Body condition score (BCS) around calving, and the typical BCS loss for up to 100 d after parturition, is associated with both production and reproductive performance of dairy cattle. In addition, there is public concern that thin cows may have impaired welfare, particularly in early lactation where feed demand exceeds pasture growth, and a lag exists between peak milk energy requirements and intake. The aim of this experiment was to determine how BCS at calving influences behavioral and physiological responses to a short-term feed restriction at 47 DIM. Body condition score (on a 10-point scale) at calving was manipulated by modifying the diets in the previous lactation of healthy dairy cattle to generate 3 treatment groups: low BCS (3.4; n = 17), medium BCS (4.6; n = 18), or high BCS (5.4; n = 20). Cows were tested in 4 groups for 8 consecutive days; testing consisted of different levels of feed allocation (d 1 and 2: 100%; d 3 and 4: 75%; d 5: 50%; d 6 to 8: 125%), where 100% was 15 kg of DM/cow per day. All BCS groups had similar and marked behavioral and physiological responses to feed restriction. For example, they increased vocalization, time spent eating silage and grazing, aggressive behavior, and fat metabolism (as measured by concentrations of β-hydroxybutyrate and nonesterified fatty acids), and reduced milk production. Body condition affected some of these responses. Fewer cows with low BCS engaged in aggressive interactions in a feed competition test (trough filled with silage that could be consumed in 15 min) on the first day of feed restriction (low: 32%; medium: 74%; high: 64%; standard error of difference = 15.4%). High-BCS cows had greater concentrations of β-hydroxybutyrate and nonesterified fatty acids throughout the experimental period, which suggests more fat mobilization; however, plasma leptin and fecal glucocorticosteroid metabolite concentrations were unaffected by BCS. Whereas cows demonstrated marked responses to feed restriction, the results suggest that a BCS of 3.4, 4.6, or 5.4 in healthy cows at calving does not overwhelmingly influence this response at 47 DIM.

Altered concentrations of bile acid (BA) in the colon can cause diarrhea or constipation. More than 25% of patients with irritable bowel syndrome (IBS) with diarrhea or chronic diarrhea in Western countries have BA malabsorption (BAM). As BAM is increasingly recognized, proper diagnostic methods are needed, to help direct the most effective course of treatment for the chronic bowel dysfunction. We review the methodologies, advantages, and disadvantages of tools that directly measure BAM: the (14)C-glycocholate breath and stool test, the (75)selenium homotaurocholic acid test (SeHCAT), and measurements of 7 α-hydroxy-4-cholesten-3-one (C4) and fecal BAs. The (14)C-glycocholate test is laborious and no longer widely used. The (75)SeHCAT has been validated, but is not available in the United States (US). Measurement of serum C4 is a simple and accurate method that can be used for most patients, but requires further clinical validation. Assays to quantify fecal BA (total and individual levels) are technically cumbersome and not widely available. Regrettably, none of these tests are routinely available in the US; assessment of the therapeutic effects of a BA binder is used as a surrogate for diagnosis of BAM. Recent data indicate the advantages to studying fecal excretion of individual BAs and their role in BAM; these could support the use of the fecal BA assay, compared with other tests. Measurement of fecal BA levels could become a routine addition to the measurement of fecal fat in patients with unexplained diarrhea. Availability ultimately determines whether the C4, SeHCAT, or fecal BA test is used; more widespread availability of such tests would enhance clinical management of these patients.

BACKGROUND:

&

Aims:

There is an unclear relationship among bowel symptoms, excretion of unconjugated fecal bile acid (UBA), and colonic transit in irritable bowel syndrome (IBS). We measured total and main individual UBA in fecal samples of patients with IBS, and assessed relationships among stool frequency or consistency, fecal UBA (total and individual), and colonic transit.

METHODS:

In a study of 30 healthy volunteers (controls), 31 subjects with IBS with diarrhea (IBS-D), and 30 with IBS with constipation (IBS-C) were placed on 4-day diets containing 100 g fat; we measured stool characteristics, total fecal UBA and fat levels, and overall colonic transit. We assessed univariate associations of total and individual levels of fecal UBA with phenotype (controls, IBS-D, IBS-C) using the Kruskal-Wallis test; associations between endpoints were assessed using Spearman correlations. With response surface regression models, we assessed relationships between stool, colonic transit, and fecal total and secretory UBA.

RESULTS:

There was a significant association between total fecal UBA and phenotype (P=.029); the association was greater for IBS-D than IBS-C, compared with controls. Fecal levels of primary UBAs (cholic and chenodeoxycholic acids) were higher in subjects with IBS-D, compared with controls (both P<.01). Levels of fecal secretory UBAs (chenodeoxycholic acids, P=.019; deoxycholic acid, P=.025) were lower in subjects with IBS-C compared with controls, whereas levels of the nonsecretory UBA, lithocholic acid, were higher (P=.020). There were significant univariate associations between stool number and form and total fecal UBA (including percentages of lithocholic acid, chenodeoxycholic acids, and cholic acid), fecal fat, and colonic transit at 24 and 48 h after eating. In the regression models, the relative contribution of colonic transit was consistently greater, and largely independent of the contribution of bile acids.

CONCLUSIONS:

Measurements of individual UBAs identify changes associated with stool characteristics in patients with IBS; these effects are independent of the effects of colonic transit.

To investigate the functional effects of probiotic treatment on the gut microbiota, as well as liver and adipose gene expression in diet-induced obese mice.Male C57BL/6J mice were fed a high-fat diet (HFD) for 8 weeks to induce obesity, and then randomized to receive HFD+probiotic (Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032, n = 9) or HFD+placebo (n = 9) for another 10 weeks. Normal diet (ND) fed mice (n = 9) served as non-obese controls.Diet-induced obese mice treated with probiotics showed reduced body weight gain and fat accumulation as well as lowered plasma insulin, leptin, total-cholesterol and liver toxicity biomarkers. A total of 151,061 pyrosequencing reads for fecal microbiota were analyzed with a mean of 6,564, 5,274 and 4,464 reads for the ND, HFD+placebo and HFD+probiotic groups, respectively. Gut microbiota species were shared among the experimental groups despite the different diets and treatments. The diversity of the gut microbiota and its composition were significantly altered in the diet-induced obese mice and after probiotic treatment. We observed concurrent transcriptional changes in adipose tissue and the liver. In adipose tissue, pro-inflammatory genes (TNFα, IL6, IL1β and MCP1) were down-regulated in mice receiving probiotic treatment. In the liver, fatty acid oxidation-related genes (PGC1α, CPT1, CPT2 and ACOX1) were up-regulated in mice receiving probiotic treatment.The gut microbiota of diet-induced obese mice appears to be modulated in mice receiving probiotic treatment. Probiotic treatment might reduce diet-induced obesity and modulate genes associated with metabolism and inflammation in the liver and adipose tissue.

Roux-en-Y gastric bypass (RYGB) results in rapid weight loss, reduced adiposity, and improved glucose metabolism. These effects are not simply attributable to decreased caloric intake or absorption, but the mechanisms linking rearrangement of the gastrointestinal tract to these metabolic outcomes are largely unknown. Studies in humans and rats have shown that RYGB restructures the gut microbiota, prompting the hypothesis that some of the effects of RYGB are caused by altered host-microbial interactions. To test this hypothesis, we used a mouse model of RYGB that recapitulates many of the metabolic outcomes in humans. 16S ribosomal RNA gene sequencing of murine fecal samples collected after RYGB surgery, sham surgery, or sham surgery coupled to caloric restriction revealed that alterations to the gut microbiota after RYGB are conserved among humans, rats, and mice, resulting in a rapid and sustained increase in the relative abundance of Gammaproteobacteria (Escherichia) and Verrucomicrobia (Akkermansia). These changes were independent of weight change and caloric restriction, were detectable throughout the length of the gastrointestinal tract, and were most evident in the distal gut, downstream of the surgical manipulation site. Transfer of the gut microbiota from RYGB-treated mice to nonoperated, germ-free mice resulted in weight loss and decreased fat mass in the recipient animals relative to recipients of microbiota induced by sham surgery, potentially due to altered microbial production of short-chain fatty acids. These findings provide the first empirical support for the claim that changes in the gut microbiota contribute to reduced host weight and adiposity after RYGB surgery.

The present study was designed to evaluate the hypolipidemic effect of ursolic acid stearoyl glucoside (UASG) in high-fat diet-induced obesity. Two in vivo experiments such as high-fat diet-induced obesity mice model and lipid emulsion tolerance test in normal rats were performed. In vitro inhibition of pancreatic lipase activity was further measured to substantiate the results. In high-fat diet-induced obesity mice model, female Swiss mice were fed a high fat diet (HFD; 40% fat) with or without 1 or 2% of UASG or 0.012% orlistat for nine weeks. In lipid emulsion tolerance test male Wister rats were orally administered, lipid emulsion with or without 500 or 1000mg/kg of UASG and the plasma triglycerides were measured from 0.5 to 5h. Consumption of HFD containing UASG to mice for nine weeks exhibited significant reduction in lipid parameters, body weight, parametrial adipose tissue weight, liver triglyceride (TG) and different organ weight compared to HFD fed control. Further it was noted the improvement in insulin resistance induced by the HFD alone group. Furthermore, consumption of an HFD containing 1 or 2% of UASG significantly increased the fecal content and fecal triglyceride compared with the HFD group. Pre-treatment with UASG inhibited the elevated plasma triglyceride level after the oral administration of the lipid emulsion to rats. Further, UASG significantly inhibits activity of pancreatic lipase at a concentration of 2.5mg/ml. Data obtained from the results indicated that UASG prevent high-fat diet-induced obesity in mice possibly by inhibiting pancreatic lipase activity.

High-fat (HF) diets can produce obesity and have been linked to the development of nonalcoholic fatty liver disease and changes in the gut microbiome. To test the hypothesis that HF feeding increases certain predominant hind gut bacteria and development of steatohepatitis, C57BL/6 mice were fed an HF (45% energy) or low-fat (LF) (10% energy) diet for 10 wk. At the end of the feeding period, body weights in the HF group were 34% greater than those in the LF group (P < 0.05). These changes were associated with dramatic increases in lipid droplet number and size, inflammatory cell infiltration, and inducible nitric oxide (NO) synthase protein concentration in the livers of mice fed the HF diet. Consistent with the fatty liver phenotype, plasma leptin and tumor necrosis factor-α concentrations were also elevated in mice fed the HF diet, indicative of chronic inflammation. Eight of 12 pairs of polymerase chain reaction (PCR) primers for bacterial species that typically predominate hind gut microbial ecology generated specific PCR products from the fecal DNA samples. The amount of DNA from Lactobacillus gasseri and/or Lactobacillus taiwanensis in the HF group was 6900-fold greater than that in the LF group. Many of these bacteria are bile acid resistant and are capable of bile acid deconjugation. Because bile acids are regulators of hepatic lipid metabolism, the marked increase of gut L. gasseri and/or L. taiwanensis species bacteria with HF feeding may play a role in development of steatohepatitis in this model.

Although dogs and cats are quite different than many livestock species in that they have evolved by eating diets high in fat and protein and low in carbohydrates, the gastrointestinal microbiota still play a key role in the gut and overall host health of these species. Early experiments in this field used culture-based techniques to evaluate the effects of dietary ingredients, such as fibers and prebiotics, on microbiota and indices of gut health (e.g., fecal scores, pH, fermentative end-products). Such studies, however, were limited in scope and lacked precision as it pertained to the microbiota. The DNA-based techniques that have become available over the past decade have greatly upgraded research capabilities and have provided a more encompassing view of the canine and feline gastrointestinal microbiomes. High-throughput sequencing techniques that are much cheaper and faster than Sanger sequencing have been a key development in this progress. Sequence data not only allow for the identification of all microbial taxa, but also provide information regarding functional capacity when a shotgun sequencing approach is used. The few canine and feline studies that have used 454 pyrosequencing have identified the predominant microbial taxa and metabolic functions present in healthy populations, differences between healthy and diseased dog and cat populations, and the effects of diet (e.g., dietary fibers, prebiotics, protein to carbohydrate ratio) on gastrointestinal microbiota. Although these studies have provided a foundation from which to work, more research is needed to increase our general understanding of the gastrointestinal microbiome and how it impacts host health, how its composition and activity may be altered by age, genetic, or environmental factors, and test whether specific pathogens or disease signatures can be identified and used in diagnosis and(or) treatment of disease.

BACKGROUND:

Postoperative anorectal malformation patients frequently have defecatory dysfunction. MRI may be useful in the management of these patients.

OBJECTIVE:

To analyze static and dynamic MRI findings in patients with defecatory dysfunction after correction of anorectal malformation (ARM), and compare differences between patients with constipation and fecal incontinence.

MATERIALS AND METHODS:

Pelvic MRI studies of 20 constipated and 32 incontinent postoperative ARM patients were analyzed retrospectively to determine the location and morphology of the neorectum, presence of peritoneal fat herniation, presence of scarring, development of the striated muscle complex (SMC) and any other abnormalities. The two groups were then compared using χ (2)-test. Eighteen patients also underwent MRI defecography to evaluate pelvic floor function and abnormalities are reported.

RESULTS:

The children with incontinence were more likely to have abnormal location of the neorectum (P = 0.031), increased anorectal angle (ARA) (P = 0.031) and peritoneal fat herniation (P = 0.032), and less likely to have dilation of the neorectum (P = 0.027), than the children with constipation. There were no significant differences between the two groups in incidence of focal stenosis of the neorectum (P = 0.797), presence of extensive scarring (P = 0.591) and developmental agenesis of the SMC (P > 0.05). MRI defecography showed 6 anterior rectoceles, 6 cystoceles and 18 pelvic floor descents.

CONCLUSIONS:

MRI is a helpful imaging modality in postoperative ARM patients with defecatory dysfunction, and it shows distinct differences between the children with constipation and incontinence and provides individualized information to guide further treatment.

Little nutritional or metabolic information has been collected from captive exotic cats fed raw diets. In particular, fiber types and concentrations for use in raw meat-based diets for captive exotic felids have not been well-studied. Our objective was to evaluate the effects of fiber type and concentration on apparent total tract energy and macronutrient digestibility, fecal characteristics, and fecal fermentative end-products in captive exotic felids. Four animals of each captive exotic species [jaguar (Panthera onca), cheetah (Acinonyz jubatus), Malayan tiger (Panthera tigris corbetti), and Siberian tiger (Panthera tigris altaica)] were randomized in four 4 x 4 Latin square designs (1 Latin square per species) to 1 of the 4 raw beef-based dietary treatments (94.7 to 96.7% beef trimmings): 2 or 4% cellulose, or 2 or 4% beet pulp. Felid species, fiber type, and fiber concentration all impacted digestibility and fecal fermentative end-products. Inclusion of beet pulp increased (P ≤ 0.05) fecal short-chain fatty acids and fecal output in all cats. Inclusion of 2 and 4% cellulose, and 4% beet pulp increased (P ≤ 0.05) fecal bulk and diluted fecal branched-chain fatty acid concentrations compared with 2% beet pulp. Apparent total tract DM, OM, fat, and GE digestibility coefficients decreased (P ≤ 0.05) linearly with BW of cats. Additionally, fecal moisture, fecal score, and concentrations of fermentative end-products increased (P ≤ 0.05) with BW. Although the response of many outcomes was dependent on cat size, in general, beet pulp increased wet fecal weight, fecal scores, and fecal metabolites, and reduced fecal pH. Cellulose generally reduced DM and OM digestibility, but increased dry fecal weight and fecal % DM. Although beet pulp and cellulose fibers were tested individually in this study, these data indicate that the optimum fiber type and concentration for inclusion in captive exotic felid diets is likely a combination of fermentable and non-fermentable fibers, with the optimal fiber blend being dependent on species. Smaller cats, such as cheetahs and jaguars, tolerated fermentable fibers, while larger cats, such as Malayan and Siberian tigers, appeared to require more insoluble fibers that limit fermentation and provide fecal bulk. Further research is required to test whether these trends hold true when fed in combination.