L-Rhamnose

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Thomas M. S. Wolever - One of the best experts on this subject based on the ideXlab platform.

  • L-Rhamnose and lactulose decrease serum triacylglycerols and their rates of synthesis, but do not affect serum cholesterol concentrations in men.
    The Journal of nutrition, 2006
    Co-Authors: Janet A. Vogt, Katrin B. Ishii-schrade, Paul B. Pencharz, Peter Jones, Thomas M. S. Wolever
    Abstract:

    Colonic short-chain fatty acids (SCFA) may affect hepatic lipid metabolism. Lactulose increases colonic acetate production, whereas L-Rhamnose increases propionate. To test the effects of oral L-Rhamnose and lactulose for 28 d on fasting concentrations and hepatic synthesis of lipids in humans, 18 men were administered 25 g/d of L-Rhamnose, lactulose, or d-glucose for 4 wk in a partially randomized crossover design, with blood collected from fasting subjects on the first and last day of each period. Cholesterol and triacylglycerol (TG) synthesis rates were determined using deuterated water uptake rate over the last 24 h of each period. Postprandial blood lipids, and glucose and insulin were assessed in 11 subjects on d 28. Fasting serum cholesterol was unchanged; however, when expressed as a percentage change, TG were decreased, relative to baseline (P < 0.04), by L-Rhamnose (-10%) and lactulose (-10%), compared with D-glucose, which increased serum TG (+11%). Net TG-fatty acid (TGFA) synthesis on d 28 was lower with L-Rhamnose (2.42 +/- 0.38 g/d) and lactulose (2.62 +/- 0.35 g/d) than with D-glucose (2.96 +/- 0.31 g/d, P < 0.01). We conclude that these results do not support a primary role for propionate in the cholesterol-lowering effect of soluble fiber. However, both lactulose and L-Rhamnose lowered serum TG (expressed as a percentage change) and TGFA synthesis, compared with d-glucose, which increased them. Although these data are consistent with inhibition of TGFA synthesis by SCFA, other aspects of the metabolism of these sugars cannot be ruled out as putative agents of their TG-lowering effects.

  • L-Rhamnose increases serum propionate after long-term supplementation, but lactulose does not raise serum acetate
    The American journal of clinical nutrition, 2004
    Co-Authors: Janet A. Vogt, Katrin B. Ishii-schrade, Paul B. Pencharz, Thomas M. S. Wolever
    Abstract:

    Background: Acute ingestion of the unabsorbed sugar L-Rhamnose in humans raises serum propionate, whereas acute ingestion of lactulose raises serum acetate. It is not known whether short-chain fatty acid concentrations in urine and feces reflect those in blood. Objective: The objective was to test the effects of oral L-Rhamnose and lactulose for 28 d on acetate and propionate concentrations in serum, urine, and feces. Design: Eleven subjects ingested 25 g L-Rhamnose, lactulose, or D-glucose (control) for 28 d in a partially randomized crossover design. One fecal sample, hourly blood samples, and all urine samples were collected over 12 h on the last day of each phase. Results: The increase in serum propionate was greater after i.-rhamnose than after lactulose (P < 0.05). The effect of lactulose on serum acetate was not significant, but lactulose raised the acetate: propionate ratio compared with D-glucose or L-Rhamnose in serum (P < 0.005) and urine (P < 0.02). Flatulence was significantly greater after lactulose and L-rhamnnse than after D-glucose (P < 0.0001), an effect that lasted 4 wk with lactulose but only I wk with L-Rhamnose. Conclusions: This study confirmed that L-Rhamnose ingestion over 28 d continues to selectively raise serum propionate in humans. Although serum acetate did not increase significantly after lactulose, the serum acetate:propionate ratio was significantly different after L-Rhamnose and lactulose, which suggests that these substrates could be used to examine the role of colonic acetate and propionate production in the effect of dietary fiber on lipid metabolism. Changes in the ratio of urinary acetate to propionate reflected those in serum.

  • L-Rhamnose increases serum propionate in humans
    The American journal of clinical nutrition, 2004
    Co-Authors: Janet A. Vogt, Paul B. Pencharz, Thomas M. S. Wolever
    Abstract:

    Background: Acetic and propionic acids are produced by colonic bacterial fermentation of unabsorbed carbohydrates and are absorbed into the portal circulation. From there, they travel to the liver, where acetate is a lipogenic substrate and propionate can inhibit lipogenesis. The extent to which peripheral blood short-chain fatty acid concentrations reflect differences in colonic fermentation is uncertain. The unabsorbed sugar lactulose produces mainly acetate when fermented in vitro, whereas L-Rhamnose yields propionate. Objective: The objective of the study was to ascertain whether ingestion of L-Rhamnose and lactulose would have different acute effects on peripheral acetate and propionate concentrations and on breath hydrogen and methane concentrations. Design: Twenty-two subjects were fed 25 g L-Rhamnose, lactulose, or glucose on 3 separate occasions in a randomized crossover design. Blood and breath samples were collected hourly for 12 h. Results: Serum propionate was significantly higher with ingestion of L-Rhamnose than with that of lactulose or glucose (P 0.001). The area under the curve for serum acetate was significantly higher with ingestion of lactulose than with that of glucose (P 0.03). The ratio of serum acetate to propionate was significantly higher with ingestion of lactulose than with that of glucose or L-Rhamnose (P 0.01). Breath hydrogen was significantly higher with ingestion of lactulose than with that of L-Rhamnose or glucose (P 0.0001). Conclusions: The selective increases in serum acetate and propionate concentrations in humans were obtained by feeding specific fermentable substrates. Presumably, these changes in serum concentrations reflect changes in colonic production. Selective alteration of colonic fermentation products could yield a new mechanism for modifying blood lipids. Am J Clin Nutr 2004;80:89 –94.

Margarita Orejas - One of the best experts on this subject based on the ideXlab platform.

  • Catabolism of L-Rhamnose in A. nidulans proceeds via the non-phosphorylated pathway and is glucose repressed by a CreA-independent mechanism.
    Microbial cell factories, 2020
    Co-Authors: Andrew Maccabe, Elpinickie Ninou, Ester Pardo, Margarita Orejas
    Abstract:

    L-Rhamnose (6-deoxy-mannose) occurs in nature mainly as a component of certain plant structural polysaccharides and bioactive metabolites but has also been found in some microorganisms and animals. The release of L-Rhamnose from these substrates is catalysed by extracellular enzymes including α-l-rhamnosidases, the production of which is induced in its presence. The free sugar enters cells via specific uptake systems where it can be metabolized. Of two L-Rhamnose catabolic pathways currently known in microorganisms a non-phosphorylated pathway has been identified in fungi and some bacteria but little is known of the regulatory mechanisms governing it in fungi. In this study two genes (lraA and lraB) are predicted to be involved in the catabolism of L-Rhamnose, along with lraC, in the filamentous fungus Aspergillus nidulans. Transcription of all three is co-regulated with that of the genes encoding α-l-rhamnosidases, i.e. induction mediated by the L-Rhamnose-responsive transcription factor RhaR and repression of induction in the presence of glucose via a CreA-independent mechanism. The participation of lraA/AN4186 (encoding L-Rhamnose dehydrogenase) in L-Rhamnose catabolism was revealed by the phenotypes of knock-out mutants and their complemented strains. lraA deletion negatively affects both growth on L-Rhamnose and the synthesis of α-l-rhamnosidases, indicating not only the indispensability of this pathway for L-Rhamnose utilization but also that a metabolite derived from this sugar is the true physiological inducer.

  • The Aspergillus nidulans Zn(II)_2Cys_6transcription factor AN5673/RhaR mediates L-Rhamnose utilization and the production of α-L-rhamnosidases
    Microbial Cell Factories, 2014
    Co-Authors: Ester Pardo, Margarita Orejas
    Abstract:

    Background Various plant-derived substrates contain L-Rhamnose that can be assimilated by many fungi and its liberation is catalyzed by α-L-rhamnosidases. Initial data obtained in our laboratory focussing on two Aspergillus nidulans α-L-rhamnosidase genes ( rhaA and rhaE ) showed α-L-rhamnosidase production to be tightly controlled at the level of transcription by the carbon source available. Whilst induction is effected by L-Rhamnose, unlike many other glycosyl hydrolase genes repression by glucose and other carbon sources occurs in a manner independent of CreA. To date regulatory genes affecting L-Rhamnose utilization and the production of enzymes that yield L-Rhamnose as a product have not been identified in A. nidulans . The purpose of the present study is to characterize the corresponding α-L-rhamnosidase transactivator. Results In this study we have identified the rhaR gene in A. nidulans and Neurospora crassa (AN5673, NCU9033) encoding a putative Zn(II)_2Cys_6 DNA-binding protein. Genetic evidence indicates that its product acts in a positive manner to induce transcription of the A. nidulans L-Rhamnose regulon. rhaR -deleted mutants showed reduced ability to induce expression of the α-L-rhamnosidase genes rhaA and rhaE and concomitant reduction in α-L-rhamnosidase production. The rhaR deletion phenotype also results in a significant reduction in growth on L-Rhamnose that correlates with reduced expression of the L-rhamnonate dehydratase catabolic gene lraC (AN5672). Gel mobility shift assays revealed RhaR to be a DNA binding protein recognizing a partially symmetrical CGG-X_11-CCG sequence within the rhaA promoter. Expression of rhaR alone is insufficient for induction since its mRNA accumulates even in the absence of L-Rhamnose, therefore the presence of both functional RhaR and L-Rhamnose are absolutely required. In N. crassa , deletion of rhaR also impairs growth on L-Rhamnose. Conclusions To define key elements of the L-Rhamnose regulatory circuit, we characterized a DNA-binding Zn(II)_2Cys_6 transcription factor (RhaR) that regulates L-Rhamnose induction of α-L-rhamnosidases and the pathway for its catabolism in A. nidulans , thus extending the list of fungal regulators of genes encoding plant cell wall polysaccharide degrading enzymes. These findings can be expected to provide valuable information for modulating α-L-rhamnosidase production and L-Rhamnose utilization in fungi and could eventually have implications in fungal pathogenesis and pectin biotechnology.

  • The Aspergillus nidulans Zn(II)2Cys6 transcription factor AN5673/RhaR mediates L-Rhamnose utilization and the production of α-L-rhamnosidases.
    Microbial cell factories, 2014
    Co-Authors: Ester Pardo, Margarita Orejas
    Abstract:

    Background Various plant-derived substrates contain L-Rhamnose that can be assimilated by many fungi and its liberation is catalyzed by α-L-rhamnosidases. Initial data obtained in our laboratory focussing on two Aspergillus nidulans α-L-rhamnosidase genes (rhaA and rhaE) showed α-L-rhamnosidase production to be tightly controlled at the level of transcription by the carbon source available. Whilst induction is effected by L-Rhamnose, unlike many other glycosyl hydrolase genes repression by glucose and other carbon sources occurs in a manner independent of CreA. To date regulatory genes affecting L-Rhamnose utilization and the production of enzymes that yield L-Rhamnose as a product have not been identified in A. nidulans. The purpose of the present study is to characterize the corresponding α-L-rhamnosidase transactivator.

Janet A. Vogt - One of the best experts on this subject based on the ideXlab platform.

  • L-Rhamnose and lactulose decrease serum triacylglycerols and their rates of synthesis, but do not affect serum cholesterol concentrations in men.
    The Journal of nutrition, 2006
    Co-Authors: Janet A. Vogt, Katrin B. Ishii-schrade, Paul B. Pencharz, Peter Jones, Thomas M. S. Wolever
    Abstract:

    Colonic short-chain fatty acids (SCFA) may affect hepatic lipid metabolism. Lactulose increases colonic acetate production, whereas L-Rhamnose increases propionate. To test the effects of oral L-Rhamnose and lactulose for 28 d on fasting concentrations and hepatic synthesis of lipids in humans, 18 men were administered 25 g/d of L-Rhamnose, lactulose, or d-glucose for 4 wk in a partially randomized crossover design, with blood collected from fasting subjects on the first and last day of each period. Cholesterol and triacylglycerol (TG) synthesis rates were determined using deuterated water uptake rate over the last 24 h of each period. Postprandial blood lipids, and glucose and insulin were assessed in 11 subjects on d 28. Fasting serum cholesterol was unchanged; however, when expressed as a percentage change, TG were decreased, relative to baseline (P < 0.04), by L-Rhamnose (-10%) and lactulose (-10%), compared with D-glucose, which increased serum TG (+11%). Net TG-fatty acid (TGFA) synthesis on d 28 was lower with L-Rhamnose (2.42 +/- 0.38 g/d) and lactulose (2.62 +/- 0.35 g/d) than with D-glucose (2.96 +/- 0.31 g/d, P < 0.01). We conclude that these results do not support a primary role for propionate in the cholesterol-lowering effect of soluble fiber. However, both lactulose and L-Rhamnose lowered serum TG (expressed as a percentage change) and TGFA synthesis, compared with d-glucose, which increased them. Although these data are consistent with inhibition of TGFA synthesis by SCFA, other aspects of the metabolism of these sugars cannot be ruled out as putative agents of their TG-lowering effects.

  • L-Rhamnose increases serum propionate after long-term supplementation, but lactulose does not raise serum acetate
    The American journal of clinical nutrition, 2004
    Co-Authors: Janet A. Vogt, Katrin B. Ishii-schrade, Paul B. Pencharz, Thomas M. S. Wolever
    Abstract:

    Background: Acute ingestion of the unabsorbed sugar L-Rhamnose in humans raises serum propionate, whereas acute ingestion of lactulose raises serum acetate. It is not known whether short-chain fatty acid concentrations in urine and feces reflect those in blood. Objective: The objective was to test the effects of oral L-Rhamnose and lactulose for 28 d on acetate and propionate concentrations in serum, urine, and feces. Design: Eleven subjects ingested 25 g L-Rhamnose, lactulose, or D-glucose (control) for 28 d in a partially randomized crossover design. One fecal sample, hourly blood samples, and all urine samples were collected over 12 h on the last day of each phase. Results: The increase in serum propionate was greater after i.-rhamnose than after lactulose (P < 0.05). The effect of lactulose on serum acetate was not significant, but lactulose raised the acetate: propionate ratio compared with D-glucose or L-Rhamnose in serum (P < 0.005) and urine (P < 0.02). Flatulence was significantly greater after lactulose and L-rhamnnse than after D-glucose (P < 0.0001), an effect that lasted 4 wk with lactulose but only I wk with L-Rhamnose. Conclusions: This study confirmed that L-Rhamnose ingestion over 28 d continues to selectively raise serum propionate in humans. Although serum acetate did not increase significantly after lactulose, the serum acetate:propionate ratio was significantly different after L-Rhamnose and lactulose, which suggests that these substrates could be used to examine the role of colonic acetate and propionate production in the effect of dietary fiber on lipid metabolism. Changes in the ratio of urinary acetate to propionate reflected those in serum.

  • L-Rhamnose increases serum propionate in humans
    The American journal of clinical nutrition, 2004
    Co-Authors: Janet A. Vogt, Paul B. Pencharz, Thomas M. S. Wolever
    Abstract:

    Background: Acetic and propionic acids are produced by colonic bacterial fermentation of unabsorbed carbohydrates and are absorbed into the portal circulation. From there, they travel to the liver, where acetate is a lipogenic substrate and propionate can inhibit lipogenesis. The extent to which peripheral blood short-chain fatty acid concentrations reflect differences in colonic fermentation is uncertain. The unabsorbed sugar lactulose produces mainly acetate when fermented in vitro, whereas L-Rhamnose yields propionate. Objective: The objective of the study was to ascertain whether ingestion of L-Rhamnose and lactulose would have different acute effects on peripheral acetate and propionate concentrations and on breath hydrogen and methane concentrations. Design: Twenty-two subjects were fed 25 g L-Rhamnose, lactulose, or glucose on 3 separate occasions in a randomized crossover design. Blood and breath samples were collected hourly for 12 h. Results: Serum propionate was significantly higher with ingestion of L-Rhamnose than with that of lactulose or glucose (P 0.001). The area under the curve for serum acetate was significantly higher with ingestion of lactulose than with that of glucose (P 0.03). The ratio of serum acetate to propionate was significantly higher with ingestion of lactulose than with that of glucose or L-Rhamnose (P 0.01). Breath hydrogen was significantly higher with ingestion of lactulose than with that of L-Rhamnose or glucose (P 0.0001). Conclusions: The selective increases in serum acetate and propionate concentrations in humans were obtained by feeding specific fermentable substrates. Presumably, these changes in serum concentrations reflect changes in colonic production. Selective alteration of colonic fermentation products could yield a new mechanism for modifying blood lipids. Am J Clin Nutr 2004;80:89 –94.

Johann Orlygsson - One of the best experts on this subject based on the ideXlab platform.

Elias Westermarck - One of the best experts on this subject based on the ideXlab platform.

  • Urinary recovery of orally administered chromium 51–labeled EDTA, lactulose, rhamnose, d-xylose, 3-O-methyl-d-glucose, and sucrose in healthy adult male Beagles
    American Journal of Veterinary Research, 2012
    Co-Authors: Rafael Frias, Satu Sankari, David A. Williams, Jörg M. Steiner, Elias Westermarck
    Abstract:

    Objective—To provide values for gastrointestinal permeability and absorptive function tests (GIPFTs) with chromium 51 (51Cr)-labeled EDTA, lactulose, rhamnose, d-xylose, 3-O-methyl-d-glucose, and sucrose in Beagles and to evaluate potential correlations between markers. Animals—19 healthy adult male Beagles. Procedures—A test solution containing 3.7 MBq of 51Cr-labeled EDTA, 2 g of lactulose, 2 g of rhamnose, 2 g of d-xylose, 1 g of 3-O-methyl-d-glucose, and 8 g of sucrose was administered intragastrically to each dog. Urinary recovery of each probe was determined 6 hours after administration. Results—Mean ± SD (range) percentage urinary recovery was 6.3 ± 1.6% (4.3% to 9.7%) for 51Cr-labeled EDTA, 3.3 ± 1.1% (1.7% to 5.3%) for lactulose, 25.5 ± 5.0% (16.7% to 36.9%) for rhamnose, and 58.8% ± 11.0% (40.1% to 87.8%) for 3-O-methyl-d-glucose. Mean (range) recovery ratio was 0.25 ± 0.06 (0.17 to 0.37) for 51Cr-labeled EDTA to rhamnose, 0.13 ± 0.04 (0.08 to 0.23) for lactulose to rhamnose, and 0.73 ± 0.09 (0....

  • urinary recovery of orally administered chromium 51 labeled edta lactulose rhamnose d xylose 3 o methyl d glucose and sucrose in healthy adult male beagles
    American Journal of Veterinary Research, 2012
    Co-Authors: Satu Sankari, Rafael Frias, David A. Williams, Jörg M. Steiner, Elias Westermarck
    Abstract:

    Objective—To provide values for gastrointestinal permeability and absorptive function tests (GIPFTs) with chromium 51 (51Cr)-labeled EDTA, lactulose, rhamnose, d-xylose, 3-O-methyl-d-glucose, and sucrose in Beagles and to evaluate potential correlations between markers. Animals—19 healthy adult male Beagles. Procedures—A test solution containing 3.7 MBq of 51Cr-labeled EDTA, 2 g of lactulose, 2 g of rhamnose, 2 g of d-xylose, 1 g of 3-O-methyl-d-glucose, and 8 g of sucrose was administered intragastrically to each dog. Urinary recovery of each probe was determined 6 hours after administration. Results—Mean ± SD (range) percentage urinary recovery was 6.3 ± 1.6% (4.3% to 9.7%) for 51Cr-labeled EDTA, 3.3 ± 1.1% (1.7% to 5.3%) for lactulose, 25.5 ± 5.0% (16.7% to 36.9%) for rhamnose, and 58.8% ± 11.0% (40.1% to 87.8%) for 3-O-methyl-d-glucose. Mean (range) recovery ratio was 0.25 ± 0.06 (0.17 to 0.37) for 51Cr-labeled EDTA to rhamnose, 0.13 ± 0.04 (0.08 to 0.23) for lactulose to rhamnose, and 0.73 ± 0.09 (0....