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PubMed1986

Histamine and mucosal mast cells in gluten enteropathy.

Coeliac disease is a malabsorptive disorder caused by intolerance to gluten and is characterized by a remodelling of the intestinal mucosa including villus atrophy, crypt hyperplasia and net increase of mucosal volume. Changes of the number of mucosal mast cells (MMCs) in coeliac mucosa has recently been reported, suggesting that the mast cell activity could have a pathogenetic role in gluten enteropathy. MMCs located solely in the lamina propria are the main repository for small-gut mucosal histamine. A consecutive prospective study was designed to study the histamine content, MMC numbers, and the relative volume of lamina propria in intestinal biopsies from adult patients suffering from unexplained diarrhea and/or malnutrition. Histamine was measured by a HPLC-method, the number of MMC was counted after long toluidine-blue staining, and the relative volumes of lamina propria and epithelium were estimated morphometrically. The findings were correlated to the histopathological appearance of the mucosa. As compared to controls the histamine content increased by 80% and MMC numbers by about 60% in the coeliac mucosa. There was also a correlation between MMC numbers and histamine content for both normal and coeliac mucosae (r = 0.81). The morphometric estimation of the relative volumes of epithelium and lamina propria revealed that the lamina-propria compartment was increased by approximately 40% in coeliac mucosa. Taking the changes in compartmental volumes of the remodelled coeliac mucosa into account, our results suggest that the histamine content and MMC population were significantly increased. MMC and MMC-associated histamine may therefore be involved in the pathogenesis of gluten enteropathy.

Celiac Disease↗
PubMed2005

Gluten Ataxia and Post-Streptococcal Central Nervous System Syndromes: Emerging Immune-mediated Disorders of the Central Nervous System?

There is an "emerging concept" that central nervous system dysfunction can be caused by an aberrant immune response triggered by exogenous antigens such as the food allergen gluten or streptococcal infection. The hypothesis of a gluten sensitive ataxia remains unproven, but is worthy of consideration. The data in support of this hypothesis require critical review before any treatment recommendations can be formulated. The idea that anti-gliadin antibody seropositivity per se justifies the term "gluten sensitivity" is important because it offers potential therapeutic possibilities, including simple exclusion diets, for patients with anti-gliadin antibody-associated ataxia. Post-streptococcal basal ganglia dysfunction has various manifestations, all of which fall into a relatively well-defined symptom complex or syndrome. Anti-basal ganglia antibodies that are associated with serologic evidence of recent streptococcal infection are a potential diagnostic marker for this group of disorders, which includes Sydenham's chorea (SC) as the prototype. More recently subjects with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection, Tourette's syndrome, obsessive-compulsive disorder and other movement disorders have been described in association with anti-basal ganglia antibodies. The apparent overlap between the clinical phenotype of SC, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections, Tourette's syndrome, and obsessive-compulsive disorder suggests that they may represent one disease entity. The current working hypothesis is that antibodies induced in response to streptococcal infection cross-react with antigenic determinants in the basal ganglia resulting in basal ganglia dysfunction. Although the experimental evidence is incomplete, there is sufficient evidence to support immune-mediated basal ganglia dysfunction as an emerging clinical entity. This has important implications for the diagnosis and treatment of subjects with these disorders. The latter includes the judicious use of antibiotic prophylaxis and immunomodulatory therapies. Apart from the diagnosis and management of SC, no consensus exists regarding the diagnosis and management of the other clinical entities within this group of disorders.

Journal Article↗
PubMed1990

Dermatitis herpetiformis and gluten sensitive enteropathy (including celiac disease)--increased subepithelial extracellular matrix viscosity due to gliadin.

It is now firmly established that dermatitis herpetiformis (DH) is associated with gluten sensitive enteropathy (GSE), although the GSE of DH is generally milder than that form which occurs in celiac disease. The toxic fraction of gluten is in the gliadin, a protein fraction. Gliadin is absorbed in GSE and antigliadin antibodies are present in both DH and celiac disease. There is a question of a cross reactivity between reticulin and gliadin. Gliadin is reported to bind to reticulin. Reticulin has a glycosaminoglycan component. Fibronectin, another component of ground substance, also binds to reticulin. Reticulin and fibronectin are important in basement membrane areas and play a role in basement membrane attachment. Gluten may also exert a lectin effect on gastrointestinal mucosa which contributes to the underlying extracellular matrix. DH and GSE have different pathologies because of their different anatomical sites. The pathomechanisms of both diseases can be explained by one mechanism. Gliadin, or a peptide fraction from it, enters or combines with the extracellular matrix and increases tissue viscosity. The protein fraction of glycosaminoglycans in the extracellular matrix is known to control viscosity. In DH the increased extracellular matrix viscosity would interfere with the diffusion of tissue fluid in the dermal papillae and leads to vesicle formation. The intestinal villi serve a very different function. In GSE the increased extracellular matrix viscosity would decrease adsorption from the intestinal tract producing villi with less volume (shortened or atrophic). The shortened villi decrease the production of digestive enzymes and the absorptive surface. The decreased movement of nutrient tissue fluid supplied to the intestinal epithelial cells also eliminates the microvilli.(ABSTRACT TRUNCATED AT 250 WORDS)

Celiac Disease↗
PubMed2004

Transcriptional downregulation of tight junction protein ZO-1 in active coeliac disease is reversed after a gluten-free diet.

UNLABELLED: Coeliac disease is an autoimmune enteropathy characterized by an enhanced permeability of the intestinal epithelial barrier. In epithelial cells paracellular permeability is regulated by intercellular tight junction. The cytoplasmic protein ZO-1 interacts directly with F-actin and plays a pivotal role in the structural and functional organization of tight junction. AIM: The aim of this study was to investigate the expression and localization of ZO-1 in the intestinal mucosa of coeliac patients. PATIENTS AND METHODS: Twenty patients with active coeliac disease, seven of whom underwent a repeat biopsy following a gluten-free diet and 27 control subjects, were studied. In all subjects, three biopsies were obtained from distal duodenum during upper gastrointestinal endoscopy. ZO-1 protein localization and levels were detected by immunofluorescence followed by confocal microscopy analysis and immunoblotting. ZO-1 mRNA expression was assessed by RT-PCR. F-actin distribution was also investigated. RESULTS: In patients with active coeliac disease, both ZO-1 protein levels and mRNA were clearly reduced. Cytoskeletal organization was disrupted with F-actin staining concentrated at the subcortical and basal surface regions. Abnormalities in ZO-1 expression and actin organization were reversed after a gluten-free diet. CONCLUSIONS: In active coeliac disease, ZO-1 protein expression is downregulated at the transcriptional level in association with F-actin redistribution. These changes are completely reversed after a gluten-free diet and could contribute to the increased intestinal paracellular permeability observed in this disorder.

Actins↗
PubMed1982

Gluten-sensitive enteropathy: sequence of villous regrowth as viewed by scanning electron microscopy.

Small-intestinal biopsy specimens from five children with gluten-sensitive enteropathy (GSE) were studied by scanning electron microscopy (SEM) before dietary treatment and sequentially after removal of gluten from the the diet. Compared with biopsy specimens from patients without evidence of villous atrophy, these specimens showed marked architectural changes. In patients with total villous atrophy observed by light microscopy, absent villi and prominent crypts were observed by SEM. Patients with subtotal villous atrophy had the first stages of villous formation characterized by semicircular ridge formation. Biopsy specimens obtained from the five patients with GSE after dietary treatment demonstrated a sequence of changes characterizing villous repair. The earliest change consisted of semicircular elevations of cells around the crypts. Unequal cellular repletion around the crypts and migration of the cells led to the formation of parallel ridges. Increased cell proliferation resulted in thickening and twisting of the ridges to form convoluted ridges. Increased complexity of the ridges appears to lead to the formation of cerebriform ridges, and septation at various points in the ridges results in the formation of mitten-like villi. In biopsy specimens from patients with villous atrophy from other causes, similar reparative changes were seen by SEM. Scanning electron microscopy is a useful adjunct to the light microscopic and dissecting microscopic assessment of small intestine biopsy specimens, and may be more sensitive tan light microscopy in documenting early morphologic response to dietary treatment for gluten-sensitive enteropathy.

Adolescent↗
PubMed1997

[Common variable immunodeficiency and total villous atrophy regressive after gluten-free diet].

A patient with a commun variable immunodeficiency (CVID) is hospitalized for chronic symptoms of malabsorption (weigh loss and diarrhea). The duodenal histology show a total villous atrophy. Investigations are negative and a gluten free diet is given. Symptoms of malabsorption disappear and improvement is histologically confirmed. Our observation suggest that the coincidence of gluten sensitive enteropathy and CVID is possible and clinicians should be aware of this association and should consider giving a gluten free diet. The sensitivity of serologic testing in this conditions is unknown.

Agammaglobulinemia↗
PubMed2003

Gluten sensitivity and 'normal' histology: is the intestinal mucosa really normal?

BACKGROUND: Early pathogenetic events of gluten intolerance may be overlooked in patients with serologic markers of celiac disease and normal intestinal mucosa by both conventional histology and immunohistochemistry. AIMS: To investigate if a submicroscopical damage of the absorptive cell surface was associated with developing gluten sensitivity. PATIENTS AND METHODS: Duodenal biopsies of seven subjects with positive anti-endomysial antibodies and normal histology underwent ultrastructural evaluation of the epithelial surface by means of both scanning and transmission electron microscopy. Specimens of intestinal mucosa of 14 children with non-celiac conditions were used as controls. RESULTS: In four patients, electron microscopy revealed alterations of the enterocyte brush border with a significant reduction of the height of microvilli. After several months, three of them had a second biopsy that eventually showed histological modifications suggestive of celiac disease. In the other three patients, no significant alteration of enterocyte ultrastructure was observed. One of them, rebiopsied after 12 months, still showed a normal duodenal histology. CONCLUSIONS: Gluten sensitivity can be associated with 'minimal' mucosal changes not detectable with conventional light microscopy. Such lesions, which primarily involve microvillous structure, may imply a reduction of intestinal absorptive surface already in the latent stage of the disease.

Adolescent↗
PubMedDate not supplied

Eosinophilic gastroenteritis and gluten-sensitive enteropathy in the same patient.

We report the clinical and laboratory features of a 19-year-old man with findings of both eosinophilic gastroenteritis and gluten-sensitive enteropathy. Before the onset of clinical symptoms, the patient had received a series of hepatitis B vaccinations but had not developed a measurable antibody response or any allergic reaction. Radioallergosorbent test results were positive to several foods, and the total serum immunoglobulin E (IgE) level was elevated. Adherence to a gluten-free diet caused a normalization in the endomysial antibody titer; however, the total serum IgE level continued to increase, and the total eosinophil count remained elevated. Symptoms of recurrent vomiting and abdominal pain necessitated prednisone burst therapy. The simultaneous occurrence of eosinophilic gastroenteritis and gluten-sensitive enteropathy is rare; therapy should be directed to each disorder individually.

Adult↗
PubMed2003

The symptomatic and histologic response to a gluten-free diet in patients with borderline enteropathy.

GOALS: A clinical problem is posed by patients with symptoms suggestive of gluten sensitivity (diarrhea, weight loss, unresponsive iron-deficiency anemia, etc.); however, small intestinal biopsies reveal only minor abnormalities, such as lymphocytosis with or without crypt hyperplasia (Marsh I-II). Our aim was to assess the benefit of a gluten-free diet (GFD) in patients with these small bowel mucosal abnormalities. STUDY: We studied 35 patients (11 men, 24 women; mean age, 28 years; range, 22-51 years) referred to us for gastrointestinal symptoms or unexplained or unresponsive diseases. Because celiac disease was suspected to be the underlying pathology, small intestinal biopsies were taken. These revealed only minor abnormalities: 11 patients showed Marsh I type lesions, whereas 24 patients demonstrated Marsh II type lesions. Although the histologic lesions were inconsistent for celiac disease and a suspicion of a borderline celiac disease persisted, all patients were motivated to adhere to GFD. RESULTS Only 23 patients adhered to our advice and followed a GFD; follow-up biopsies were taken after 8 to 12 months. In the Marsh I lesion group (seven patients), five patients showed mucosal normalization to Marsh 0 and two showed persistence of Marsh I lesions. In the Marsh II lesion group (16 patients), 9 patients revealed mucosal normalization, 5 improved to a Marsh I lesion, and 3 revealed persistence of Marsh II lesions. A dramatic clinical improvement in symptoms was noted in all patients who were on a GFD, with symptoms virtually disappearing in all patients. Seven patients who refused GFD were reevaluated 8 to 12 months later. Symptoms and histologic lesions were unchanged in six, all of whom refused again to adhere to a GFD. One of the seven with Marsh I lesions had a worsening of symptoms and of histologic lesions (from Marsh I to Marsh IIIa); so, this last patient adhered to a GFD. CONCLUSIONS: Symptoms disappeared after GFD in patients suspected to have celiac disease but with slight histologic lesions. Although Marsh I-II lesions cannot be classified as celiac lesions (ESPGAN criteria), the patients' symptoms at presentation and the clear improvement of symptoms when on GFD, with or without improvement of histologic lesions, supports the assumption that these patients are sensitive to gluten and may justify treatment with a GFD.

Adult↗
PubMed2001

Defining gluten refractory enteropathy.

OBJECTIVE: The diagnosis of coeliac disease (CD) is based on the responsiveness of the enteropathy to a gluten-free diet (GFD). This implies that terms such as 'non-responsive CD' and 'refractory CD' are almost paradoxical. In spite of this, these terms are commonly used in the literature, often with different and confusing meanings. METHODS: On the basis of both a review of the literature and our clinical experience, we propose the following classification. A condition characterized by a refractory enteropathy, not due to lymphoma, ulcerative jejunoileitis or collagenous sprue, but in which gluten sensitivity has been shown previously or could be shown while the patients were on an immunosuppressive therapy should be indicated as refractory CD. Those patients in whom gluten sensitivity can be excluded should be considered to be affected by non-coeliac refractory sprue. Finally, patients in whom the presence of CD cannot be either confirmed or excluded should be considered to be affected by undefined sprue. RESULTS: Twenty-four certain refractory patients are described in the literature. The data suggest a diagnosis of refractory CD in 13 patients, non-coeliac refractory sprue in three patients, and undefined sprue in eight patients. CONCLUSIONS: We define refractory CD as a form of CD that no longer responds to a GFD. Non-coeliac refractory sprue is a condition unrelated to CD. It could be either an independent condition or a common end point of different enteropathies.

Adult↗
PubMed2005

Anti-Saccharomyces cerevisiae and perinuclear anti-neutrophil cytoplasmic antibodies in coeliac disease before and after gluten-free diet.

BACKGROUND: Anti-Saccharomyces cerevisiae and perinuclear anti-neutrophil cytoplasmic autoantibodies are markers of Crohn's disease and ulcerative colitis respectively. AIM: To determine the prevalence of anti-S. cerevisiae and perinuclear anti-neutrophil cytoplasmic autoantibodies in a large series of coeliac disease patients before and after gluten free diet, and to correlate anti-S. cerevisiae-positivity with intestinal mucosal damage. METHODS: One hundred and five consecutive coeliac disease patients and 141 controls (22 ulcerative colitis, 24 Crohn's disease, 30 primary sclerosing cholangitis, 15 postenteritis syndrome, 50 blood donors) were tested for anti-S. cerevisiae by enzyme-linked immunosorbent assay and for perinuclear anti-neutrophil cytoplasmic autoantibodies by indirect immunofluorescence. RESULTS: In coeliac disease anti-S. cerevisiae (immunoglobulin G and/or immunoglobulin A) were slightly less frequent (59%) than in Crohn's disease (75%, P = 0.16) and significantly more frequent than in ulcerative colitis (27%), primary sclerosing cholangitis (30%), postenteritis syndrome (26%) and blood donors (4%) (P = 0.009, P = 0.0002, P = 0.025, P < 0.0001). No correlation was found between anti-S. cerevisiae and degree of mucosal damage. Perinuclear anti-neutrophil cytoplasmic autoantibodies were detected only in one coeliac. After gluten free diet the disappearance of anti-S. cerevisiae-immunoglobulin A (93%) was more frequent than that of immunoglobulin G (17%, P = 0.0001); perinuclear anti-neutrophil cytoplasmic autoantibodies disappeared in the only coeliac positive at diagnosis. CONCLUSION: More than half of untreated coeliacs are anti-S. cerevisiae-positive irrespective of the severity of mucosal damage. Differently from immunoglobulin A, anti-S. cerevisiae-immunoglobulin G persisted in more than 80% after gluten free diet. The high prevalence of anti-S. cerevisiae in coeliac disease suggests that they may be the effect of a non-specific immune response in course of chronic small bowel disease.

Adolescent↗
PubMed2006

Spectrum of gluten-sensitive enteropathy in first-degree relatives of patients with coeliac disease: clinical relevance of lymphocytic enteritis.

BACKGROUND: Limited data on a short series of patients suggest that lymphocytic enteritis (classically considered as latent coeliac disease) may produce symptoms of malabsorption, although the true prevalence of this situation is unknown. Serological markers of coeliac disease are of little diagnostic value in identifying these patients. AIMS: To evaluate the usefulness of human leucocyte antigen-DQ2 genotyping followed by duodenal biopsy for the detection of gluten-sensitive enteropathy in first-degree relatives of patients with coeliac disease and to assess the clinical relevance of lymphocytic enteritis diagnosed with this screening strategy. PATIENTS AND METHODS: 221 first-degree relatives of 82 DQ2+ patients with coeliac disease were consecutively included. Duodenal biopsy (for histological examination and tissue transglutaminase antibody assay in culture supernatant) was carried out on all DQ2+ relatives. Clinical features, biochemical parameters and bone mineral density were recorded. RESULTS: 130 relatives (58.8%) were DQ2+, showing the following histological stages: 64 (49.2%) Marsh 0; 32 (24.6%) Marsh I; 1 (0.8%) Marsh II; 13 (10.0%) Marsh III; 15.4% refused the biopsy. 49 relatives showed gluten sensitive enteropathy, 46 with histological abnormalities and 3 with Marsh 0 but positive tissue transglutaminase antibody in culture supernatant. Only 17 of 221 relatives had positive serological markers. Differences in the diagnostic yield between the proposed strategy and serology were significant (22.2% v 7.2%, p<0.001). Relatives with Marsh I and Marsh II-III were more often symptomatic (56.3% and 53.8%, respectively) than relatives with normal mucosa (21.1%; p = 0.002). Marsh I relatives had more severe abdominal pain (p = 0.006), severe distension (p = 0.047) and anaemia (p = 0.038) than those with Marsh 0. The prevalence of abnormal bone mineral density was similar in relatives with Marsh I (37%) and Marsh III (44.4%). CONCLUSIONS: The high number of symptomatic patients with lymphocytic enteritis (Marsh I) supports the need for a strategy based on human leucocyte antigen-DQ2 genotyping followed by duodenal biopsy in relatives of patients with coeliac disease and modifies the current concept that villous atrophy is required to prescribe a gluten-free diet.

Adolescent↗
PubMed1992

Do adults with high gliadin antibody concentrations have subclinical gluten intolerance?

Gliadin antibodies of the IgG and IgA isotypes and IgG subclasses were measured in 200 adults who were randomly selected from the Icelandic National Register. Those with the highest gliadin antibody concentrations were invited with negative controls to participate in a clinical evaluation. Neither the study subjects nor the physicians who recorded and evaluated the clinical findings were aware of the antibody levels. Significantly higher proportion of the gliadin antibody positive individuals reported unexplained attacks of diarrhoea (p = 0.03), and IgA gliadin antibodies were associated with increased prevalence of chronic fatigue (p = 0.0037). The gliadin antibody positive group also showed significantly decreased transferrin saturation, mean corpuscular volume and mean corpuscular haemoglobin compared with the gliadin antibody negative controls. Serum folic acid concentrations were significantly lower in the IgA gliadin antibody positive individuals. On blind global assessment 15 of the 48 participants were thought to have clinical and laboratory features that are compatible with gluten sensitive enteropathy, and 14 of these were in the gliadin antibody positive group (p = 0.013). Complaints that have not been associated with gluten intolerance had similar prevalence in both groups with the exception of persistent or recurrent headaches that were more common in the gliadin antibody positive group. These findings raise the possibility that a subclinical form of gluten intolerance may be relatively common.

Adult↗
PubMed2005

Cerebellar abnormalities on proton MR spectroscopy in gluten ataxia.

Gluten sensitivity can manifest with ataxia. The metabolic status of the cerebellum was investigated in 15 patients with gluten ataxia and 10 controls using proton MR spectroscopy. Significant differences were present in mean N-acetyl aspartate levels at short echo time and N-acetyl aspartate/choline ratios at long echo time between the patient and control groups. These data support the hypothesis that cerebellar neuronal physiology differs between patients with gluten ataxia and healthy controls.

Adult↗
PubMed1997

Effect of celiac disease and gluten-free diet on growth hormone-binding protein, insulin-like growth factor-I, and insulin-like growth factor-binding proteins.

Failure to thrive is common in children with celiac disease. As alterations in the growth hormone-insulin-like growth factor I (GH-IGF-I) growth axis have been reported in these patients, we studied the behavior of growth hormone-binding proteins (GH-BPs I and II), IGF-I and its binding proteins in 14 children with celiac disease, either before or after a 6-month gluten-free diet. GH-BP II levels were significantly lower in patients during the active phase of the disease than after the diet or in comparison with control subjects, appropriate for age and sex. There was no difference in the GH-BP-I levels of patients and controls, nor did they change after the diet. Blood levels of IGF-I and IGFBP-3 were reduced before the diet in all patients while ligand blotting showed that IGFBP-2 and 1 were increased. All of these parameters normalized after the gluten-free diet. IGFBP-4 was not greatly influenced by the disease. Furthermore, we found a significant, positive correlation between GH-BP II and IGF-I or IGFBP-3 levels. The height standard deviation scores and body mass indices of the patients improved significantly after the diet. The body mass index significantly and positively correlated with GH-BP II, IGF-I or IGFBP-3 levels. In conclusion, our data show that celiac children had multiple alterations in the growth axis during the active phase of the disease which disappeared during the gluten-free diet.

Body Height↗
PubMed1983

Gluten-sensitive enteropathy. Immunoglobulin G heavy-chain (Gm) allotypes and the immune response to wheat gliadin.

Anti-gliadin antibody was measured by radioimmunoassay in 30 Caucasians with gluten-sensitive enteropathy (GSE). 22 GSE patients maintained on a gluten-free diet for 1.5 to 20 yr (mean duration 76 mo) had elevated serum concentrations of IgG antigliadin antibody. Among GSE patients on a gluten-free diet, antigliadin antibody was seen only in those having the chromosome 14-encoded IgG immunoglobulin heavy chain allotype marker G2m(n). IgG antigliadin antibody was found in GSE patients with G2m(n) regardless of whether the HLA-B8 and/or -DR3 major histocompatibility complex antigens that occur frequently in GSE were present. No patient lacking G2m(n) had significant levels of antigliadin antibody. The association between antigliadin antibody and the immunoglobulin heavy chain allotype marker G2m(n) in GSE patients likely reflects the presence of Gmn-linked variable region genes or Gmn-linked genes that regulate variable region gene expression.

Adolescent↗
PubMed2004

Non-gluten sensitivity-related small bowel villous flattening with increased intraepithelial lymphocytes: not all that flattens is celiac sprue.

Seven patients (mean age, 37.6 years; 5 women) had several weeks of gluten sensitivity (GS)-like symptoms; 2 had flu-like symptom prodromes. The 7 cases had morphologically similar biopsy specimens; all tissue fragments had uniform injury--increased lymphoplasmacytic lamina propria inflammation, moderate to complete villous flattening, numerous crypt mitoses, and markedly increased villous intraepithelial lymphocytes (IELs). All patients were diagnosed with GS and prescribed a gluten-free diet; all returned 9 to 38 weeks later questioning their diagnosis because symptoms had resolved substantially or completely. Clinical improvement was unrelated to gluten abstinence or ingestion. Repeated endoscopy and colonoscopy performed 4.1 to 16 months later showed normal mucosa in all 7 patients. Diseases other than GS can cause marked villous flattening and increased villous IELs in adults. The cause of small bowel mucosal injury is unknown. A similar non-GS-associated clinicopathologic complex, assumed to be due to a protracted viral enteritis or slow regression of a virus-induced immune reaction, occurs in children. The temporal aspects of symptom improvement and mucosal restitution in these 7 patients are similar to "acute self-limited colitis." An overly exuberant immune response to an infectious agent is possible.

Adult↗
PubMed2004

Effects of wet corn gluten feed and intake level on diet digestibility and ruminal passage rate in steers.

Twelve ruminally cannulated Jersey steers (BW = 534 kg) were used in an incomplete Latin square design experiment with a 2 x 2 factorial arrangement of treatments to determine the effects of wet corn gluten feed (WCGF) and total DMI level on diet digestibility and ruminal passage rate. Treatments consisted of diets formulated to contain (DM basis) steam-flaked corn, 20% coarsely ground alfalfa hay, and either 0 or 40% WCGF offered once daily for ad libitum consumption or limited to 1.6% of BW (DM basis). Two consecutive 24-d periods were used, each consisting of 18 d for adaptation, 4 d for collection, and a 2-d in situ period. Rumens of all steers were evacuated once daily at 0, 4, 8, and 12 h after feeding. Chromic oxide (10 g/[steer*d]) was fed as a digestibility marker, and steers were pulse-dosed with Yb-labeled alfalfa hay to measure ruminal particulate passage rate. Dacron bags containing 5 g of steam-flaked corn, WCGF, or ground (2-mm screen) alfalfa hay were placed into the rumens of all steers and removed after 3, 6, 12, or 48 h. Wet corn gluten feed increased percent apparent total-tract digestion of OM (P < 0.01), NDF (P < 0.01), and starch (P < 0.03), decreased (P < 0.01) ruminal total VFA concentration, increased (P < 0.01) ruminal NH3 concentration, and increased (P < 0.01) ruminal pH. Wet corn gluten feed also increased (P < 0.01) ruminal passage rate of Yb. Limit feeding decreased (P < 0.01) percent apparent total-tract digestion of both OM and NDF, ruminal total VFA concentration (P < 0.01), and ruminal fill (P < 0.01), but increased (P < 0.01) ruminal NH3 concentration. Apparent total-tract digestion of starch was not affected (P = 0.70) by level of DMI. A DMI level x hour interaction (P < 0.01) occurred for ruminal pH. Limit feeding increased ruminal pH before and 12 h after feeding, but decreased ruminal pH 4 h after feeding compared with diets offered ad libitum. A diet x DMI level interaction (P < 0.02) occurred for in situ degradation of alfalfa hay, with dietary addition of WCGF increasing (P < 0.02) the extent of in situ alfalfa hay degradation in steers fed for ad libitum consumption. This study suggests that WCGF increases OM and NDF digestion, and that limit feeding diets once daily might depress OM and NDF digestion, possibly due to decreased stability of the ruminal environment.

Animal Feed↗