fumarates and lauric-acid

Two experiments were conducted to assess the effects of a mixture of dietary additives on enteric methane production, rumen fermentation, diet digestibility, energy balance, and animal performance in lactating dairy cows. Identical diets were fed in both experiments. The mixture of feed additives investigated contained lauric acid, myristic acid, linseed oil, and calcium fumarate. These additives were included at 0.4, 1.2, 1.5, and 0.7% of dietary dry matter, respectively (treatment ADD). Experimental fat sources were exchanged for a rumen inert source of fat in the control diet (treatment CON) to maintain isolipidic rations. Cows (experiment 1, n=20; experiment 2, n=12) were fed restricted amounts of feed to avoid confounding effects of dry matter intake on methane production. In experiment 1, methane production and energy balance were studied using open-circuit indirect calorimetry. In experiment 2, 10 rumen-fistulated animals were used to measure rumen fermentation characteristics. In both experiments animal performance was monitored. The inclusion of dietary additives decreased methane emissions (g/d) by 10%. Milk yield and milk fat content tended to be lower for ADD in experiment 1. In experiment 2, milk production was not affected by ADD, but milk fat content was lower. Fat- and protein-corrected milk was lower for ADD in both experiments. Milk urea nitrogen content was lowered by ADD in experiment 1 and tended to be lower in experiment 2. Apparent total tract digestibility of fat, but not that of starch or neutral detergent fiber, was higher for ADD. Energy retention did not differ between treatments. The decrease in methane production (g/d) was not evident when methane emission was expressed per kilogram of milk produced. Feeding ADD resulted in increases of C12:0 and C14:0 and the intermediates of linseed oil biohydrogenation in milk in both experiments. In experiment 2, ADD-fed cows tended to have a decreased number of protozoa in rumen fluid when compared with that in control cows. Total volatile fatty acid concentrations were lower for ADD, whereas molar proportions of propionate increased at the expense of acetate and butyrate.

Topics: Animal Feed; Animals; Cattle; Diet; Digestion; Energy Metabolism; Female; Fermentation; Food Additives; Fumarates; Lactation; Lauric Acids; Linseed Oil; Methane; Myristic Acid; Rumen

We investigated whether the direct renin inhibitor aliskiren can affect metabolism in cardiomyocytes from rat, mouse and human sources.. At 10-50 μmol/L, aliskiren significantly increased medium-chain-fatty-acid uptake in primary-cultured neonatal-rat and HL-1 adult-mouse-derived cardiomyocytes (BODIPY-induced fluorescence intensity). The fatty-acid transporter CD-36 was correspondingly translocated to, but the glucose transporter Glut-4 away from, the sarcoplasmic reticulum/plasma membrane, in primary-cultured neonatal-rat (CD-36, Glut-4) and adult-human (CD-36) cardiomyocytes (confocal immunocytochemistry). Immunoblotting showed that aliskiren induced phosphorylation of ERK1/2 in cardiomyocytes from all three sources; responses were dose- and time-dependent, unaffected by renin treatment, and did not cause alterations in expression of (P)R or Igf2/M6P receptors. Microarray analysis of the complete genome of aliskiren-treated neonatal-rat cardiomyocytes, with RT-qPCR and immunoblot confirmation assays in rat and human primary cardiomyocytes, showed that aliskiren up-regulated mRNA and increased protein expression of several enzymes important in lipid and glucose metabolism and in cholesterol biosynthesis. Cardiomyocyte cell-cycle and viability were unaffected by aliskiren.. Aliskiren can induce changes in fatty-acid and glucose uptake and expression of key enzymes of lipid and cholesterol metabolism, which are not associated with increased expression of (P)R or Igf2/M6P receptors, in cultured cardiomyocytes.

Topics: Amides; Animals; CD36 Antigens; Cell Cycle; Cell Survival; Cells, Cultured; Cholesterol; Extracellular Signal-Regulated MAP Kinases; Fatty Acids; Fumarates; Glucose Transporter Type 4; Humans; Lauric Acids; Lipid Metabolism; Myocytes, Cardiac; Oligonucleotide Array Sequence Analysis; Rats; Receptor, IGF Type 2; Renin