Soy and Gastrointestinal Health: A Review.

Soybean is the most economically important legume globally, providing a major source of plant protein for millions of people; it offers a high-quality, cost-competitive and versatile base-protein ingredient for plant-based meat alternatives. The health benefits of soybean and its constituents have largely been attributed to the actions of phytoestrogens, which are present at high levels. Additionally, consumption of soy-based foods may also modulate gastrointestinal (GI) health, in particular colorectal cancer risk, via effects on the composition and metabolic activity of the GI microbiome. The aim of this narrative review was to critically evaluate the emerging evidence from clinical trials, observational studies and animal trials relating to the effects of consuming soybeans, soy-based products and the key constituents of soybeans (isoflavones, soy proteins and oligosaccharides) on measures of GI health. Our review suggests that there are consistent favourable changes in measures of GI health for some soy foods, such as fermented rather than unfermented soy milk, and for those individuals with a microbiome that can metabolise equol. However, as consumption of foods containing soy protein isolates and textured soy proteins increases, further clinical evidence is needed to understand whether these foods elicit similar or additional functional effects on GI health.

Effects of dietary oat supplementation on carcass traits, muscle metabolites, amino acid profiles, and its association with meat quality of Small-tail Han sheep.

Oat supplementation of the ruminant diet can improve growth performance and meat quality traits, but the role of muscle metabolites has not been evaluated. This study aimed to establish whether oat grass supplementation (OS) of Small-tail Han sheep improved growth performance and muscle tissue metabolites that are associated with better meat quality and flavor. After 90-day, OS fed sheep had higher live-weight and carcass-weight, and lower carcass fat. Muscle metabolomics analysis showed that OS fed sheep had higher levels of taurine, l-carnitine, inosine-5'-monophospgate, cholic acid, and taurocholic acid, which are primarily involved in taurine and hypotaurine metabolism, purine metabolism, and bile acid biosynthesis and secretion, decreased fat accumulation and they promote functional or flavor metabolites. OS also increased muscle levels of amino acids that are attributed to better quality and flavorsome mutton. These findings provided further evidence for supplementing sheep with oat grass to improve growth performance and meat quality.

Fructan extracts from wheat stem and barley grain stimulate large bowel fermentation in rats.

The benefits of inulin-type fructans for bowel health are well established, but less so for other fructan sources. In vitro data suggest that fructans extracted from cereals are readily fermented and produce favorable short-chain fatty acid profiles; however, whether this occurs in vivo is unknown. We hypothesized that in rats, fructans extracted from wheat stem and barley grain would have similar effects on fermentation as oligofructose (OF). Fifty-six male Sprague-Dawley rats were randomly assigned to 1 of 7 dietary treatments that contained either 2% or 5% fructan, provided by a barley grain fructan extract (BGFE), a wheat stem fructan extract, or OF or no added fructan (control). The duration of the feeding study was 14 days. Rats fed diets containing 5% fructan had higher cecal digesta weights; larger acetate, propionate, and total short-chain fatty acid pools; and lower pHs in comparison with the control group. In addition, only the 5% OF and 5% BGFE groups increased cecal butyrate pools, and 5% BGFE was the only group in which colonic digesta pH was lower than that of the control. Diets containing 2% fructan did not affect any of these fermentation end points. Whereas bifidobacteria numbers in cecal digesta of 2% and 5% OF were higher than that in the control group, they were not different from those in rats fed diets containing BGFE and wheat stem fructan extract. Barley grain and wheat stem fructans produced similar large bowel fermentation patterns to OF when fed to rats at 5% of the diet.

Adiponectin relates to smooth muscle function and folate in obese children.

OBJECTIVE: Adiponectin, an adipocyte-specific protein, stimulates nitric oxide production and may mediate associations between visceral obesity and vascular dysfunction. Adiponectin is lower in obese children but its relationship with vascular function has not been clarified in childhood. We aimed to evaluate the association between adiponectin and vascular function in obese and healthy children. METHODS: Forty-nine obese and thirty-three non-obese children (aged 13.4+/-2.8 years, 37 males) participated in a cross-sectional study. We measured adiponectin, vascular endothelial and smooth muscle function (Flow mediated dilatation [FMD] and glyceryl trinitrate induced dilatation [GTN]), serum folate, red cell folate (RCF), homocysteine, lipids, glucose and insulin. Because adiponectin related to RCF we examined the effect of folate supplementation on adiponectin levels in obese children in a previously conducted randomized folate intervention trial. This included two assessments prior to intervention and two post intervention. RESULTS: Adiponectin, FMD and GTN were lower in obese compared with non-obese children (p = 0.002, p = 0.03 and p < 0.001, respectively). In obesity, adiponectin related to GTN (beta = 0.46, p < 0.001), RCF (beta = 0.4, p = 0.001) and LDL cholesterol (beta = 0.33, p = 0.004). Adiponectin associations were affected by gender and adiponectin related to female gender (B = 0.22, p = 0.03). During the intervention trial, folic acid did not improve adiponectin levels (p = 0.8) in spite of increasing serum folate and RCF (p < 0.001, p < 0.001, respectively) and decreasing homocysteine levels (p = 0.008). CONCLUSIONS: Obese children have lower adiponectin, which relates to decreased smooth muscle function and lower folate status. Despite adiponectin relating to folate status, folic acid supplementation does not improve adiponectin in obese children.

Effect of testosterone and a nutritional supplement, alone and in combination, on hospital admissions in undernourished older men and women.

BACKGROUND: In older people, undernutrition is associated with increased hospitalization rates and mortality. Because weight loss in older people often reflects a disproportionate reduction of skeletal muscle, anabolic treatments may be beneficial. OBJECTIVE: Our aim was to evaluate the hypothesis that testosterone treatment and a nutritional supplement have additive benefits. DESIGN: Oral testosterone undecanoate (40 mg daily for women, 80 mg twice daily for men) and an oral nutritional supplement (475 kcal/d) were administered, alone or combined, for 1 y to 49 community-dwelling, undernourished people [Mini Nutritional Assessment score <24 and low body weight (body mass index, in kg/m(2): <22) or recent weight loss (>7.5% over 3 mo)] aged >65 y (mean age: 77 y; 26 women and 23 men). Hospital admissions and other variables were assessed. RESULTS: In subjects receiving combined testosterone and nutritional supplements (n = 11), there were no hospital admissions, whereas there were 9 admissions (2 elective) in 13 subjects in the no-treatment group, 4 in the testosterone-treated group (n = 12), and 5 in the supplement-treated group (n = 13); P = 0.06 with no-treatment compared with combined treatment. When compared with the no-treatment group, the combined-treatment group had significantly fewer subjects admitted to hospital (0 compared with 5, P = 0.03), fewer days in hospital (0 compared with 74, P = 0.041), and a longer time to hospital admission (P = 0.017). CONCLUSIONS: In undernourished older people, combined treatment with testosterone and nutritional supplementation reduced the number of people hospitalized and the duration of hospital admissions, which are important endpoints in this group. Larger, confirmatory studies are now needed. This trial was registered before commencement at clinical trials.gov as NCT00117000.