| 1. |
- Cowan, Theresa, et al.
(författare)
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Chronic coffee consumption in the diet-induced obese rat: impact on gut microbiota and serum metabolomics
- 2014
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Ingår i: Journal of Nutritional Biochemistry. - : Elsevier BV. - 0955-2863 .- 1873-4847. ; 25:4, s. 489-495
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Tidskriftsartikel (refereegranskat)abstract
- Epidemiological data confirms a strong negative association between regular coffee consumption and the prevalence of type 2 diabetes. Coffee is initially absorbed in the stomach and small intestine but is further fermented in the colon by gut microbiota. The bioavailability, production and biological activity of coffee polyphenols is modulated, in part, by gut microbiota. The purpose of this study was to determine if chronic coffee consumption could mitigate negative gut microbiota and metabolomic profile changes induced by a high-fat diet. Male Sprague-Dawley rats were randomized to chow (12% kcal fat) or high-fat (60% kcal fat) diet. Each group was further divided into water or caffeinated coffee for 10 weeks. Coffee consumption in high-fat-fed rats was associated with decreased body weight, adiposity, liver triglycerides and energy intake. Despite a more favorable body composition, rats displayed profound systemic insulin resistance, likely due to caffeine. Coffee consumption attenuated the increase in Firmicutes (F)-to-Bacteroidetes (B) ratio and Clostridium Cluster XI normally associated with high-fat feeding but also resulted in augmented levels of Enterobacteria. In the serum metabolome, coffee had a distinct impact, increasing levels of aromatic and circulating short-chain fatty acids while lowering levels of branched-chain amino acids. In summary, coffee consumption is able to alter gut microbiota in high-fat-fed rats although the role of these changes in reducing diabetes risk is unclear given the increased insulin resistance observed with coffee in this study.
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| 2. |
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| 3. |
- Ji, Chenlin, et al.
(författare)
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Postnatal overfeeding promotes early onset and exaggeration of high-fat diet-induced nonalcoholic fatty liver disease through disordered hepatic lipid metabolism in rats
- 2014
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Ingår i: Journal of Nutritional Biochemistry. - : Elsevier. - 0955-2863 .- 1873-4847. ; 25:11, s. 1108-1116
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Tidskriftsartikel (refereegranskat)abstract
- Exposure to overnutrition in critical or sensitive developmental periods may increase the risk of developing obesity and metabolic syndrome in adults. Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome, but the relationship among postnatal nutrition, lipid metabolism, and NAFLD progression during development remains poorly understood. Here we investigated in a rat model whether postnatal overfeeding increases susceptibility to NAFLD in response to a high-fat diet. Litters from Sprague-Dawley dams were culled to three (small litters) or ten (normal litters) pups and then weaned onto a standard or high-fat diet at postnatal day 21 to generate normal-litter, small-litter, normal-litter/high-fat, and small-litter/high-fat groups. At age 16 weeks, the small-litter and both high-fat groups showed obesity, dyslipidemia, and insulin resistance. Hepatic disorders appeared earlier in the small-litter/high-fat rats with greater liver mass gain and higher hepatic triglycerides and steatosis score versus normal-litter/high-fat rats. Hepatic acetyl-CoA carboxylase activity and mRNA expression were increased in small-litter rats and aggravated in small-litter/high-fat rats but not in normal-litter/high-fat rats. The high expression in small-litter/high-fat rats coincided with high sterol regulatory element-binding protein-1c mRNA and protein expression. However, mRNA expression of enzymes involved in hepatic fatty acid oxidation (carnitine palmitoyltransferase 1) and output (microsomal triglyceride transfer protein) was decreased under a high-fat diet regardless of litter size. In conclusion, overfeeding related to small-litter rearing during lactation contributes to the NAFLD phenotype when combined with a high-fat diet, possibly through up-regulated hepatic lipogenesis. (C) 2014 Elsevier Inc. All rights reserved.
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| 4. |
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| 5. |
- Roberts, Carol L., et al.
(författare)
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Soluble plantain fibre blocks adhesion and M-cell translocation of intestinal pathogens
- 2013
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Ingår i: Journal of Nutritional Biochemistry. - : Elsevier. - 0955-2863 .- 1873-4847. ; 24:1, s. 97-103
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Tidskriftsartikel (refereegranskat)abstract
- Dietary fibres may have prebiotic effects mediated by promotion of beneficial bacteria. This study explores the possibility that soluble plant fibre may also improve health by inhibiting epithelial adhesion and translocation by pathogenic bacteria. We have focussed on soluble non-starch polysaccharide (NSP) from plantain bananas (Musa spp.) which previous studies showed to be particularly effective at blocking Escherichia coli epithelial adherence. In vitro and ex vivo studies assessed the ability of plantain NSP to inhibit epithelial cell adhesion and invasion of various bacterial pathogens, and to inhibit their translocation through microfold (M)-cells and human Peyers patches mounted in Ussing chambers. Plantain NSP showed dose-related inhibition of epithelial adhesion and M-cell translocation by a range of pathogens. At 5 mg/ml, a concentration readily achievable in the gut lumen, plantain NSP inhibited adhesion to Caco2 cells by Salmonella Typhimurium (85.0 +/- 8.2%, Pandlt;.01), Shigella sonnei (46.6 +/- 29.3%. Pandlt;.01), enterotoxigenic E.coli (56.1 +/- 23.7%, Pandlt;.05) and Clostridium difficile (67.6 +/- 12.3%, Pandlt;.001), but did not inhibit adhesion by enteropathogenic E.coli. Plantain NSP also inhibited invasion of Caco2 cells by S. Typhimurium (80.2 +/- 9.7%) and Sh. sonnei (46.7 +/- 13.4%); Pandlt;.01. Plantain NSP, 5 mg/ml, also inhibited translocation of S. Typhimurium and Sh. sonnei across M-cells by 73.3 +/- 5.2% and 46.4 +/- 7.7% respectively (Pandlt;.05). Similarly, S. Typhimurium translocation across Peyers patches was reduced 65.9 +/- 8.1% by plantain NSP (Pandlt;.01). Soluble plantain fibre can block epithelial adhesion and M-cell translocation of intestinal pathogens. This represents an important novel mechanism by which soluble dietary fibres can promote intestinal health and prevent infective diarrhoea. Crown Copyright
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| 6. |
- Scheers, Nathalie, 1974, et al.
(författare)
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Proposing a Caco-2/HepG2 cell model for in vitro iron absorption studies
- 2014
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Ingår i: Journal of Nutritional Biochemistry. - : Elsevier BV. - 0955-2863 .- 1873-4847. ; 25:7, s. 710-715
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Tidskriftsartikel (refereegranskat)abstract
- The Caco-2 cell line is well established as an in vitro model for iron absorption. However, the model does not reflect the regulation of iron absorption by hepcidin produced in the liver. We aimed to develop the Caco-2 model by introducing human liver cells (HepG2) to Caco-2 cells. The Caco-2 and HepG2 epithelia were separated by a liquid compartment, which allowed for epithelial interaction. Ferritin levels in cocultured Caco-2 controls were 21.7 +/- 10.3 ng/mg protein compared to 7.7 +/- 5.8 ng/mg protein in monocultured Caco-2 cells. The iron transport across Caco-2 layers was increased when liver cells were present (8.1% +/- 1.5% compared to 3.5% +/- 2.5% at 120 mu M Fe). Caco-2 cells were exposed to 0, 80 and 120 mu M Fe and responded with increased hepcidin production at 1201 mu M Fe (3.6 +/- 0.3 ng/ml compared to 2.7 +/- 0.3 ng/ml). The expression of iron exporter ferroportin in Caco-2 cells was decreased at the hepcidin concentration of 3.6 ng/ml and undetectable at external addition of hepcidin (10 ng/ml). The apical transporter DMT1 was also undetectable at 10 ng/ml but was unchanged at the lower concentrations. In addition, we observed that sourdough bread, in comparison to heat-treated bread, increased the bioavailability of iron despite similar iron content (53% increase in ferritin formation, 97% increase in hepcidin release). This effect was not observed in monocultured Caco-2 cells. The Caco-2/HepG2 model provides an alternative approach to in vitro iron absorption studies in which the hepatic regulation of iron transport must be considered. (c) 2014 The Authors. Published by Elsevier Inc.
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| 7. |
- Zou, Jun, et al.
(författare)
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Lycopene suppresses proinflammatory response in lipopolysaccharide-stimulated macrophages by inhibiting ROS-induced trafficking of TLR4 to lipid raft-like domains
- 2013
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Ingår i: Journal of Nutritional Biochemistry. - : Elsevier BV. - 1873-4847 .- 0955-2863. ; 24:6, s. 1117-1122
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Tidskriftsartikel (refereegranskat)abstract
- We recently showed that lycopene inhibited lipopolysaccharide (LPS)-induced productions of nitric oxide (NO) and interleukin-6 (IL-6) in murine RAW264.7 macrophages by mechanisms related to inhibition of ERK and nuclear factor-kappa B. Since the assembly of Toll-like receptor 4 (TLR4) in lipid rafts is a key element in LPS induced signaling, we investigated whether this process would be influenced by lycopene. We found that pretreatment of RAW264.7 cells with lycopene inhibited LPS-induced recruitment of TLR4 into fractions - enriched with lipid raft marker. By the methods of immunoprecipitation and immunoblotting, we also found that lycopene inhibited the subsequent formation of the complex of TLR4 with its adaptors including myeloid differentiation primary-response protein 88 and TIR domain-containing adaptor-inducing IFN-beta. We also found that the lycopene induced inhibition was associated with reduced formation of reactive oxygen species (ROS), which was an upstream mechanism for the effects of lycopene, because treating the cells with the antioxidant N-acetyl-L-cysteine and NADPH oxidase inhibitor diphenyleneiodonium chloride significantly inhibited LPS-induced recruitment of TLR4 into lipid raft-like domains as well as the production of proinflammatory molecule NO and IL-6. Thus, our findings suggest that lycopene may prevent LPS-induced TLR4 assembly into lipid rafts through reducing intracellular ROS level. (C) 2013 Elsevier Inc. All rights reserved.
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| 8. |
- Yuniarto, Adhi, et al.
(författare)
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Bio-fouling reducers for improving the performance of an aerobic submerged membrane bioreactor treating palm oil mill effluent
- 2013
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Ingår i: Desalination. - : Elsevier BV. - 1873-4464 .- 0011-9164. ; 316, s. 146-153
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Tidskriftsartikel (refereegranskat)abstract
- A bench scale aerobic submerged membrane bioreactor (ASMBR) was used to treat diluted palm oil mill effluent (POME). For further improving the effluent quality and reduction of bio-fouling, powdered activated carbon (PAC) and zeolite were used as bio-fouling reducers (BM). We compared the performances of ASMBR without BFR (called BFR0) with ASMBR using BFR, namely 2 g/L PAC (BFR1), 4 g/L PAC (BFR2) and 2 g/L zeolite (BFR3) for a period of about 70 days. Each system with BFR showed distinct performances by producing higher effluent quality as compared with BFR0. On average, the systems with and without BFR removed COD by 97.5-98.5% and 95.2%, respectively. The ASMBR with BFR also produced permeate with average residual color between 16 and 26 Pt-Co, as compared to 80 Pt-Co by BFR0. The addition of BFR increased the critical flux from 20 LMH (BFR0) to 36, 42 and 30 LMH (BFR1, BFR2, and BFR3). Furthermore, the ASMBR systems with BFR formed lower operational trans-membrane pressure (TMP), lowered the concentration of soluble microbial products (SMP) and increased the concentration of EPS. (C) 2013 Elsevier B.V. All rights reserved.
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