Changes in satiety hormone concentrations and feed intake in rats in response to lactic acid bacteria.

A negative energy balance can be accomplished by reducing the caloric intake which results in an increased feeling of hunger. This physiological state is regulated by secretion of satiety hormones. The secretion of these hormones can be influenced by ingestion of e.g. fat. Fat, dairy beverage and synbiotic mixture have been found to have satiety-inducing effects in humans and rats. Thus, the aim of this study was to investigate the change of satiety hormone concentration in rats in response to feeding of fermented milks containing lactic acid bacteria. Two studies were conducted with Wistar rats randomly allocated into groups receiving Lactobacillus fermented (2 L. acidophilus, L. bulgaricus, L. salivarius and L. rhamnosus) milk. A single isocaloric oral dose with the test item or control was given to the rats. Blood samples were taken after dosing with the test product and the satiety hormones were measured. For the test groups, significant changes could be detected in PYY concentrations after 60 min, although some groups had a significant lower feed intake. In conclusion, some probiotic Lactobacillus strains may modify satiety hormones production. However, more studies are needed to evaluate their potential of prolonging satiety.

Effect of clays, metal oxides, and organic matter on rhamnolipid biosurfactant sorption by soil.

Rhamnolipids produced by Pseudomonas aeruginosa have been proposed as soil washing agents for enhanced removal of metal and organic contaminants from soil. A potential limitation for the application of rhamnolipids is sorption by soil matrix components. The objective of this study is to empirically determine the contribution of representative soil constituents (clays, metal oxides, and organic matter) to sorption of the rhamnolipid form most efficient at metal complexation (monorhamnolipid). Sorption studies show that monorhamnolipid (R1) sorption is concentration dependent. At low R1 concentrations that are relevant for enhancing organic contaminant biodegradation, R1 sorption followed the order: hematite (Fe(2)O(3))>kaolinite>MnO(2) approximately illite approximately Ca-montmorillonite>gibbsite (Al(OH)(3))>humic acid-coated silica. At high R1 concentrations, relevant for use in complexation/removal of metals or organics, R1 sorption followed the order: illite>>humic acid-coated silica>Ca-montmorillonite>hematite>MnO(2)>gibbsite approximately kaolinite. These results allowed prediction of R1 sorption by a series of six soils. Finally, a comparison of R1 and R2 (dirhamnolipid) shows that the R1 form sorbs more strongly alone than when in a mixture of both the R1 and R2 forms. The information presented can be used to estimate, on an individual soil basis, the extent of rhamnolipid sorption. This is important for determining: (1) whether rhamnolipid addition is a feasible remediation option and (2) the amount of rhamnolipid required to efficiently remove the contaminant.

The enhancement by surfactants of hexadecane degradation by Pseudomonas aeruginosa varies with substrate availability.

The rhamnolipid biosurfactant produced by Pseudomonas aeruginosa influences various processes related to hydrocarbon degradation. However, degradation can only be enhanced by the surfactant when it stimulates a process that is rate limiting under the applied conditions. Therefore we determined how rhamnolipid influences hexadecane degradation by P. aeruginosa UG2 under conditions differing in hexadecane availability. The rate of hexadecane degradation in shake flask cultures was lower for hexadecane entrapped in a matrix with 6 nm pores (silica 60) or in quartz sand than for hexadecane immobilized in matrices with pore sizes larger than 300 nm or for hexadecane present as a separate liquid phase. This indicates that the availability of hexadecane decreased with decreasing pore size under these conditions. The rate-limiting step for hexadecane entrapped in silica 60 was the mass transfer of substrate from the matrix to the bulk liquid phase, whereas for hexadecane present as a second liquid phase it was the uptake of the substrate by the cells. Hexadecane degradation in batch incubations was accelerated by the addition of rhamnolipid or other surfactants in all experiments except in those where hexadecane was entrapped in silica 60, indicating that the surfactants stimulated uptake of hexadecane by the cells. Since rhamnolipid stimulated the degradation rate in batch experiments to a greater extent than any of the other 14 surfactants tested, hexadecane uptake was apparently more enhanced by rhamnolipid than by the other surfactants. Although rhamnolipid did not stimulate the release of hexadecane from silica 60 under conditions of intense agitation, it significantly enhanced this rate during column experiments in the absence of strain UG2. The results demonstrate that rhamnolipid enhances degradation by stimulating release of entrapped substrate in column studies under conditions of low agitation and by stimulating uptake of substrate by the cells, especially when degradation is not limited by release of substrate from the matrices.

Rhamnolipid stimulates uptake of hydrophobic compounds by Pseudomonas aeruginosa.

The biodegradation of hexadecane by five biosurfactant-producing bacterial strains (Pseudomonas aeruginosa UG2, Acinetobacter calcoaceticus RAG1, Rhodococcus erythropolis DSM 43066, R. erythropolis ATCC 19558, and strain BCG112) was determined in the presence and absence of exogenously added biosurfactants. The degradation of hexadecane by P. aeruginosa was stimulated only by the rhamnolipid biosurfactant produced by the same organism. This rhamnolipid did not stimulate the biodegradation of hexadecane by the four other strains to the same extent, nor was degradation of hexadecane by these strains stimulated by addition of their own biosurfactants. This suggests that P. aeruginosa has a mode of hexadecane uptake different from those of the other organisms. Rhamnolipid also enhanced the rate of epoxidation of the aliphatic hydrocarbon alpha,omega-tetradecadiene by a cell suspension of P. aeruginosa. Furthermore, the uptake of the hydrophobic probe 1-naphthylphenylamine by cells of P. aeruginosa was enhanced by rhamnolipid, as indicated by stopped-flow fluorescence experiments. Rhamnolipid did not stimulate the uptake rate of this probe in de-energized cells. These results indicate that an energy-dependent system is present in P. aeruginosa strain UG2 that mediates fast uptake of hydrophobic compounds in the presence of rhamnolipid.