Methodology was developed for measuring the gastrointestinal endogenous phosphorus (P) outputs and true P digestibility values in studies with piglets. Four barrows, average initial body weight 6.8 kg, were fitted with a simple T-cannula at the distal ileum and fed four diets according to a 4 x 4 Latin square design. Four cornstarch-based diets containing four levels of P (1.1, 2.1, 3.2 and 4.3 g/kg diet) on a dry matter (DM) basis were formulated from soybean meal (SBM). Each experimental period comprised 8 d with a 4-d adaptation and 4-d collection of ileal digesta and feces. The apparent ileal and fecal P digestibility values in SBM were affected (P < 0.05) by P levels in the assay diets. The ileal and fecal P digestibility values increased from -24.8 to 37.1% and from 18.8 to 42.5%, respectively, as P contents increased from 1.1 to 4.3 g/kg DM diet. Linear relationships (P < 0.05), expressed as g/kg DM diet intake, between ileal and fecal outputs and dietary inputs of P, suggested that the endogenous P outputs can be determined by linear regression analysis. The endogenous P output was higher (P < 0.05) in ileal digesta than in feces (0.86 +/- 0.09 vs. 0.31 +/- 0.06 g/kg DM diet intake). There was no difference (P > 0.05) between the true ileal (50.7 +/- 7.1%) and fecal (48.5 +/- 5.4%) P digestibility values in SBM. These results suggest that differences in P contents between assay diets are primarily responsible for the large variability in apparent P digestibility values reported within the same ingredient. Apparent digestibility values underestimate the true digestive utilization of P by approximately 25%. True rather than apparent P digestibility values should be determined and used in diet formulation for pigs. In addition, this study shows that the gastrointestinal endogenous P output is important in whole-body P requirement and homeostasis.

An increase in ALA intake resulting in increased plasma EPA composition may be cardioprotective, especially in minor allele homozygotes. This trial was registered at www.clinicaltrials.gov as NCT00927199.

BackgroundGiven the highly debated role of dairy food consumption in modulating biomarkers of metabolic syndrome, this study was conducted to examine the influence of long-term (6 month) dairy consumption on metabolic parameters in healthy volunteers under free-living conditions without energy restriction.MethodsTwenty-three healthy subjects completed a randomized, crossover trial of 12 months. Participants consumed their habitual diets and were randomly assigned to one of two treatment groups: a high dairy supplemented group instructed to consume 4 servings of dairy per day (HD); or a low dairy supplemented group limited to no more than 2 servings of dairy per day (LD). Baseline, midpoint, and endpoint metabolic responses were examined.ResultsEndpoint measurements of body weight and composition, energy expenditure, blood pressure, blood glucose, and blood lipid and lipoprotein responses did not differ (p > 0.05) between the LD and HD groups. HD consumption improved (p < 0.05) plasma insulin (-9%) and insulin resistance (-11%, p = 0.03) as estimated by HOMA-IR compared with the LD group.ConclusionsStudy results suggest that high dairy consumption (4 servings/d) may improve insulin resistance without negatively impacting bodyweight or lipid status under free-living conditions.Trial registrationTrial registration: NCT01761955

The mammalian target of rapamycin (mTOR) plays key roles in cellular metabolism and hypertrophic-hyperplasic growth, and it acts as a central regulator of protein synthesis and ribosome biogenesis at the transcriptional and translational levels by sensing and integrating signals from mitogens and nutrients. Hormonal and stress factors can affect the mTOR-signaling pathway via their receptors and signal transduction pathways. Nutritional regulation of the mTOR-signaling pathway is mediated by their corresponding plasma membrane transporters, other unknown mechanisms, or both. Adenine monophosphate-activated protein kinase, an important cellular energy sensor, can interact with the mTOR-signaling pathway to maintain cellular energy homeostasis. Interactions of mTOR with regulatory-associated protein of TOR or rapamycin-insensitive companion of mTOR result in 2 mTOR complexes, with the former (mTOR complex-1) being the primary controller of cell growth and the latter (mTOR complex-2) mediating effects that are insensitive to rapamycin, such as cytoskeletal organization. Upstream elements of the mTOR-signaling pathway include Ras-homolog enriched in brain, and tuberous sclerosis complex 1 and 2, with tuberous sclerosis complex 2 as the linker between phosphatidylinositol 3-kinase/protein kinase B or Ras-Raf-mitogen-activated protein kinase-extracellular signal-regulated protein kinase pathways and the mTOR pathway. Ribosomal protein S6 protein kinase 1 and eukaryotic initiation factor 4E binding protein 1 are currently the 2 best-known downstream effectors of mTOR signaling. Hormonal factors, stressors, and nutrients can differentially mediate cellular metabolism and growth via the mTOR pathway with effectors specific to the organ or tissue types involved.

To investigate emerging clinical data suggesting a triglyceride (TAG)-lowering response to plant sterol (PS) therapy, we characterized changes in TAG metabolism in 16 C57BL/6J mice fed a basal control diet (CON) or the CON diet supplemented with 2% PS for 6 wk. PS consumption reduced (p<0.05) plasma (-28%) and hepatic (-30%) TAG concentrations compared with CON mice. PS consumption increased (p<0.05) hepatic lipogenic gene expression (sterol-regulatory-element-binding protein 1c, 2.4-fold of CON; fatty acid synthase, 6.5-fold of CON) and de novo lipogenesis (4.51+/-0.72 versus 2.82+/-0.61%/day) compared with CON. PS consumption increased (p<0.05) fecal palmitate and stearate excretion and reduced body weight gain compared with CON mice. Although no change in the transcription of intestinal fatty acid absorptive genes was observed, peroxisome proliferator-activated receptor alpha mRNA was reduced (p<0.05, 2.0-fold of CON) in the PS-fed mice. In conclusion, PS-fed C57BL/6J mice showed pronounced reductions in plasma and hepatic TAG concentrations despite increases in hepatic lipogenic gene expression and de novo lipogenesis. Interference with intestinal fatty acid/TAG metabolism as suggested by increased fecal fatty acid loss and reduced weight gain may be associated with the TAG-lowering response to PS consumption.