Of note, the bGH mice also had significantly impaired intestinal fat absorption with increased fecal output. Collectively, these findings suggest that excess GH alters the gut microbiome in an age-dependent manner with distinct longitudinal microbial and predicted metabolic pathway signatures.

Dietary Management of Chronic Kidney Disease and Secondary Hyperoxaluria in Patients with Short Bowel Syndrome and Type 3 Intestinal Failure.

Short gut syndrome can lead to type 3 intestinal failure, and nutrition and hydration can only be achieved with parenteral nutrition (PN). While this is a lifesaving intervention, it carries short- and long-term complications leading to complex comorbidities, including chronic kidney disease. Through a patient with devastating inflammatory bowel disease’s journey, this review article illustrates the effect of short gut and PN on kidney function, focusing on secondary hyperoxaluria and acute precipitants of glomerular filtration. In extensive small bowel resections colon in continuity promotes fluid reabsorption and hydration but predisposes to hyperoxaluria and stone disease through the impaired gut permeability and fat absorption. It is fundamental, therefore, for dietary intervention to maintain nutrition and prevent clinical deterioration (i.e., sarcopenia) but also to limit the progression of renal stone disease. Adaptation of both enteral and parenteral nutrition needs to be individualised, keeping in consideration not only patient comorbidities (short gut and jejunostomy, cirrhosis secondary to PN) but also patients’ wishes and lifestyle. A balanced multidisciplinary team (renal physician, gastroenterologist, dietician, clinical biochemist, pharmacist, etc.) plays a core role in managing complex patients, such as the one described in this review, to improve care and overall outcomes.

Low production of 12α-hydroxylated bile acids prevents hepatic steatosis in Cyp2c70−/− mice by reducing fat absorption

Bile acids (BAs) play important roles in lipid homeostasis, and BA signaling pathways serve as therapeutic targets for nonalcoholic fatty liver disease (NAFLD). Recently, we generated cytochrome P450, family 2, subfamily C, polypeptide 70 (Cyp2c70−/−) mice with a human-like BA composition lacking mouse-/rat-specific muricholic acids to accelerate translation from mice to humans. We employed this model to assess the consequences of a human-like BA pool on diet-induced obesity and NAFLD development. Male and female Cyp2c70−/− mice and WT littermates were challenged with a 12-week high-fat Western-type diet (WTD) supplemented with 0.25% cholesterol. Cyp2c70 deficiency induced a hydrophobic BA pool with high abundances of chenodeoxycholic acid, particularly in females, because of sex-dependent suppression of sterol 12α-hydroxylase (Cyp8b1). Plasma transaminases were elevated, and hepatic fibrosis was present in Cyp2c70−/− mice, especially in females. Surprisingly, female Cyp2c70−/− mice were resistant to WTD-induced obesity and hepatic steatosis, whereas male Cyp2c70−/− mice showed similar adiposity and moderately reduced steatosis compared with WT controls. Both intestinal cholesterol and FA absorption were reduced in Cyp2c70−/− mice, the latter more strongly in females, despite unaffected biliary BA secretion rates. Intriguingly, the biliary ratio 12α-/non-12α-hydroxylated BAs significantly correlated with FA absorption and hepatic triglyceride content as well as with specific changes in gut microbiome composition. The hydrophobic human-like BA pool in Cyp2c70−/− mice prevents WTD-induced obesity in female mice and NAFLD development in both genders, primarily because of impaired intestinal fat absorption. Our data point to a key role for 12α-hydroxylated BAs in control of intestinal fat absorption and modulation of gut microbiome composition.

Grasp55\u2212/\u2212 mice display impaired fat absorption and resistance to high-fat diet-induced obesity

The Golgi apparatus plays a central role in the intracellular transport of macromolecules. However, molecular mechanisms of Golgi-mediated lipid transport remain poorly understood. Here, we show that genetic inactivation of the Golgi-resident protein GRASP55 in mice reduces whole-body fat mass via impaired intestinal fat absorption and evokes resistance to high-fat diet induced body weight gain. Mechanistic analyses reveal that GRASP55 participates in the Golgi-mediated lipid droplet (LD) targeting of some LD-associated lipases, such as ATGL and MGL, which is required for sustained lipid supply for chylomicron assembly and secretion. Consequently, GRASP55 deficiency leads to reduced chylomicron secretion and abnormally large LD formation in intestinal epithelial cells upon exogenous lipid challenge. Notably, deletion of dGrasp in Drosophila causes similar defects of lipid accumulation in the midgut. These results highlight the importance of the Golgi complex in cellular lipid regulation, which is evolutionary conserved, and uncover potential therapeutic targets for obesity-associated diseases.

Characterization of an intestine-specific GH receptor knockout (IntGHRKO) mouse

ObjectiveGrowth hormone (GH) has been reported to enhance the intestinal barrier; as such, recombinant GH has been administered for several intestinal diseases. However, excess GH action has been implicated in increasing the risk of intestinal dysfunction. The goal of this study was to examine the direct effects of GH on the small and large intestines to clarify the role GH plays in intestinal function through the use of a mouse model. DesignAn intestinal epithelial-specific GH receptor (GHR) knockout (IntGHRKO) mouse line was generated using Cre-lox with the villin promoter driving Cre expression. The generated mice were characterized with respect to growth and intestinal phenotypes. ResultsIntGHRKO mice showed no significant changes in body length, weight, or composition compared to floxed controls. Male IntGHRKO mice had significantly shorter large intestines at 4 and 12 months of age. Intestinal barrier function was assessed by measuring the expression of tight junction related genes, as well as levels of serum endotoxin and fecal albumin. Results showed sex differences as males had an increase in occludin levels but normal serum endotoxin and fecal albumin; while, females had changes in fecal albumin levels with normal occludin and serum endotoxin. Evaluation of glucose tolerance and fat absorption also showed sex differences as females were glucose intolerant, while males had impaired fat absorption. Histopathology revealed a trend towards decreased villus height in males, which could explain the sex difference in glucose homeostasis. ConclusionsOverall, the data demonstrate that disruption of GH on the intestinal epithelial cells modestly affects the intestinal gross anatomy, morphology, and function in a sex-specific manner.

Abstract 186: Cyp8b1 Ablation Prevents Western Diet-Induced Weight Gain and Hepatic Steatosis due to Impaired Fat Absorption

Bile acids (BAs) are cholesterol derivatives that are well-known for their role in facilitating intestinal lipid absorption. Furthermore, they can regulate glucose and lipid metabolism by activating nuclear and cell surface receptors. Insulin resistance is correlated with alterations in bile acid composition, in particular higher levels of 12&amp;#945;-hydroxylated BAs. These BA species are generated by the enzyme Cyp8b1. We hypothesized that elevated levels of 12&amp;#945;-hydroxylated BAs could be a link between insulin resistance and defects of lipid metabolism. To study the role of Cyp8b1 in the regulation of lipid metabolism, we used Cyp8b1 deficient mice-which are unable to produce 12&amp;#945;-hydroxy BAs-and challenged them with a western type diet. We found that Cyp8b1-/- mice gained less weight compared to controls, which was entirely accounted for by fat mass. Triglyceride and cholesterol accumulation in the liver of Cyp8b1-/- mice were also strongly reduced. We found that these improvements were due to reduced lipid absorption in the intestine of Cyp8b1-/- mice, which could be rescued by replenishing the pool with taurocholic acid. The lipid malabsorption resulted in higher caloric excretion in the feces, due to excess excretion of hydrolyzed dietary lipids. When we fed the mice with a fat-free diet, these differences between genotypes were normalized, confirming the central role of BA composition-not just overall levels-in intestinal lipid absorption and whole-body lipid homeostasis. Based on these findings, it is possible that reducing 12&amp;#945;-hydroxy BAs could be a therapeutic option for the control of obesity and lipid homeostasis.

Cyp8b1 ablation prevents Western diet-induced weight gain and hepatic steatosis because of impaired fat absorption.

Bile acids (BAs) are cholesterol derivatives that regulate lipid metabolism, through their dual abilities to promote lipid absorption and activate BA receptors. However, different BA species have varying abilities to perform these functions. Eliminating 12α-hydroxy BAs in mice via Cyp8b1 knockout causes low body weight and improved glucose tolerance. The goal of this study was to determine mechanisms of low body weight in Cyp8b1-/- mice. We challenged Cyp8b1-/- mice with a Western-type diet and assessed body weight and composition. We measured energy expenditure, fecal calories, and lipid absorption and performed lipidomic studies on feces and intestine. We investigated the requirement for dietary fat in the phenotype using a fat-free diet. Cyp8b1-/- mice were resistant to Western diet-induced body weight gain, hepatic steatosis, and insulin resistance. These changes were associated with increased fecal calories, due to malabsorption of hydrolyzed dietary triglycerides. This was reversed by treating the mice with taurocholic acid, the major 12α-hydroxylated BA species. The improvements in body weight and steatosis were normalized by feeding mice a fat-free diet. The effects of BA composition on intestinal lipid handling are important for whole body energy homeostasis. Thus modulating BA composition is a potential tool for obesity or diabetes therapy.

The effect of impaired angiogenesis on intestinal function following massive small bowel resection

PurposeIntestinal adaptation involves villus lengthening, crypt deepening, and increased capillary density following small bowel resection (SBR). Mice lacking the proangiogenic chemokine CXCL5 have normal structural adaptation but impaired angiogenesis. This work evaluates the impact of incomplete adaptive angiogenesis on the functional capacity of the intestine after SBR. MethodsCXCL5 knockout (KO) and C57BL/6 wild-type (WT) mice underwent 50% SBR. Magnetic resonance imaging measured weekly body composition. Intestinal absorptive capacity was evaluated through fecal fat analysis. Gene expression profiles for select macronutrient transporters were measured via RT-PCR. Postoperative crypt and villus measurements were assessed for structural adaptation. Submucosal capillary density was measured through CD31 immunohistochemistry. ResultsComparable postoperative weight gain occurred initially. Diminished weight gain, impaired fat absorption, and elevated steatorrhea occurred in KO mice after instituting high-fat diet. Greater postoperative upregulation of ABCA1 fat transporter occurred in WT mice, while PEPT1 protein transporter was significantly downregulated in KO mice. KO mice had impaired angiogenesis but intact structural adaptation. ConclusionAfter SBR, KO mice display an inefficient intestinal absorption profile with perturbed macronutrient transporter expression, impaired fat absorption, and slower postoperative weight gain. In addition to longer villi and deeper crypts, an intact angiogenic response may be required to achieve functional adaptation to SBR.

Partial Pancreatic Resection for Pancreatic Malignancy Is Associated with Sustained Pancreatic Exocrine Failure and Reduced Quality of Life: A Prospective Study

Objectives: Pancreatic resection for cancer may produce pancreatic exocrine insufficiency (PEI), which is poorly understood. This study examined the coefficient of fat absorption (CFA), symptoms, quality of life (QoL) and the accuracy of faecal elastase-1 (FE-1) measurement to predict PEI. Methods: Forty patients were analysed following resection for pancreatic malignancy. The primary endpoint was PEI diagnosis defined by CFA !93%; secondary endpoints were PEI diagnosis using FE-1 <200 μg/g, body mass index (BMI), and symptom and QoL analysis. Interventions were 3-day stool collection, EORTC QLQ-C30 (version 1) questionnaire and patient's diary, at 6 weeks and 3,6 and 12 months after surgery. Results: CFA <93% was presentin 67% of patients at 6 weeks and in 55% at 12 months. PEI using FE-1 was present in 77 and 83% of patients, respectively. No significant changes between time-points were observed. Sensitivity, specificity, PPV, NPV and accuracy for FE-1 in detecting CFA <93% were 91, 35, 70, 71 and 70%, respectively. CFA and FE-1 levels were uncorrelated. Overall, QoL increased at 6 (p = 0.0212) and 12 (p < 0.0001) months after surgery, mainly driven by physical, role and social functioning, and by appetite. Importantly, however, BMI and symptoms were unaffected by PEI, which suggests a subclinical presentation; such patients had attributes indicating poorer QoL (notably insomnia, p = 0.0012). Conclusions: PEI was common and sustained following resection and not associated with significant symptoms. These patients had a tendency toward poorer QoL. FE-1 is a poor surrogate for diagnosing impaired fat absorption. Postoperative pancreatic enzyme replacement should be considered more routinely.

Fat burners: nutrition supplements that increase fat metabolism.

The term 'fat burner' is used to describe nutrition supplements that are claimed to acutely increase fat metabolism or energy expenditure, impair fat absorption, increase weight loss, increase fat oxidation during exercise, or somehow cause long-term adaptations that promote fat metabolism. Often, these supplements contain a number of ingredients, each with its own proposed mechanism of action and it is often claimed that the combination of these substances will have additive effects. The list of supplements that are claimed to increase or improve fat metabolism is long; the most popular supplements include caffeine, carnitine, green tea, conjugated linoleic acid, forskolin, chromium, kelp and fucoxanthin. In this review the evidence for some of these supplements is briefly summarized. Based on the available literature, caffeine and green tea have data to back up its fat metabolism-enhancing properties. For many other supplements, although some show some promise, evidence is lacking. The list of supplements is industry-driven and is likely to grow at a rate that is not matched by a similar increase in scientific underpinning.

Fibrinogen Storage Disease Caused by Aguadilla Mutation Presenting With Hypobeta‐lipoproteinemia and Considerable Liver Disease

Fibrinogen Storage Disease Caused by Aguadilla Mutation Presenting With Hypobeta‐lipoproteinemia and Considerable Liver Disease

Appetite and obesity: a gastroenterologist's perspective

This review focuses on the gastrointestinal tract's control of appetite and interventions directed to the gut that are effective in the treatment of obesity. It examines the evidence linking gut hormones to the control of both appetite and upper gastrointestinal motility, the evidence that stomach function is altered and contributes to satiation in obesity and outlines the principles of therapy for obesity which are directed at the gastrointestinal tract. These therapies impair fat absorption or alter stomach functions through pharmacological, device, endoscopic, or surgical approaches. Gastroenterologists need to understand the role of factors controlling appetite in order to effectively manage the increasing number of obese patients and the ways the gut function may be altered as a result of the treatments and their complications.

The Farnesoid X Receptor Modulates Adiposity and Peripheral Insulin Sensitivity in Mice

The farnesoid X receptor (FXR) is a bile acid (BA)-activated nuclear receptor that plays a major role in the regulation of BA and lipid metabolism. Recently, several studies have suggested a potential role of FXR in the control of hepatic carbohydrate metabolism, but its contribution to the maintenance of peripheral glucose homeostasis remains to be established. FXR-deficient mice display decreased adipose tissue mass, lower serum leptin concentrations, and elevated plasma free fatty acid levels. Glucose and insulin tolerance tests revealed that FXR deficiency is associated with impaired glucose tolerance and insulin resistance. Moreover, whole-body glucose disposal during a hyperinsulinemic euglycemic clamp is decreased in FXR-deficient mice. In parallel, FXR deficiency alters distal insulin signaling, as reflected by decreased insulin-dependent Akt phosphorylation in both white adipose tissue and skeletal muscle. Whereas FXR is not expressed in skeletal muscle, it was detected at a low level in white adipose tissue in vivo and induced during adipocyte differentiation in vitro. Moreover, mouse embryonic fibroblasts derived from FXR-deficient mice displayed impaired adipocyte differentiation, identifying a direct role for FXR in adipocyte function. Treatment of differentiated 3T3-L1 adipocytes with the FXR-specific synthetic agonist GW4064 enhanced insulin signaling and insulin-stimulated glucose uptake. Finally, treatment with GW4064 improved insulin resistance in genetically obese ob/ob mice in vivo. Although the underlying molecular mechanisms remain to be unraveled, these results clearly identify a novel role of FXR in the regulation of peripheral insulin sensitivity and adipocyte function. This unexpected function of FXR opens new perspectives for the treatment of type 2 diabetes.

Disrupted fat absorption attenuates obesity induced by a high-fat diet in Clock mutant mice

The Clock gene is a core component of the circadian clock in mammals. We show here that serum levels of triglyceride and free fatty acid were significantly lower in circadian Clock mutant ICR than in wild-type control mice, whereas total cholesterol and glucose levels did not differ. Moreover, an increase in body weight induced by a high-fat diet was attenuated in homozygous Clock mutant mice. We also found that dietary fat absorption was extremely impaired in Clock mutant mice. Circadian expressions of cholecystokinin-A (CCK-A) receptor and lipase mRNAs were damped in the pancreas of Clock mutant mice. We therefore showed that a Clock mutation attenuates obesity induced by a high-fat diet in mice with an ICR background through impaired dietary fat absorption. Our results suggest that circadian clock molecules play an important role in lipid homeostasis in mammals.

Clostridial constipation’s broad pathology

Clostridia are normally found in the healthy colon, where their numbers are kept in check by other bacteria. However, when they establish themselves in the ileum they become formidable foes. They produce medium-length fatty acids that increase water absorption, causing hypertension and drying up the feces, causing constipation.Furthermore, they can deconjugate bile (impaired fat absorption), metabolyze tryptophan (the most scarce of the essential amino acids), digest fiber (so that the more fiber the patient takes, the more the constipation is exacerbated), digest lecithin, produce carcinogenic metabolites and copious amounts of extremely foul smelling gas, etc. They can also prevent vitamin B12 absorption in the ileum, causing anemia.The synthetic sugar lactulose, which can only be digested by lactobacilli, can help displace the clostridia and resolve the constipation by causing the lactobacilli to produce short fatty acids that have the opposite effect to that of the medium fatty acids produced by clostridia and their accomplices: they cause water retention in the intestines.

Effect of zinc bacitracin and salinomycin on intestinal microflora and performance of broilers

A feeding experiment was carried out over 42 d with four groups of broiler chickens fed experimental diets formulated to provide no supplementation, 20 mg zinc bacitracin, 60 mg salinomycin, or both feed additives in combination. During the fifth week of the experiment, four chickens from each pen were killed, and the contents of gizzard, duodenum, jejunum, ileum, ceca, and rectum were separately collected and pooled. In all intestinal segments, the pH and the concentration of lactic acid were measured, and the numbers of anaerobic bacteria, coliforms, lactic acid bacteria, lactobacilli, enterococci, and Clostridium perfringens were counted. In homogenates of pancreas obtained from four animals, the activities of amylase, lipase, trypsin, and chymotrypsin were measured. A significant growth-promoting effect was observed in the group receiving zinc bacitracin in combination with salinomycin. Zinc bacitracin significantly reduced the number of coliform bacteria in the ileum and increased the activities of amylase and lipase in pancreas homogenates. Supplementation with salinomycin and zinc bacitracin, alone or in combination, resulted in significantly lower counts of C. perfringens as well as Lactobacillus salivarius, which was a dominant lactic acid bacterium found in broiler intestinal contents. High numbers of these lactobacilli may play a role in broiler growth depression related to competition in nutrient uptake or impaired fat absorption due to bile acid deconjugation.