Whole-body protein turnover response to short-term high-protein diets during weight loss: a randomized controlled trial.

To determine whole-body protein turnover responses to high-protein diets during weight loss, 39 adults (age, 21±1 years; VO2peak, 48±1 ml kg(-1) min(-1); body mass index, 25±1 kg m(2)) were randomized to diets providing protein at the recommend dietary allowance (RDA), 2 × -RDA or 3 × -RDA. A 10-day weight maintenance period preceded a 21-day, 40% energy deficit. Postabsorptive (FASTED) and postprandial (FED) whole-body protein turnover was determined during weight maintenance (day 10) and energy deficit (day 31) using [1-(13)C]leucine. FASTED flux, synthesis and breakdown were lower (P<0.05) for energy deficit than weight maintenance. Protein flux and synthesis were higher (P<0.05) for FED than FASTED. Feeding attenuated (P<0.05) breakdown during weight maintenance but not energy deficit. Oxidation increased (P<0.05) between dietary protein levels and feeding stimulated oxidation, although oxidative responses to feeding were higher (P<0.05) for energy deficit than weight maintenance. FASTED net balance decreased between dietary protein levels, but in the FED state, net balance was lower for 3 × -RDA as compared with RDA and 2 × -RDA (diet-by-state, P<0.05). Consuming dietary protein at levels above the RDA, particularly 3 × -RDA, during short-term weight loss increases protein oxidation with concomitant reductions in net protein balance.

Efficacy of mineral supplementation to growing cattle grazing winter-wheat pasture in northwestern Oklahoma.

Two experiments were conducted to evaluate the efficacy of mineral supplementation to cattle grazing winter-wheat pasture. In experiment 1 (fall), 120 steers and heifers (body weight [BW] = 232 ± 11.4 kg) were assigned randomly to four blocks of replicated pastures during the second week of November in 2008 and 2009 and all herds (6 animals/pasture; 4.9 ha/pasture) were allowed to graze for 84 d. In experiment 2 (spring), 216 steers (BW = 248 ± 7.9 kg) were assigned randomly to five blocks of replicated pastures during the second week of February in 2009 and 2010 and all herds (12 or 6 animals/pasture; 4.9 ha/pasture) were allowed to graze for 84 d. Half the pastures in both experiments received a free-choice mineral mixture (Wheat Pasture Pro; Land O'Lakes Purina Feed, LLC; St. Paul, MN; Ca, 16% and P, 4%); mineral feeders were weighed weekly to determine mineral intake. All pastures were planted in early September of each year (67 kg of seed/ha) and fertilized with 50 kg of urea-N/ha. Standing herbage dry matter was determined midway between weigh dates by clipping wheat forage to the ground along 122 cm of drill rows at 10 locations/pasture. Data were analyzed by ANOVA, with treatment as the fixed effect and pasture, animal sex (experiment 1), and block as random effects. In experiment 1, cattle offered minerals had a 43% faster average daily gain (ADG; P = 0.02, 0.73 kg) than cattle not offered minerals (0.51 kg); hence, supplemented cattle weighed 6% more (P = 0.04; 286 kg) after 84 d than nonsupplemented cattle (271 kg). In experiment 2, cattle offered the mineral supplement had a faster ADG (20% increase; P = 0.04; 1.00 kg) than cattle not offered minerals (0.83 kg). Further, supplemented cattle weighed 4% more (P = 0.03; 326 kg) after 84 d than nonsupplemented cattle (312 kg). In both experiments, daily standing herbage dry matter averaged 1,381 kg/animal and never differed (P ≥ 0.47) between treatments. Mineral intakes averaged 135 (experiment 1) and 124 (experiment 2) g/d, resulting in a cost of supplement to kilogram of added BW gain of $0.53 and $0.64, respectively (assuming a mineral cost of $0.88/kg). Overall, supplementing an appropriate mineral mixture to cattle grazing winter-wheat pasture increased ADG in a cost-effective manner.

Selective inhibition of selenocysteine tRNA maturation and selenoprotein synthesis in transgenic mice expressing isopentenyladenosine-deficient selenocysteine tRNA.

Selenocysteine (Sec) tRNA (tRNA([Ser]Sec)) serves as both the site of Sec biosynthesis and the adapter molecule for donation of this amino acid to protein. The consequences on selenoprotein biosynthesis of overexpressing either the wild type or a mutant tRNA([Ser]Sec) lacking the modified base, isopentenyladenosine, in its anticodon loop were examined by introducing multiple copies of the corresponding tRNA([Ser]Sec) genes into the mouse genome. Overexpression of wild-type tRNA([Ser]Sec) did not affect selenoprotein synthesis. In contrast, the levels of numerous selenoproteins decreased in mice expressing isopentenyladenosine-deficient (i(6)A(-)) tRNA([Ser]Sec) in a protein- and tissue-specific manner. Cytosolic glutathione peroxidase and mitochondrial thioredoxin reductase 3 were the most and least affected selenoproteins, while selenoprotein expression was most and least affected in the liver and testes, respectively. The defect in selenoprotein expression occurred at translation, since selenoprotein mRNA levels were largely unaffected. Analysis of the tRNA([Ser]Sec) population showed that expression of i(6)A(-) tRNA([Ser]Sec) altered the distribution of the two major isoforms, whereby the maturation of tRNA([Ser]Sec) by methylation of the nucleoside in the wobble position was repressed. The data suggest that the levels of i(6)A(-) tRNA([Ser]Sec) and wild-type tRNA([Ser]Sec) are regulated independently and that the amount of wild-type tRNA([Ser]Sec) is determined, at least in part, by a feedback mechanism governed by the level of the tRNA([Ser]Sec) population. This study marks the first example of transgenic mice engineered to contain functional tRNA transgenes and suggests that i(6)A(-) tRNA([Ser]Sec) transgenic mice will be useful in assessing the biological roles of selenoproteins.

Chemopreventive agents: selenium.

The element selenium (Se) was recognized only 40 years ago as being essential in the nutrition of animals and humans. It is recognized as being an essential component of a number of enzymes, in which it is present as the amino acid selenocysteine. Se compounds have also been found to inhibit tumorigenesis in a variety of animal models, and recent studies indicate that supplemental Se in human diets may reduce cancer risk. The antitumorigenic activities have been associated with Se intakes that correct nutritionally deficient status in animals, as well as higher intakes that are substantially greater than those associated with maximal expression of the selenocysteine-containing enzymes. Therefore, it is proposed that while some cancer protection, particularly that involving antioxidant protection, involves selenoenzymes, specific Se metabolites, which are produced in significant amounts at relatively high Se intakes, also discharge antitumorigenic functions. According to this two-stage model of the roles of Se in cancer prevention, individuals with nutritionally adequate Se intakes may benefit from Se supplementation. Evidence for chemoprevention by Se and for the apparent mechanisms underlying these effects is reviewed to the end of facilitating the development of the potential of Se compounds as cancer chemopreventive agents.

The Chakaria food system study: household-level, case-control study to identify risk factor for rickets in Bangladesh.

OBJECTIVE: A comprehensive, multiround survey of local food systems in a rickets-endemic area of Bangladesh was conducted to identify household-level risk factors for rickets. DESIGN: A household-level, case-control study was conducted in a rickets-endemic area, Chakaria, with planned comparisons between households with one or more rachitic child and neighboring households with no affected children. SETTING: A rickets-endemic area of southeastern Bangladesh, Chakaria. SUBJECTS AND METHODS: An interview-based survey was conducted in six villages in Chakaria with 199 households with at least one child showing physical signs consistent with rickets and 281 households with no affected children. RESULTS: Households with rachitic children in Chakaria had more children, more pregnant or lactating women, and fewer adults than unaffected households in that community. Affected households tended to rely on farming for their livelihood and tended to have less economic activity as indicated by less outstanding debt than their neighbors. Households with rickets were at significantly greater risk of pneumonia than were other households. Calcium undernutrition was severe and widespread in Chakaria due to a food system that offered very little of the element in accessible forms. Household diets were based on cereals and starchy vegetables. Rice and fish constituted the major source of calcium for most households, although dairy products, when used, were very important calcium sources, particularly for young children. In fact, the use of dairy products was the only household choice that led to substantial increases in the calcium intakes of children, and households that used dairy products tended to show increased calcium intakes for all of their members. CONCLUSIONS: The risk of a Chakarian household having a child with rickets appeared to be related to its economic status. Although this might be expected to be manifest as limitations in food access and/or use, rickets households failed to show a dietary pattern associated with rickets. Calcium undernutrition was prevalent and, thus, would appear to be a predisposing factor for rickets; however, calcium undernutrition was prevalent in Chakarian households with and without rickets. Therefore, it is probable that another precipitating factor(s) play a role(s) in the etiology of rickets in Chakaria.

Report on Clinical Nutrition Research Units.

The National Institutes of Health support seven Clinical Nutrition Research Units, which are designed to create or strengthen nutrition research, training, and education through coordinated effort, intellectual stimulation, and use of shared resources. Research at the participating institutions focuses on the role of nutrition in cancer, cardiovascular disease, renal disease, digestive diseases, cystic fibrosis, diabetes, and other illnesses. Contributing substantially to the development of this nutrition research base have been Clinical Nutrition Research Unit-supported pilot studies, core laboratories, and new investigators. In the clinical setting, Clinical Nutrition Research Unit Nutritional Support Services assist in the care of patients receiving total parenteral nutrition and those with anorexia nervosa, burns, cancer, and a spectrum of nutrition-related problems. Participation of Clinical Nutrition Research Unit staff in training activities range from undergraduate, graduate, and postgraduate education courses for medical students and other health professionals to continuing education workshops, lecture series, and information programs for professional and lay audiences.

Reporting the accuracy of biochemical measurements for epidemiologic and nutrition studies.

Procedures for reporting and monitoring the accuracy of biochemical measurements are presented. They are proposed as standard reporting procedures for laboratory assays for epidemiologic and clinical-nutrition studies. The recommended procedures require identification and estimation of all major sources of variability and explanations of laboratory quality control procedures employed. Variance-components techniques are used to model the total variability and calculate a maximum percent error that provides an easily understandable measure of laboratory precision accounting for all sources of variability. This avoids ambiguities encountered when reporting an SD that may taken into account only a few of the potential sources of variability. Other proposed uses of the total-variability model include estimating precision of laboratory methods for various replication schemes and developing effective quality control-checking schemes. These procedures are demonstrated with an example of the analysis of alpha-tocopherol in human plasma by using high-performance liquid chromatography.

Report on the Fourth Conference for Federally Supported Human Nutrition Research Units and Centers.

The Fourth Conference for Federally Supported Human Nutrition Research Units and Centers, sponsored by the Interagency Committee on Human Nutrition Research, addressed two topics: nutrition and function, and nutrient interactions and toxicities. This article summarizes the conference's introductory remarks and the contents of the 34 papers presented. Future meetings of federally supported nutrition research units and centers will focus on other human nutrition research topics and will be held biennially.

Serum selenium and subsequent risk of prostate cancer.

It is suspected that selenium is protective against prostate cancer. To test this hypothesis, we conducted a nested case-control study in a cohort of 9345 Japanese-American men examined between 1971 and 1977. At the time of examination, a blood specimen was obtained, and the serum was frozen. After a surveillance period of more than 20 years, 249 tissue-confirmed incident cases of prostate cancer were identified. Their stored sera and those of 249 matched controls were measured for selenium levels. Odds ratios for prostate cancer, based on quartiles of serum selenium levels, were determined using the General Estimating Equations approach. The multivariate odds ratio for the highest quartile was 0.5 (95% confidence interval, 0.3-0.9) with a two-sided P for trend of 0.02. The inverse association was more notable for cases with advanced disease and for cases diagnosed 5-15 years after phlebotomy. However, the association was mainly present in current or past cigarette smokers rather than nonsmokers, which leads to caution in the interpretation of the results.

Plasma selenium concentration predicts the prevalence of colorectal adenomatous polyps.

The objective of this cross-sectional study was to determine whether plasma selenium concentration predicts the prevalence of adenomatous polyps of the colon and rectum. The source population for the study was 101 patients undergoing sequential colonoscopies at the Veterans Affairs Medical Center, Tucson, AZ. The study population was then limited to the 48 patients (all male) undergoing their initial colonoscopy who did not have a diagnosis of colorectal cancer. For each of these patients, a prediagnostic fasting plasma selenium concentration was determined. The data from this study suggest that fasting plasma selenium concentrations may be an important risk factor for colorectal adenomas. Patients with fasting plasma selenium concentrations below the median (< 128 mcg/liter) were significantly more likely to have one or more adenomatous polyps (prevalence odds ratio 4.2) and more adenomatous polyps (3.5 times) per patient. There was also a suggestion of a more proximal distribution of adenomatous polyps in the patients with a lower level of selenium. These associations were not confounded by age or smoking. The results of this study are consistent with the experimental animal studies, geographic mortality studies, and prospective cohort studies of selenium and colorectal cancer.

Selenium in pediatric nutrition.

Se is an essential nutrient that provides antioxidant protection in concert with vitamin E. Several selenoproteins have been identified, but only one, SeGSHpx, has a known function, that of neutralizing toxic hydroperoxides. Plasma Se concentration, being responsive to changes in Se intake, is the most practical and widely used measure of nutritional Se status. The plasma Se concentrations of the majority of healthy infants and children fall within the range of 50 to 150 micrograms/L. Although SeGSHpx activity measures the metabolically functional form of Se, the lack of a standardized analytical method has limited its usefulness as an index of nutritional Se status. Se deficiency was first observed in animals, but it is now recognized to occur in humans. Two human diseases associated with severe nutritional Se deficiency have been reported from China: a juvenile cardiomyopathy named Keshan disease and a chondrodystrophy named Kaschin-Beck disease. Long-term TPN, which provides negligible amounts of intrinsic Se, has been demonstrated in some cases to result in biochemical and clinical impairment. Although there are no consistent signs and symptoms characteristic of TPN-associated Se deficiency in addition to the low blood selenium levels, some patients will experience leg muscle pain and altered serum transaminase and creatine kinase activities. These manifestation of Se deficiency usually take years to develop. Recent information about the amount of dietary Se needed to maximize plasma SeGSHpx activity in adult men has allowed for better estimates of the Se requirement for humans. Recommended daily dietary allowances published recently by the National Academy of Sciences have been revised for infants and children in this paper by making appropriate adjustments for the protein requirements of these age-groups. These recommended intakes for Se can generally be met by consuming adequate amounts of cereals, meat, eggs, dairy products, human milk, and infant formula, which are good sources of highly available Se and are of low risk of providing excess amounts of Se. Suboptimal Se intakes by pregnant women may predispose their infants to low Se status at birth, which in turn may affect the infants ability to maintain adequate Se status during the first few months of life. In those situations where protein intake is restricted, such as in phenylketonuria and maple syrup urine disease, Se-supplemented formulas should be used. The most critical situation for Se supplementation is in pediatric patients receiving long-term TPN therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Synthetic seleno-organic compound with glutathione peroxidase-like activity in the chick.

The glutathione peroxidase activity catalyzed by the seleno-organic anti-inflammatory drug Ebselen (registered under the trademark of the Natterman Corp. Cologne, FRG) [PZ51, 2-phenyl-1,2-benzisoselenazol-3(2H)on], as measured by NADPH oxidation, was inhibited in vitro by the selenium-dependent glutathione peroxidase (SeGSHpx) inhibitors aurothioglucose and D-(-)penicillamine HCl. Vitamin E- and selenium-deficient chicks were given 0, 80 or 320 ppm PZ51 in diets devoid of vitamin E and supplemented with low levels of sodium selenite (0.04 ppm selenium added to the basal diet containing ca. 0.015 ppm selenium) when a small number of chicks (ca. 13%) had exudative diathesis (ED). By 24 hr, the high PZ51 dose (320 ppm) delayed the onset of ED compared to untreated controls. Similarly, vitamin E-deficient chicks fed diets containing 0, 80, 160, 320, 640 or 1280 ppm PZ51 and supplemented with 0.04 ppm selenium showed ED in inverse proportion to log PZ51 dose. Plasma and liver post-mitochondrial supernatant samples from these chicks also exhibited log-linear relationships between dietary PZ51 level and selenium content or SeGSHpx-like activity. The amount of SeGSHpx-like activity for chicks given PZ51 above that determined for untreated chicks was extractable into ethanol, indicating that those PZ51-associated increases were not due to protein-bound selenium or SeGSHpx. This suggests that selenium from PZ51 was not available to support synthesis of SeGSHpx. Dietary PZ51 (1280 ppm) or selenium (0.1 ppm) alone or in combination decreased the acute lethalities of nitrofurantoin or paraquat in vitamin E-adequate chicks. The results indicate that SeGSHpx-like activity in selenium-deficient chicks is increased by oral administration of PZ51, which appears to mimic the true enzyme by affording protection against clinical signs of selenium deficiency (i.e. ED) and pro-oxidant drug lethality.

Food systems for improved health: linking agricultural production and human nutrition.

OBJECTIVES: Link traditional agricultural production disciplines to the food sciences and the various disciplines concerned with human nutrition and health in order to find sustainable solutions to malnutrition. DESIGN: Develop a new integrated program area within a university by forging explicit linkages within a wide array of disciplines concerned with food systems and human health. SETTING: The College of Agriculture and Life Sciences, the College of Human Ecology, the Division of Nutrition, and the Cornell International Institute for Food, Agriculture, and Development at Cornell University, Ithaca, New York, USA. INTERVENTIONS: Use food-based, system approaches to meet human nutrition goals. Current focus is on the provision of micronutrients (especially iron, vitamin A and iodine) for people globally. RESULTS: A new program area 'Food Systems for Health' has been developed at Cornell University. The program fosters effective interdisciplinary research, teaching and extension activities directed towards sustainable improvements in human nutrition and health. CONCLUSIONS: The old paradigms of agriculture, human nutrition, and public health must be shifted from current linear approaches to integrated and interactive approaches if effective long-term, food-based solutions to micronutrient malnutrition are to be found.

Food system-based approaches to improving micronutrient nutrition: the case for selenium.

Micronutrient deficiencies affect nearly half the world's population, impairing child development, reducing work productivity, and increasing mortality and morbidity rates by affecting both infectious and chronic diseases. To feed a growing world, it will be necessary to consider agriculture in the broad context of a food system as an instrument of public health and, thus, to address nutrient balance while also seeking sustainability. Such efforts would include increasing cropping system diversity, enhancing micronutrient outputs and promoting environmental sustainability. Example of this approach are presented for the essential trace element selenium (Se), which at high intakes can reduce cancer risks but is deficient in many parts of the world. Food systems-based approaches are discussed for preventing Se deficiency by enhancing intakes of any of several biologically available forms of Se, and for reducing cancer risk by enhancing intakes of forms of the element that support anti-tumorigenic Se-metabolites.

Knockout of cellular glutathione peroxidase affects selenium-dependent parameters similarly in mice fed adequate and excessive dietary selenium.

This study was to determine whether or not effects of the cellular glutathione peroxidase (GPX1) knockout on several Se-dependent parameters in mice were tissue, dietary Se concentration, and selenoprotein specific. A 2 x 3 factorial experiment was conducted with 18 GPX1 knockout mice [GPX1(-)] and 18 controls (3 weeks old, half males and females). These mice were fed a torula yeast diet supplemented with all-rac-alpha-tocopheryl acetate (50 mg/kg of feed) and Se (sodium selenite) at 0, 0.5, or 3.0 mg/kg of feed for 6 weeks. Both kidney GPX1 mRNA levels and liver, kidney, lung, and testis total GPX activities, assayed using hydrogen peroxide, were affected (p < 0.001) by the GPX1 knockout and dietary Se concentrations, whereas kidney extracellular or plasma GPX (GPX3) mRNA levels and phospholipid hydroperoxide GPX (GPX4) activities in the four tissues were affected (p < 0.001) by only dietary Se concentrations. Total GPX activity in testis was reduced approximately 90% (p < 0.01) by the GPX1 knockout. Neither the GPX1 knockout nor the dietary Se concentrations affected mRNA levels of GPX4 in testis or selenoprotein P in kidney. Total liver Se concentrations were not different between the GPX1(-) and control mice at 0 mg Se/kg of feed, but were reduced (p < 0.01) by 61 and 64% in the GPX1(-) mice at 0.5 and 3.0 mg Se/kg of feed, respectively. These results not only confirm the independent expression of GPX3, GPX4, and selenoprotein P from that of GPX1, but also show similar effects of the GPX1 knockout on Se-dependent parameters in mice between different dietary Se concentrations, tissues, and selenoproteins.

An analysis of cancer prevention by selenium.

The nutritional functions of selenium (Se) are recognized as being due to a number of Se-containing proteins. It is not clear, however, whether any of these function in the anti-tumorigenic effects of Se most of which have been demonstrated for Se exposures greater than those required for selenoprotein expression. Indeed, other anti-tumorigenic mechanisms have been demonstrated for certain Se-metabolites. The Nutritional Prevention of Cancer Trial found supplemental Se (200 microg/day, as Se-enriched yeast) to be associated with significant reductions in cancer risks in subjects with pre-treatment plasma Se concentrations below ca. 120 ng/ml (1.5 nmoles/ml), which level would appear to require food-Se intakes of ca. 1.5 microg/kg body weight/day. However, the putative anti-carcinogenic Se-metabolite(s) should be more relevant than total plasma Se as a supplementation target for cancer prevention. These may be components of the non-protein-bound fraction of Se in plasma, which constitutes 2-4% of total plasma Se.

Effects of selenium on colonic fermentation in the rat.

Studies were conducted to determine the effects of dietary selenium (Se) on the hindgut microbial activity in rats. Selenium was fed as L-selenomethionine (SeMet) at either 0 or 2 ppm Se in the presence or absence of wheat bran (WB, 10%), a known substrate for the enteric microflora. Wheat bran feeding caused the greatest fermentation, measured by the production of short-chain fatty acids (SCFAs) along the entire intestinal tract and feces; however, its effects were suppressed by SeMet in the proximal large bowel, cecum, and colon. Selenium significantly enhanced fermentation in the colon and rectum, but not in the cecum or feces. Selenium was found in association with the bacterial cell fractions of gut contents and feces: 40-46% of the total Se was associated with colonic microbes and 58% in fecal microbes. Increased acetate and reduced butyrate production were driven by the addition of Se regardless of whether WB was fed.

Effects of aurothioglucose and dietary Se on glutathione S-transferase activities and glutathione concentrations in chick tissues.

Experiments were conducted to determine whether the increased glutathione S-transferase (GSH-T) activity associated with selenium (Se) deficiency is necessarily related to losses in the activity of Se-dependent glutathione peroxidase (SeGSHpx) in chicks. Nutritional Se status was altered in two ways: by treatment with an antagonist of Se utilization, aurothioglucose (AuTG), and by feeding diets containing excess Se. Chicks given AuTG (10-30 mg AU/kg, sc) had growth rates and hepatic GSH concentrations that were comparable to those of saline-treated controls; however, their plasma GSH levels exceeded those of either Se-deficient (6-fold) or -adequate (3-fold) saline-treated chicks. Hepatic SeGSHpx activities of AuTG-treated chicks were half those of controls under conditions of Se-adequacy; however, this effect was not detected when Se was deficient. Hepatic GSH-TCDNB (assayed with 1-chloro-2,4-dinitrobenzene) activities of AuTG-treated chicks were significantly greater than those of controls when Se was deficient (i.e., when SeGSHpx activity was 12% of the Se-adequate level); however, deprivation of Se did not affect GSH-TCDNB activity in the absence of AuTG. Chicks fed excess Se (6-20 ppm as Na2SeO3) in diets containing either low (2 IU/kg) or adequate (100 IU/kg) VE, showed hepatic GSH-TCDNB activities and GSH concentrations greater than those of Se-adequate (0.2 ppm Se) chicks by 100% and 40%, respectively. That increased hepatic GSH-TCDNB activity can occur because of either AuTG or excess Se status under conditions wherein SeGSHpx activity is not affected indicates that the transferase response is not directly related to changes in the peroxidase.

Ascorbate interacts with sodium selenite to increase glutathione peroxidase activity in selenium-deficient chick duodena cultured in vitro.

Duodena from Selenium (Se)/vitamin E-depleted 19 d chick embryos were cultured in vitro for 0-30 h. The addition of sodium selenite to the culture medium was associated with increased selenium-dependent glutathione peroxidase (SeGSHpx) activity after 24 h of incubation. In the absence of Se or in the presence of sodium ascorbate supplementation alone, SeGSHpx activity showed a gradual decline over the same time period. When ascorbate was added, along with sodium selenite, SeGSHpx activity was increased earlier and to a greater extent than in the presence of Se alone. These observations show that ascorbate can influence the metabolism of sodium selenite, resulting in increased SeGSHpx activity.

Studies on the effects of selenium on rumen microbial fermentation in vitro.

The effects of selenium (Se) on ruminant microbial fermentation were investigated in vitro using rumen microflora collected from a rumen-fistulated dairy cow. First, the effects of L-selenomethionine (SeMet; at 0.2 or 2 ppm Se) in the presence or absence of wheat bran (WB, 500 mg per incubation flask) were evaluated. Second, the effects of several forms of Se (elemental Se: 50 ppm Se; sodium selenite: 2 ppm Se; SeMet: 2 ppm Se) were compared. Results showed that the amounts of short-chain fatty acids (SCFAs) tended to be increased by SeMet treatment, whereas SeMet in the presence of WB transiently suppressed fermentation. The addition of SeMet tended to increase the production of acetate while reducing the production of butyrate with the without WB supplementation. Among the different Se compounds tested, the amounts of SCFAs were greater with SeMet treatment, which yielded a higher proportion of acetate compared to other treatments. Selenite did not influence the total SCFAs concentrations; however, it increased the relative proportion of butyrate at the expense of acetate. Elemental Se did not significantly affect fermentation. Higher bacterial Se concentrations were observed for selenite than for SeMet. It was concluded that Se supplementation can influence rumen microbial fermentation and that Se compounds differ in this regard.