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Lipidomic Insight into Membrane Remodeling in Aging and Neurodegenerative Diseases
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Long-chain fatty acids (LCFA) play a crucial role in various metabolic processes, including energy storage and membrane formation; moreover, they constitute a source of bioactive lipid mediators. The LCFAs are activated by the long-chain acyl-CoA synthetases (ACSL) enzymes, which in mammals are essential for fatty acid degradation, phospholipid remodeling, and production of long acyl-CoA esters regulating various physiological processes [29].
Impairment of Lipid Metabolism in Ischemic and Reperfused Myocardial Tissue
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
Ger J. van der Vusse, Marc van Bilsen, Robert S. Reneman
In the present survey, we will attempt to describe the effect of ischemia and reperfusion on myocardial fatty acid metabolism in relation to reversible and irreversible injury of myocardial tissue. There are several reasons to focus on this particular aspect of the broad spectrum of cardiac metabolic pathways. Firstly, the energy-delivering process of fatty acid degradation does obligatorily require molecular oxygen. Impaired supply of oxygen will result in inhibition of fatty acid oxidation with a concomitant accumulation of lipid intermediates, potentially harmful by nature.5 Secondly, evidence is growing5,12,13,31,32 that membrane perturbation plays an important role in the development of irreversible ischemia-induced damage. Since phosphoglycerides, containing over 85% of all tissue fatty acids,34 are important constituents of myocardial membranes, impaired phosphoglyceride homeostasis will likely result in loss of cell membrane integrity and accumulation of fatty acids and lysophosphoglycerides. Enhanced cellular fatty acids levels, in turn, may exert a deleterious effect on the ischemic myocytes.
Carbon Dioxide Sequestration by Microalgae
Published in Gokare A. Ravishankar, Ranga Rao Ambati, Handbook of Algal Technologies and Phytochemicals, 2019
G.V. Swarnalatha, Ajam Shekh, P.V. Sijil, C.K. Madhubalaji, Vikas Singh Chauhan, Ravi Sarada
The reports indicate that the CO2 supplementation enhances the lipid content in various microalgal strains. According to Peng et al. (2016), the enhancement of lipid accumulation was caused by the significant down-regulation of the genes encoding enzymes for fatty acid degradation and the up-regulation of fatty acid synthesis.
Chronic exposure to ampicillin alters lung microbial composition in laboratory rat
Published in Experimental Lung Research, 2023
Ping Chen, Tingting Hu, Haonan Jiang, Bing Li, Guiying Li, Pixin Ran, Yumin Zhou
The present study investigated the effects of ampicillin aerosolization on lung microbiota of Sprague-Dawley rats. Results of this study demonstrated that ampicillin could modify lung community compositions by the long-term low-dose nebulization of antibiotics at a certain concentration of LA5. Brucella, Acinetobacter, Acidobacteria_Gp14, Sphingomonas, Tumebacillus, and Acidobacteria_Gp16 were the dominant and significantly different taxa between the LA5 and LC groups (Figures 2 and 3). Furthermore, alterations were identified in potential metabolites associated with Drug metabolism cytochrome P450 (map00982), Phenylalanine metabolism (map00360), Fatty acid degradation (map00071), Non_homologous end joining (map03450), beta-Alanine metabolism (map00410) and so on (Figure 4A).
Dietary manipulation of the gut microbiome in inflammatory bowel disease patients: Pilot study
Published in Gut Microbes, 2022
Barbara Olendzki, Vanni Bucci, Caitlin Cawley, Rene Maserati, Margaret McManus, Effie Olednzki, Camilla Madziar, David Chiang, Doyle V. Ward, Randall Pellish, Christine Foley, Shakti Bhattarai, Beth A. McCormick, Ana Maldonado-Contreras
We next evaluated the functional capacity of the microbiome during the intervention. At baseline, we found that the metagenomic capacity varied greatly by participant, with most samples clustering by participant (data not shown). However, we observe that during the intervention the microbiome exhibited an increased genetic capacity for 1) biosynthesis of several key amino acids (i.e., histidine, lysine, threonine, methionine, serine, glycine, isoleucine, and arginine); 2) degradation of mannan (a dietary fiber); and 3) β-oxidation for fatty acid degradation (Figure 4). Roseburia sp. and Faecalibacterium sp. – both favored during the IBD-AID intervention are main degraders of dietary mannan ultimately producing SCFA.52,53 Mannans are found in the endospermic tissue of nuts (homopolymeric mannan), barley, oats (β-glucans or mannoproteins), coffee beans, coconut palm, tomato, and legume seeds (galactomannan).54 Similarly, increased microbiome gene capacity for oxidation of fatty acids during the intervention also suggests increased availability of SCFAs. Thus, we further investigated the impact of IBD-AID on the pool of microbial genes involved in SCFA production during the intervention.
Bacteroides uniformis combined with fiber amplifies metabolic and immune benefits in obese mice
Published in Gut Microbes, 2021
Inmaculada López-Almela, Marina Romaní-Pérez, Clara Bullich-Vilarrubias, Alfonso Benítez-Páez, Eva M. Gómez Del Pulgar, Rubén Francés, Gerhard Liebisch, Yolanda Sanz
Thermogenesis, mainly fueled by fatty acids,25 was increased in HFHSD-fed mice, as indicated by overexpression of Ucp-1 in BAT and in epididymal fat, whose thermogenic potential may increase under β3 adrenergic stimulation.26 Although increased adrenergic-induced thermogenesis associated to diet-induced obesity remains controversial,27 it may be a mechanism to increase metabolic rate under a Western diet in order to maintain energy balance.28 The overexpression of Ucp-1 in epididymal fat, coupled with increased Cpt1-a expression of mice fed HFHSD and their positive correlation to fat mass and weight gain, suggests excess energy from the obesogenic diet was partially counteracted by triggering fatty acid degradation by thermogenesis and fatty acid oxidation, albeit insufficient to prevent obesity. Also, the activation of this mechanism was unnecessary in mice receiving B. uniformis and WBE. Therefore, the beneficial effect of B. uniformis and WBE on adiposity was not mediated by the activation of energy dissipating metabolic routes using lipids as fuel, which suggests that the improved whole-energy disposal was through a mechanism independent of adipose tissue.