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- Bahadoran, Zahra, et al.
(författare)
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Inorganic nitrate, a natural anti-obesity agent : A systematic review and meta-analysis of animal studies
- 2020
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Ingår i: EXCLI Journal. - 1611-2156. ; 19, s. 972-983
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Forskningsöversikt (refereegranskat)abstract
- Evidence for potential effects of inorganic nitrate (NO3) on body weight is limited to inconsistent findings of animal experiments. In this systematic review and meta-analysis, we aimed to quantify the overall effect of inorganic NO3, administered via drinking water, on body weight gain in rats. We searched PubMed, Scopus, and Embase databases, and the reference lists of published papers. Experiments on male rats, reported data on body weight in NO3-treated animals and controls, were included for quality assessment, meta-analyses, subgroup anal-yses, and meta-regressions. Of 173 initially obtained studies, 11 were eligible to be included in the analyses, which covered the years 2004 to 2019 and included a total of 43 intervention (n=395) and 43 control (n=395) arms. Overall, the final body weights were significantly lower in the NO3-supplemented groups compared to controls (WMD= –16.8 g, 95 % CI= –27.38, –6.24; P=0.002). Doses of NO3 higher than the median (> 72.94 mg L-1 d-1) and longer NO3 exposure (> 8 weeks) resulted in greater mean differences (WMD= –31.92 g, 95 % CI= –52.90, –10.94 and WMD= –23.16 g, 95 % CI= –35.64, –10.68 g). After exclusion of experiments using high doses of NO3 (> 400 mg L-1 d-1), the overall mean differences in body weights between the groups decreased by approxi-mately 37 % but remained statistically significant (WMD= –10.11 g, 95 % CI= –19.04, –1.19, P=0.026). Mean changes in body weight were affected by age, baseline values in body weight, and the duration of the studies. These preliminary experimental findings strongly support the hypothesis that NO3 can be considered as a natural anti-obesity agent.
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- Bölling, Anette, et al.
(författare)
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Pulmonary phthalate exposure and asthma - is PPAR a plausible mechanistic link?
- 2013
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Ingår i: EXCLI Journal. - : Universität Mainz. - 1611-2156. ; 12, s. 733-759
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Tidskriftsartikel (refereegranskat)abstract
- Due to their extensive use as plasticisers in numerous consumer products, phthalates have become ubiquitous environmental contaminants. An increasing number of epidemiological studies suggest that exposure to phthalates may be associated with worsening or development of airway diseases. Peroxisome Proliferation Activated Receptors (PPAR)s, identified as important targets for phthalates in early studies in rodent liver, have been suggested as a possible mechanistic link. In this review we discuss the likelihood of an involvement of PPARs in asthma development and exacerbation due to pulmonary phthalate exposure. First, we go through the literature on indoor air levels of phthalates and pulmonary phthalate kinetics. These data are then used to estimate the pulmonary phthalate levels due to inhalation exposure. Secondly, the literature on phthalate-induced activation or modulation of PPARs is summarized. Based on these data, we discuss whether pulmonary phthalate exposure is likely to cause PPAR activation, and if this is a plausible mechanism for adverse effects of phthalates in the lung. It is concluded that the pulmonary concentrations of some phthalates may be sufficient to cause a direct activation of PPARs. Since PPARs mainly mediate antiinflammatory effects in the lungs, a direct activation is not a likely molecular mechanism for adverse effects of phthalates. However, possible modulatory effects of phthalates on PPARs deserve further investigation, including partial antagonist effects and/or cross talk with other signalling pathways. Moreover other mechanisms, including interactions between phthalates and other receptors, could also contribute to possible adverse pulmonary effects of phthalates.
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- Gheibi, Sevda, et al.
(författare)
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Insulin secretion : The nitric oxide controversy
- 2020
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Ingår i: EXCLI Journal. - 1611-2156. ; 19, s. 1227-1245
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Forskningsöversikt (refereegranskat)abstract
- Nitric oxide (NO) is a gas that serves as a ubiquitous signaling molecule participating in physiological activities of various organ systems. Nitric oxide is produced in the endocrine pancreas and contributes to synthesis and secretion of insulin. The potential role of NO in insulin secretion is disputable – both stimulatory and inhibitory effects have been reported. Available data indicate that effects of NO critically depend on its concentration. Different isoforms of NO synthase (NOS) control this and have the potential to decrease or increase insulin secretion. In this review, the role of NO in insulin secretion as well as the possible reasons for discrepant findings are dis-cussed. A better understanding of the role of NO system in the regulation of insulin secretion may facilitate the development of new therapeutic strategies in the management of diabetes.
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- Mu, Qinfeng, et al.
(författare)
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Apolipoprotein m promotes growth and inhibits apoptosis of colorectal cancer cells through upregulation of ribosomal protein s27a
- 2021
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Ingår i: EXCLI Journal. - 1611-2156. ; 20, s. 145-159
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Tidskriftsartikel (refereegranskat)abstract
- Colorectal cancer (CRC) is one of the frequent malignant tumors and has a high mortality-to-incidence ratio. Apolipoprotein M (ApoM), a lipoprotein superfamily member, is primarily bound to high-density lipoprotein (HDL) particles. Our previous studies opined that ApoM crucially modulates CRC progression, but its role in CRC has not been elucidated. Here, lentivirus infection technology was used to overexpress ApoM in Caco-2 cells. Cell growth, apoptosis as well as clone formation assays were performed to explore the biological influences of ApoM in Caco-2 cells. Differentially expressed genes were analyzed via GeneChip microarrays and Quantitative real-time PCR (qPCR) along with Western blotting were applied to verify the results. Ribosomal protein S27a (RPS27A) expression in CRC and tumor-adjacent tissues was detected by qPCR, and its correlation with clinico-pathologic characteristics was explored. Our results showed that ApoM overexpression could promote Caco-2 cell proliferation and inhibit apoptosis. The microarray evaluation uncovered 2671 genes, which were differentially expressed, including RPS27A. The qPCR as well as the Western blotting data showed that ApoM overexpression significantly increased the expression of RPS27A. Moreover, RPS27A expression was remarkably higher in CRC tissues in contrast with the tumor-adjacent tissues and was positively correlated with the ApoM level in tumor tissues, and higher RPS27A expression was associated with smaller tumors and lower T stage. Functional recovery experiments indicated that knockdown of RPS27A counteracted the apoptosis inhibition and clone formation pro-motion induced by ApoM overexpression in Caco-2 cells. In conclusion, ApoM promotes CRC cell growth and inhibits apoptosis through upregulation of RPS27A.
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- Tangkosakul, Teerawit, et al.
(författare)
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Native And Chimeric Metal-Binding Lactate Dehydrogenase As Detection And Protection Tools For Oxidative Stress Induced By Fenton'S Reaction
- 2009
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Ingår i: EXCLI Journal. - 1611-2156. ; 8, s. 1-11
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Tidskriftsartikel (refereegranskat)abstract
- In the present study, a simple and reliable antioxidant screening technique based on lactate dehydrogenase (LDH) oxidation by Cu2+-mediated Fenton's reaction has successfully been developed. Oxidation of LDH by hydroxyl radical consequently leads to enzymatic inactivation, while addition of antioxidants can protect and regain enzyme activity. This method demonstrated a high feasibility on detecting of antioxidative activity of lipophilic (e.g. alpha-Tocopherol and beta-Carotene) and hydrophilic compounds (e. g. glutathione, mannitol and thiourea) in a single assay. Results from linear correlation curves revealed that the IC50 were in the order of beta-carotene (3.45 mu g/ml) > alpha-Tocopherol (52.31 mu g/ml) > Mn(II)-bacitracin (109.37 mu g/ml) > glutathione (122.63 mu g/ml). Detailed investigations revealed that oxidation of LDH resulted in enzyme degradation, which was metal- and time-dependent mechanism. Therefore, further experiments were conducted to determine whether extension of the N-terminus of LDH with metal- binding regions possesses protective effect against the inactivation process. Genetic construction of chimeric LDH carrying two and four repetitive sequences of cadmium binding peptide (CdBP), designated as CdBP2LDH and CdBP4LDH, has been carried out. From our findings, the CdBP2LDH and the CdBP4LDH exhibited protective action and enzyme activity regained 20-30 % and 70 % higher than that of the native LDH, respectively. Two possible mechanisms have been proposed to play important role in protection against metal- mediated Fenton's reaction: i) changing in redox potential of Cu2+ in metal-peptide complex, and ii) taking away of Cu2+ ion from the crucial amino acids by metal saturation at the cadmium-binding peptides.
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