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      Worldwide flavor enhancer monosodium glutamate combined with high lipid diet provokes metabolic alterations and systemic anomalies: An overview

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          Highlights

          • Flavor enhancing high lipid diet acts as silent killer.

          • Monosodium glutamate mixed with high lipid diet alters redox-status.

          • Monosodium glutamate mixed with high lipid diet induces systemic anomalies.

          Abstract

          In this fast-food era, people depend on ready-made foods and engage in minimal physical activities that ultimately change their food habits. Majorities of such foods have harmful effects on human health due to higher percentages of saturated fatty acids, trans-fatty acids, and hydrogenated fats in the form of high lipid diet (HLD). Moreover, food manufacturers add monosodium glutamate (MSG) to enhance the taste and palatability of the HLD. Both MSG and HLD induce the generation of reactive oxygen species (ROS) and thereby alter the redox-homeostasis to cause systemic damage. However, MSG mixed HLD (MH) consumption leads to dyslipidemia, silently develops non-alcoholic fatty liver disease followed by metabolic alterations and systemic anomalies, even malignancies, via modulating different signaling pathways. This comprehensive review formulates health care strategies to create global awareness about the harmful impact of MH on the human body and recommends the daily consumption of more natural foods rich in antioxidants instead of toxic ingredients to counterbalance the MH-induced systemic anomalies.

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          A core gut microbiome in obese and lean twins

          The human distal gut harbors a vast ensemble of microbes (the microbiota) that provide us with important metabolic capabilities, including the ability to extract energy from otherwise indigestible dietary polysaccharides1–6. Studies of a small number of unrelated, healthy adults have revealed substantial diversity in their gut communities, as measured by sequencing 16S rRNA genes6–8, yet how this diversity relates to function and to the rest of the genes in the collective genomes of the microbiota (the gut microbiome) remains obscure. Studies of lean and obese mice suggest that the gut microbiota affects energy balance by influencing the efficiency of calorie harvest from the diet, and how this harvested energy is utilized and stored3–5. To address the question of how host genotype, environmental exposures, and host adiposity influence the gut microbiome, we have characterized the fecal microbial communities of adult female monozygotic and dizygotic twin pairs concordant for leanness or obesity, and their mothers. Analysis of 154 individuals yielded 9,920 near full-length and 1,937,461 partial bacterial 16S rRNA sequences, plus 2.14 gigabases from their microbiomes. The results reveal that the human gut microbiome is shared among family members, but that each person’s gut microbial community varies in the specific bacterial lineages present, with a comparable degree of co-variation between adult monozygotic and dizygotic twin pairs. However, there was a wide array of shared microbial genes among sampled individuals, comprising an extensive, identifiable ‘core microbiome’ at the gene, rather than at the organismal lineage level. Obesity is associated with phylum-level changes in the microbiota, reduced bacterial diversity, and altered representation of bacterial genes and metabolic pathways. These results demonstrate that a diversity of organismal assemblages can nonetheless yield a core microbiome at a functional level, and that deviations from this core are associated with different physiologic states (obese versus lean).
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            Richness of human gut microbiome correlates with metabolic markers.

            We are facing a global metabolic health crisis provoked by an obesity epidemic. Here we report the human gut microbial composition in a population sample of 123 non-obese and 169 obese Danish individuals. We find two groups of individuals that differ by the number of gut microbial genes and thus gut bacterial richness. They contain known and previously unknown bacterial species at different proportions; individuals with a low bacterial richness (23% of the population) are characterized by more marked overall adiposity, insulin resistance and dyslipidaemia and a more pronounced inflammatory phenotype when compared with high bacterial richness individuals. The obese individuals among the lower bacterial richness group also gain more weight over time. Only a few bacterial species are sufficient to distinguish between individuals with high and low bacterial richness, and even between lean and obese participants. Our classifications based on variation in the gut microbiome identify subsets of individuals in the general white adult population who may be at increased risk of progressing to adiposity-associated co-morbidities.
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              Pharmacological inhibition of cystine–glutamate exchange induces endoplasmic reticulum stress and ferroptosis

              Exchange of extracellular cystine for intracellular glutamate by the antiporter system xc − is implicated in numerous pathologies. Pharmacological agents that inhibit system xc − activity with high potency have long been sought, but have remained elusive. In this study, we report that the small molecule erastin is a potent, selective inhibitor of system xc −. RNA sequencing revealed that inhibition of cystine–glutamate exchange leads to activation of an ER stress response and upregulation of CHAC1, providing a pharmacodynamic marker for system xc − inhibition. We also found that the clinically approved anti-cancer drug sorafenib, but not other kinase inhibitors, inhibits system xc − function and can trigger ER stress and ferroptosis. In an analysis of hospital records and adverse event reports, we found that patients treated with sorafenib exhibited unique metabolic and phenotypic alterations compared to patients treated with other kinase-inhibiting drugs. Finally, using a genetic approach, we identified new genes dramatically upregulated in cells resistant to ferroptosis. DOI: http://dx.doi.org/10.7554/eLife.02523.001
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                Author and article information

                Contributors
                Journal
                Toxicol Rep
                Toxicol Rep
                Toxicology Reports
                Elsevier
                2214-7500
                29 April 2021
                2021
                29 April 2021
                : 8
                : 938-961
                Affiliations
                [0005]Department of Physiology (UG & PG), Serampore College, 9 William Carey Road, Serampore, Hooghly, 712201, West Bengal, India
                Author notes
                [* ]Corresponding author. bm_scp@ 123456yahoo.in
                Article
                S2214-7500(21)00085-8
                10.1016/j.toxrep.2021.04.009
                8120859
                34026558
                18f031b4-a934-4482-9bbf-cd4ae2ebd9f6
                © 2021 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 24 September 2020
                : 20 April 2021
                : 25 April 2021
                Categories
                Regular Article

                food habits,monosodium glutamate,high lipid diet,human health,harmful effects

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