Academic literature on the topic 'Lipid anabolism'
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Journal articles on the topic "Lipid anabolism"
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Krycer, James R., Lake-Ee Quek, Deanne Francis, Armella Zadoorian, Fiona C. Weiss, Kristen C. Cooke, Marin E. Nelson, et al. "Insulin signaling requires glucose to promote lipid anabolism in adipocytes." Journal of Biological Chemistry 295, no. 38 (July 28, 2020): 13250–66. http://dx.doi.org/10.1074/jbc.ra120.014907.
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Adipose tissue is essential for metabolic homeostasis, balancing lipid storage and mobilization based on nutritional status. This is coordinated by insulin, which triggers kinase signaling cascades to modulate numerous metabolic proteins, leading to increased glucose uptake and anabolic processes like lipogenesis. Given recent evidence that glucose is dispensable for adipocyte respiration, we sought to test whether glucose is necessary for insulin-stimulated anabolism. Examining lipogenesis in cultured adipocytes, glucose was essential for insulin to stimulate the synthesis of fatty acids and glyceride–glycerol. Importantly, glucose was dispensable for lipogenesis in the absence of insulin, suggesting that distinct carbon sources are used with or without insulin. Metabolic tracing studies revealed that glucose was required for insulin to stimulate pathways providing carbon substrate, NADPH, and glycerol 3-phosphate for lipid synthesis and storage. Glucose also displaced leucine as a lipogenic substrate and was necessary to suppress fatty acid oxidation. Together, glucose provided substrates and metabolic control for insulin to promote lipogenesis in adipocytes. This contrasted with the suppression of lipolysis by insulin signaling, which occurred independently of glucose. Given previous observations that signal transduction acts primarily before glucose uptake in adipocytes, these data are consistent with a model whereby insulin initially utilizes protein phosphorylation to stimulate lipid anabolism, which is sustained by subsequent glucose metabolism. Consequently, lipid abundance was sensitive to glucose availability, both during adipogenesis and in Drosophila flies in vivo. Together, these data highlight the importance of glucose metabolism to support insulin action, providing a complementary regulatory mechanism to signal transduction to stimulate adipose anabolism.
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Sanchez-Alvarez, Miguel, Qifeng Zhang, Fabian Finger, Michael J. O. Wakelam, and Chris Bakal. "Cell cycle progression is an essential regulatory component of phospholipid metabolism and membrane homeostasis." Open Biology 5, no. 9 (September 2015): 150093. http://dx.doi.org/10.1098/rsob.150093.
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We show that phospholipid anabolism does not occur uniformly during the metazoan cell cycle. Transition to S-phase is required for optimal mobilization of lipid precursors, synthesis of specific phospholipid species and endoplasmic reticulum (ER) homeostasis. Average changes observed in whole-cell phospholipid composition, and total ER lipid content, upon stimulation of cell growth can be explained by the cell cycle distribution of the population. TORC1 promotes phospholipid anabolism by slowing S/G2 progression. The cell cycle stage-specific nature of lipid biogenesis is dependent on p53. We propose that coupling lipid metabolism to cell cycle progression is a means by which cells have evolved to coordinate proliferation with cell and organelle growth.
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Bensinger, Steven, Yoko Kidani, M. Benjamin Hock, Joseph Argus, Evangelia Komisopoulou, and Thomas Graeber. "An essential role for SREBP signaling in T cell blastogenesis (47.17)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 47.17. http://dx.doi.org/10.4049/jimmunol.188.supp.47.17.
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Abstract Accumulating evidence indicates that cellular metabolism is an important regulator of T cell immunity. We and others have shown that activation of T cell rapidly initiates a robust genetic and biochemical program that drives the biosynthesis of lipids. Surprisingly, inhibiting lipid synthesis markedly decreases DNA synthesis and lymphocyte proliferation, suggesting a fundamental link between lipid anabolism and cell cycle progression. To date, the molecular mechanisms underlying these intriguing observations are largely undefined. The Sterol Regulatory Element Binding Proteins (SREBP) are b-HLH transcription factors with a well-placed role in lipid homeostasis. The impact of SREBPs on T cell development and function has not been evaluated. Herein we demonstrate an essential role for SREBPs in CD8 T cell blastogenesis. Gene expression and ChIP studies coupled with metabolic flux analysis revealed an essential role for SREBP signaling in the acquisition of a lipid anabolic program by blasting T cells. In the absence of SREBP activity, mitogen-stimulated T cells do not efficiently enlarge and arrest in G0/G1 of cell cycle before undergoing apoptosis-independent cell death. Homeostatic proliferation and antigen-specific viral immunity is also compromised in the absence of SREBP activity. Taken together, these data delineate a critical role for SREBPs in T cell growth and provide a mechanistic understanding of how SREBPs regulate the acquisition of anabolic metabolism in T cells.
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Wang, Shuang, Rasool Kamal, Yue Zhang, Renhui Zhou, Liting Lv, Qitian Huang, Siriguleng Qian, Sufang Zhang, and Zongbao Kent Zhao. "Expression of VHb Improved Lipid Production in Rhodosporidium toruloides." Energies 13, no. 17 (August 27, 2020): 4446. http://dx.doi.org/10.3390/en13174446.
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The oleaginous yeast Rhodosporidium toruloides has emerged as a robust host for production of microbial lipids as alternative biofuel feedstocks. Oxygen supply is a limiting factor for microbial lipid production, as lipid biosynthesis is highly oxygen-demanding. Vitreoscilla hemoglobin (VHb) is a protein capable of promoting oxygen delivery for anabolism. In this study, we developed R. toruloides with VHb expression for improved lipid production. The VHb expression cassette was integrated into the R. toruloides chromosome via the Agrobacterium-mediated transformation. In shake flask cultures, the engineered strain 4#-13 produced 34% more lipids than the parental strain did. Results obtained under reduced aeration conditions in 3 L bioreactor showed that lipid titer and lipid yield of the engineered strain 4#-13 were 116% and 71%, respectively, higher than those of the parental strain. Under high cell density culture conditions, the engineered strain 4#-13 grew faster and produced 72% more lipids. Our results demonstrated that the VHb gene is functional in R. toruloides for promoting lipid production. The strains described here may be further engineered by integrating extra genetic parts to attain robust producers for more valuable products. This should improve the economics of microbial lipids to facilitate a sustainable production of biodiesel and other lipid-based biofuels.
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De Oliveira, Matheus Pinto, and Marc Liesa. "The Role of Mitochondrial Fat Oxidation in Cancer Cell Proliferation and Survival." Cells 9, no. 12 (December 4, 2020): 2600. http://dx.doi.org/10.3390/cells9122600.
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Tumors remodel their metabolism to support anabolic processes needed for replication, as well as to survive nutrient scarcity and oxidative stress imposed by their changing environment. In most healthy tissues, the shift from anabolism to catabolism results in decreased glycolysis and elevated fatty acid oxidation (FAO). This change in the nutrient selected for oxidation is regulated by the glucose-fatty acid cycle, also known as the Randle cycle. Briefly, this cycle consists of a decrease in glycolysis caused by increased mitochondrial FAO in muscle as a result of elevated extracellular fatty acid availability. Closing the cycle, increased glycolysis in response to elevated extracellular glucose availability causes a decrease in mitochondrial FAO. This competition between glycolysis and FAO and its relationship with anabolism and catabolism is conserved in some cancers. Accordingly, decreasing glycolysis to lactate, even by diverting pyruvate to mitochondria, can stop proliferation. Moreover, colorectal cancer cells can effectively shift to FAO to survive both glucose restriction and increases in oxidative stress at the expense of decreasing anabolism. However, a subset of B-cell lymphomas and other cancers require a concurrent increase in mitochondrial FAO and glycolysis to support anabolism and proliferation, thus escaping the competing nature of the Randle cycle. How mitochondria are remodeled in these FAO-dependent lymphomas to preferably oxidize fat, while concurrently sustaining high glycolysis and increasing de novo fatty acid synthesis is unclear. Here, we review studies focusing on the role of mitochondrial FAO and mitochondrial-driven lipid synthesis in cancer proliferation and survival, specifically in colorectal cancer and lymphomas. We conclude that a specific metabolic liability of these FAO-dependent cancers could be a unique remodeling of mitochondrial function that licenses elevated FAO concurrent to high glycolysis and fatty acid synthesis. In addition, blocking this mitochondrial remodeling could selectively stop growth of tumors that shifted to mitochondrial FAO to survive oxidative stress and nutrient scarcity.
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Song, Rui, Mengxiao Hu, Xiyu Qin, Lili Qiu, Pengjie Wang, Xiaoxu Zhang, Rong Liu, and Xiaoyu Wang. "The Roles of Lipid Metabolism in the Pathogenesis of Chronic Diseases in the Elderly." Nutrients 15, no. 15 (August 3, 2023): 3433. http://dx.doi.org/10.3390/nu15153433.
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Lipid metabolism plays crucial roles in cellular processes such as hormone synthesis, energy production, and fat storage. Older adults are at risk of the dysregulation of lipid metabolism, which is associated with progressive declines in the physiological function of various organs. With advancing age, digestion and absorption commonly change, thereby resulting in decreased nutrient uptake. However, in the elderly population, the accumulation of excess fat becomes more pronounced due to a decline in the body’s capacity to utilize lipids effectively. This is characterized by enhanced adipocyte synthesis and reduced breakdown, along with diminished peripheral tissue utilization capacity. Excessive lipid accumulation in the body, which manifests as hyperlipidemia and accumulated visceral fat, is linked to several chronic lipid-related diseases, including cardiovascular disease, type 2 diabetes, obesity, and nonalcoholic fatty liver disease. This review provides a summary of the altered lipid metabolism during aging, including lipid digestion, absorption, anabolism, and catabolism, as well as their associations with age-related chronic diseases, which aids in developing nutritional interventions for older adults to prevent or alleviate age-related chronic diseases.
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Stuani, Lucille, Fabien Riols, Pierre Millard, Marie Sabatier, Aurélie Batut, Estelle Saland, Fanny Viars, et al. "Stable Isotope Labeling Highlights Enhanced Fatty Acid and Lipid Metabolism in Human Acute Myeloid Leukemia." International Journal of Molecular Sciences 19, no. 11 (October 25, 2018): 3325. http://dx.doi.org/10.3390/ijms19113325.
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Background: In Acute Myeloid Leukemia (AML), a complete response to chemotherapy is usually obtained after conventional chemotherapy but overall patient survival is poor due to highly frequent relapses. As opposed to chronic myeloid leukemia, B lymphoma or multiple myeloma, AML is one of the rare malignant hemopathies the therapy of which has not significantly improved during the past 30 years despite intense research efforts. One promising approach is to determine metabolic dependencies in AML cells. Moreover, two key metabolic enzymes, isocitrate dehydrogenases (IDH1/2), are mutated in more than 15% of AML patient, reinforcing the interest in studying metabolic reprogramming, in particular in this subgroup of patients. Methods: Using a multi-omics approach combining proteomics, lipidomics, and isotopic profiling of [U-13C] glucose and [U-13C] glutamine cultures with more classical biochemical analyses, we studied the impact of the IDH1 R132H mutation in AML cells on lipid biosynthesis. Results: Global proteomic and lipidomic approaches showed a dysregulation of lipid metabolism, especially an increase of phosphatidylinositol, sphingolipids (especially few species of ceramide, sphingosine, and sphinganine), free cholesterol and monounsaturated fatty acids in IDH1 mutant cells. Isotopic profiling of fatty acids revealed that higher lipid anabolism in IDH1 mutant cells corroborated with an increase in lipogenesis fluxes. Conclusions: This integrative approach was efficient to gain insight into metabolism and dynamics of lipid species in leukemic cells. Therefore, we have determined that lipid anabolism is strongly reprogrammed in IDH1 mutant AML cells with a crucial dysregulation of fatty acid metabolism and fluxes, both being mediated by 2-HG (2-Hydroxyglutarate) production.
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MacKinnon, Barbara M., and D. L. Lee. "Age-related changes in Heligmosomoides polygyrus (Nematoda): neutral lipid content in developing oocytes." Canadian Journal of Zoology 66, no. 12 (December 1, 1988): 2791–96. http://dx.doi.org/10.1139/z88-407.
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Changes in neutral lipid content of developing female gametes in Heligmosomoides polygyrus at 8, 12, 20, 40, 80, and 140 days postinfection (p.i.) were investigated and correlated with egg production by the worms over the same period. Egg production increased to day 20 p.i. when the average egg output for one female reached approximately 700 eggs/day. A decline in egg production occurred from 80 days p.i. until the end of the experiment (140 days p.i.). Neutral lipid content was low in oogonia from worms of all ages. Developing oocytes contained the highest levels of neutral lipid. There was a significant loss of lipid just before fertilization of the oocytes. An increase in lipid occurred in all developmental stages of gametes from day 8 to day 40 p.i., and a significant decline occurred thereafter to day 140 p.i. Although egg production and lipid content of the female reproductive tract showed similar trends, there was not a precise correlation. It is felt that nuclear and cytoplasmic processes other than lipid anabolism or catabolism within the developing gametes play a more important role in influencing egg output.
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Liu, L., Y. Yang, F. Yang, Y. Lin, K. Liu, X. Wang, and Y. Zhang. "A mechanistic investigation about hepatoxic effects of borneol using zebrafish." Human & Experimental Toxicology 42 (January 2, 2023): 096032712211490. http://dx.doi.org/10.1177/09603271221149011.
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Except for clinical value, borneol is routinely used in food and cosmetics with seldom safety evaluation. To investigate its hepatoxicity, we exposed 3 dpf (days post fertilization) larval zebrafish to borneol at a gradient of concentrations (200–500 μM) for 3 days. Herein, our results revealed that high doses of borneol (300–500 μM) caused liver size decrease or lateral lobe absence. Borneol also seriously disturbed the hepatic protein metabolism presented with the increased activity of alanine aminotransferase (ALT) and lipid metabolism shown with the increased level of triglycerides (TG) and total cholesterol (TC). The lipid accumulation (oil red staining) was detected as well. Additionally, significant upregulation of genes was detected that related to oxidative stress, lipid anabolism, endoplasmic reticulum stress (ERS), and autophagy. Conversely, the lipid metabolism-related genes were markedly downregulated. Moreover, the changes in the superoxide dismutase activity and the level of glutathione and malondialdehyde raised the likelihood of lipid peroxidation. The outcomes indicated the involvement of oxidative stress, ERS, lipid metabolism, and autophagy in borneol-induced lipid metabolic disorder and hepatic injury. This study will provide a more comprehensive understanding of borneol hepatoxicity and the theoretical basis for the safe use of this compound.
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Altumairah, Mohammed A. H., and Ravindra P. Choudhary. "Overview on Diabetes Mellitus." Journal of Medical and Health Studies 2, no. 2 (September 21, 2021): 63–69. http://dx.doi.org/10.32996/jmhs.2021.2.2.7.
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Diabetes mellitus is a group of diverse illnesses that often show hyperglycemia and glucose intolerance via insulin shortage, insulin impairment or both (Sicree et al., 2006). These difficulties occur due to disruptions in regulation systems controlling the storage and movement of metabolic fuels, including carbohydrate, lipid and protein catabolism and anabolism, induced by poor insulin production, insulin activity or both (Shillitoe, 1988; Votey and Peters, 2004). With more than 62 million diabetics already diagnosed in India, the situation of a potential pandemic is approaching fast.
Dissertations / Theses on the topic "Lipid anabolism"
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Liang, Chao. "Aptamer-functionalized lipid nanoparticles targeting osteoblasts as a novel RNA Interference-based bone anabolic strategy." HKBU Institutional Repository, 2016. https://repository.hkbu.edu.hk/etd_oa/325.
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Osteoporosis remain major clinical challenges. RNA interference (RNAi) provides a promising approach for promoting osteoblastic bone formation to settle the challenges. However, the major bottleneck for translating RNAi with efficacy and safety to clinical bone anabolic strategy is lack of osteoblast-specific delivery systems for osteogenic siRNAs. Previously, we developed a targeting system involving DOTAP-based cationic liposomes attached to oligopeptides (AspSerSer)6, (also known as (DSS)6), which had good affinity for bone formation surface. Using this system, osteogenic Pleckstrin Homology Domain Containing, Family O Member 1 (Plekho1) siRNA could be specifically delivered to bone formation surface at tissue level and promoted bone formation in osteopenic rodents. However, concerns still exist regarding indirect osteoblast-specific delivery, detrimental retention in hepatocytes, mononuclear phagocyte system (MPS)-induced dose reduction and inefficient nanoparticle extravasation. Aptamers, selected by cell-based Systematic evolution of ligands by exponential enrichment (cell-SELEX), are single-stranded DNA (ssDNA) or RNA which binds to target cells specifically by distinct tertiary structures. By performing positive selection with osteoblasts and negative selection with hepatocytes and peripheral blood mononuclear cells (PBMCs), we aimed to screen an aptamer that could achieve direct osteoblast-specific delivery and minimal hepatocyte and PBMCs accumulation of Plekho1 siRNAs. In addition, lipid nanoparticles (LNPs) have been widely used as nanomaterials encapsulating siRNA due to their small particle size below 90 nm. Polyethylene glycol¡(PEG) as the mostly used hydrophilic polymer, could efficiently prevent LNPs from MPS uptake. So, LNPs with PEG shielding could serve as siRNA carriers to realize efficient extravasation from fenestrated capillaries to osteoblasts and help reduce MPS uptake of the siRNAs. Recently, we screened an aptamer (CH6) by cell-SELEX specifically targeting both rat and human osteoblasts and developed the aptamer-functionalized LNPs encapsulating osteogenic Plekho1 siRNA, i.e., CH6-LNPs-siRNA. Our results demonstrated that CH6-LNPs-siRNA had an average particle size below 90 nm and no significant cytotoxicity in vitro. CH6 aptamer facilitated osteoblast-selective uptake of Plekho1 siRNA and gene silencing in vitro. In this study, we further found that CH6 aptamer facilitated the bone-specific distribution of siRNA by biophotonic imaging and quantitative analysis. Immunohistochemistry results showed that CH6 achieved in vivo osteoblast-specific delivery of Plekho1 siRNA. Dose-response experiment indicated that CH6-LNPs-siRNA achieved almost 80% gene knockdown at the siRNA dose of 1.0 mg/kg and maintained 12 days for over 50% gene silencing. microCT, bone histomorphometry and mechanical testing confirmed that CH6 facilitated bone formation, leading to improved bone micro-architecture, increased bone mass and enhanced mechanical properties in osteoporotic rodents. Furthermore, CH6-LNPs-siRNA achieved better bone anabolic action when compared to the previously developed (AspSerSer)6-liposome-siRNA. There was no obvious toxicity in rats injected with CH6-LNPs-siRNA. All these results indicated that osteoblast-specific aptamer-functionalized LNPs could act as a novel RNAi-based bone anabolic strategy and advance selectivity of targeted delivery for osteogenic siRNAs from tissue level toward cellular level. In addition, the generation of ssDNA from double-stranded PCR products is an essential step in selection of aptamers in SELEX. We found that the size separation derived from unequal primers with chemical modification could be a satisfactory alternative to the classic magnetic separation.
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Sander, Simone [Verfasser], and Britta [Akademischer Betreuer] Brügger. "Relevance of ACSL3-mediated ACS activity and ACSL3 localization in anabolic and catabolic lipid droplet metabolism / Simone Sander ; Betreuer: Britta Brügger." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1177695626/34.
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Martins, Danieli Brolo. "SISTEMA COLINÉRGICO E PEROXIDAÇÃO LIPÍDICA DE RATOS TRATADOS COM SULFATO DE VINCRISTINA E DECANOATO DE NANDROLONA." Universidade Federal de Santa Maria, 2008. http://repositorio.ufsm.br/handle/1/10011.
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Coordenação de Aperfeiçoamento de Pessoal de Nível SuperiorVincristine sulphate is antitumor agent widely used in small animal clinical oncology; therefore it can cause a number of adverse effects including marrow and neuronal cytotoxicity. Nandrolone decanoate, an anabolic-androgenic steroid (AAS), has been used in association with vincristine in order to ease effects such as moderate myelosuppression. The present dissertation presents data related to the isolated or associated employment of vincristine sulphate and nandrolone decanoate, as well as their effects on the cholinergic system and oxidative profile of Wistar rats. The animals were submitted to four different doses of AAS for three weeks and its action on acetylcholinesterase (AChE) activity in four different structures of brain tissue (cerebellum, hippocampus, striatum and cerebral cortex) was studied. The second experiment shows the effects of vincristine and/or nandrolone decanoate in the brain (same parts studied previously) and blood through measurement of brain and red blood cell AChE (RBC-AChE) enzyme activity as well as brain and blood serum lipid peroxidation of rats treated for two weeks. Results show that the two highest doses used in the first experiment increased enzyme activity, suggesting interference in the cholinergical system of the striatum and cerebellum. The results obtained in the latter experiment demonstrate that the isolated use of this AAS and its association with vincristine sulphate altered brain and RBC-AChE action, both in a stimulatory and inhibitory fashion. Lipid peroxidation, in the brain and blood, increased due to the isolated use of both vincristine and nandrolone decanoate, as well as to their associated use at the highest dose of ester used. Furthermore, the data show that the association between the therapeutic dose of nandrolone decanoate and vincristine is capable of neutralizing the free radical production induced by their isolated use in brain and blood serum. Serum RBC-AChE activity and the oxidative profile presented in this study are similar to those exhibited for brain tissue. Based on these data, it can be concluded that nandrolone decanoate is capable of interfering in AChE activity, affecting the cholinergic system, which could cause an alteration of its neurotransmitter, as well as a low or high stimulation of post-synaptic receptors. Therefore, the use of the therapeutic dose of AAS studied here in association with vincristine has been shown to be beneficial, as it could protect the organism from damaging processes caused by the production of free radicals.
O sulfato de vincristina é um agente anti-tumoral bastante usado na oncologia clínica de pequenos animais, porém seus efeitos colaterais incluem citotoxicidade medular e neuronal. O decanoato de nandrolona, um esteróide anabólico androgênico (EAA), tem sido usado em associação a este medicamento para amenizar alguns de seus efeitos, como a mielossupressão moderada. Esta dissertação apresenta dados referentes ao uso isolado ou associado do sulfato de vincristina e do decanoato de nandrolona, seus efeitos no sistema colinérgico e no perfil oxidativo de ratos Wistar. Primeiramente, verificou-se quatro diferentes doses do EAA, por três semanas, e sua ação sobre a atividade da acetilcolinesterase (AChE) em quatro partes do tecido cerebral (cerebelo, estriado, hipocampo e córtex cerebral). O segundo experimento apresenta grupos tratados durante duas semanas com sulfato de vincristina e/ou decanoato de nandrolona e as ações destes no cérebro (mesmas partes pesquisadas anteriormente) e no sangue, através da mensuração da atividade enzimática da AChE cerebral e eritrocitária (RBC-AChE) e peroxidação lipídica cerebral e sérica. As duas doses mais altas utilizadas no primeiro trabalho aumentam a atividade da enzima, sugerindo que haja interferência no sistema colinérgico, no estriado e no cerebelo. Os resultados obtidos, no estudo posterior, demonstram que o uso isolado deste EAA e suas associações com o sulfato de vincristina alteram a ação da AChE cerebral e RBC-AChE, tanto de forma estimulatória quanto inibitória. A peroxidação lipídica, cerebral e sangüínea, aumenta devido ao uso isolado da vincristina e do decanoato de nandrolona, e na associação do quimioterápico com a dose mais alta usada do éster. A dose terapêutica do decanoato de nandrolona e a vincristina utilizadas são capazes de neutralizar a produção de radicais livres tanto no cérebro quanto no soro sangüíneo. A atividade da RBC-AChE e o valor do perfil oxidativo do soro apresentados nesta pesquisa são similares àqueles exibidos pelo tecido cerebral. Diante destes dados, pode-se concluir que o decanoato de nandrolona é capaz de influenciar a atividade da AChE, afetando o sistema colinérgico, o que poderia ocasionar em uma ação alterada do seu neurotransmissor, além de uma baixa ou alta estimulação dos receptores póssinápticos. Entretanto, o uso da dose terapêutica estudada deste EAA associada à vincristina mostra-se benéfico, pois poderia proteger o organismo de processos prejudiciais relacionados a produção de radicais livres.
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Shee, Somnath. "Manipulating Bacterial and Host Reactive Oxygen Species (ROS)- based mechanisms to potentiate killing of Mycobacterium tuberculosis (Mtb)." Thesis, 2021. https://etd.iisc.ac.in/handle/2005/5680.
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Mycobacterium tuberculosis (Mtb) is evolutionarily equipped to resist exogenous reactive oxygen species but shows vulnerability to an increase in endogenous ROS (eROS). Since eROS is an unavoidable consequence of aerobic metabolism, understanding how eROS levels are controlled is essential yet remains uncharacterized. By combining the Mrx1-roGFP2 redox biosensor with transposon mutagenesis, we identified 368 genes (redoxosome) responsible for maintaining non-toxic levels of eROS in Mtb. Integrating redoxosome with a global network of protein-protein interactions and transcriptional regulators revealed a hypothetical protein (rv0158) as a top node managing eROS and redox homeostasis in Mtb. RNA sequencing, seahorse XF flux measurements, and lipid analysis indicate that rv0158 is required to balance the deployment of fatty acid substrates between lipid anabolism and oxidation. Disruption of rv0158 perturbed redox balance in a carbon-source-specific manner, promoted killing in response to anti-TB drugs, reduced survival in macrophages, and lowered persistence in mice.
We describe a novel pathogen response to moxifloxacin. Mtb, unlike Escherichia coli, decreases respiration in response to moxifloxacin. Nevertheless, cells were killed, as ROS increased due to NADH-dependent reductive stress. Moxifloxacin lethality was mitigated by supplementing bacterial cultures with a ROS scavenger (thiourea), and an iron chelator (bipyridyl), indicating ROS is part and not a consequence of death processes. Treatment with N-acetyl cysteine (NAC) accelerated respiration and ROS production, increased moxifloxacin lethality, and lowered the mutant prevention concentration. Thus, redox and bioenergetic imbalance contribute to the moxifloxacin-mediated killing of Mtb. These results provide a way to make fluoroquinolones more effective anti-tuberculosis agents.
We have previously reported that Mtb H37Rv sets up a gradient of mycothiol redox potential: EMSH-oxidized (-240 mV) to EMSH-reduced (-320 mV) inside macrophages, where the EMSH -reduced Mtb subpopulation are significantly more tolerant to anti-TB drugs. Therefore, one of the keys to subverting drug-tolerance is to impede the emergence of EMSH -reduced subpopulation by inducing overwhelming oxidative stress. In this study, we exposed THP1-macrophages infected with Mtb H37Rv expressing Mrx1-roGFP2-biosensor, to a library of FDA-approved drugs (Enzo Life Sciences; BML-2842) and scored for the oxidative shift in the Mtb- EMSH at 24 hours post infection. Based on their activity to trigger oxidative stress inside the bacterium, non-cytotoxicity to host, and inhibition of bacterial growth inside macrophages, C5 molecule emerged as the top hit. Pre-treatment with C5 potentiated killing of Mtb by all tested antibiotics (isoniazid, rifampicin, and moxifloxacin) and reduced drug-tolerance.Welcome-DBT
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Smith, Kerry Ruth. "The effect of anabolic implant and dietary lipid source on intramusuclar lipid deposition in finished beef cattle." 2004. http://purl.galileo.usg.edu/uga%5Fetd/smith%5Fkerry%5Fr%5F200405%5Fphd.
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Long, Jared Woodrow. "Effects of supplemental lipid and anabolic growth implants on carcass characteristics, meat quality, and fatty acid composition of finishing beef cattle." 2005. http://purl.galileo.usg.edu/uga%5Fetd/long%5Fjared%5Fw%5F200512%5Fms.
Full textBooks on the topic "Lipid anabolism"
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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0032.
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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_001.
Full textAbstract:
Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_002.
Full textAbstract:
Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
Book chapters on the topic "Lipid anabolism"
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Saito, Mariko, and Abraham Rosenberg. "Regulation of Glycosphingolipid Anabolism in Fibroblasts by Ionophores, Plasma Membrane ATP-ase Inhibition, and Growth Factors." In Enzymes of Lipid Metabolism II, 591–95. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5212-9_73.
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Lackner, K. J., W. März, G. Wolter, H. Sartor, and W. Gross. "Anabolic Steroids do not Change mRNA Levels and Protein Secretion of Apolipoprotein A-I and B-100 in HepG2 Cells." In Recent Developments in Lipid and Lipoprotein Research, 151–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84855-1_18.
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Sasako, Takayoshi, and Kohjiro Ueki. "ER Stress Response Failure and Steatohepatitis Comorbid with Diabetes." In Psychology and Patho-physiological Outcomes of Eating [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100054.
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Dynamic metabolic changes occur in the liver during the transition between fasting and eating, which is mainly mediated by insulin, a hormone to promote anabolism and suppress catabolism. In obesity and diabetes, insulin resistance is induced via various mechanisms, and among them is endoplasmic reticulum (ER) stress. We recently reported that eating induces transient ER stress and consequent ER stress response in the liver. During eating, expression of Sdf2l1, an ER-resident molecule involved in ER stress-associated degradation, is induced as a part of ER stress response. XBP-1s regulates expression of Sdf2l1 at the transcription level, and Sdf2l1 terminates eating-induced ER stress in the liver, consequently regulating glucose and lipid metabolism. In obesity and diabetes, however, ER stress response is impaired, partly because insulin-mediated translocation of XBP-1s to the nucleus is suppressed, which results in further excessive ER stress. Induction of Sdf2l1 by XBP-1s is highly down-regulated, but restoration of Sdf2l1 ameliorates glucose intolerance and fatty liver. In diabetic patients, hepatic insulin resistance induces enhanced ER stress and ER stress response failure in the liver, which in turn promote hepatic fibrosis and contribute to the development of steatohepatitis comorbid with diabetes.
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Clark, Gregory O., and William J. Kovacs. "Glucose, Lipid, and Protein Metabolism." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0018.
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The maintenance of life requires a constant supply of substrate for the generation of energy and preservation of the structure of cells and tissues. The process in principle is simple, yet the individual metabolic pathways and the regulation of substrate fluxes through these pathways can be complex. Energy is derived when fuel substrates are oxidized to carbon dioxide and water in the presence of oxygen, generating adenosine triphosphate (ATP). A portion of the ingested foodstuff is also utilized, either directly or after transformation into other substrates, to repair and replace cell membranes, structural proteins, and organelles. The remainder is stored as potential energy in the form of glycogen or fat. Under normal circumstances, each individual remains in a near-steady state where weight and appearance are stable over prolonged periods. In the short term, fuel metabolism changes dramatically several times a day during alternating periods of feeding and fasting. An anabolic phase begins with food ingestion and lasts for several hours. Energy storage occurs during this period when caloric intake exceeds caloric demands. The catabolic phase usually begins 4 to 6 hours after a meal and lasts until the person eats once again. During this phase, utilization shifts from exogenous to endogenous fuels, a change heralded by the mobilization of substrate stored in liver, muscle, and adipose tissue. Both anabolic and catabolic phases are characterized by specific biochemical processes regulated by distinct hormonal profiles. In the anabolic phase that follows ingestion of a mixed meal, substrate flux is directed from the intestine through the liver to storage and utilization sites. Glucose, triglyceride, and amino acid concentrations increase in plasma, whereas those of fatty acids, ketones (acetoacetic and β -hydroxy-butyric acids), and glycerol decrease. Both glycogen and protein synthesis begin in liver and muscle, while fatty acid synthesis and triglyceride esterification are stimulated in hepatocytes and adipose tissue. In the catabolic phase, the biochemical activities are reversed and the flux of fuel is directed from storage depots to liver and other utilization sites.
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Infante, Marco. "The Insulin Journey in the Human Body." In Evolving Concepts in Insulin Resistance [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.107906.
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Insulin represents the paramount anabolic hormone and the master regulator of glucose, lipid, and protein metabolism. This chapter describes the sequential stages of the physiologic journey of insulin in the human body, from its synthesis/secretion to its action in peripheral tissues and, ultimately, to its clearance and degradation. These stages include i) insulin synthesis and release from pancreatic beta cells; ii) insulin first-pass metabolism and partial clearance in the liver; iii) insulin action on the vasculature and exit from the capillary beds; iv) insulin action in peripheral and central target tissues (skeletal muscle, adipose tissue, liver, and central nervous system); and v) final insulin degradation in the kidney. Each of these stages is regulated by complex intracellular mechanisms that take place in different tissues and allow for the anabolic actions of insulin. Understanding the abovementioned stages is pivotal to comprehending the clinical consequences of impaired insulin secretion and action, as defects in one or more of these stages can be associated with the development of insulin resistance, metabolic syndrome, and type 2 diabetes mellitus. Additionally, a thorough knowledge of the insulin bodily journey can assist clinicians in therapeutic decision-making for diabetic patients on exogenous insulin therapy in different clinical settings.
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"Metabolic Logic through the Lens of Coenzyme Forms of Human Vitamins." In The Chemical Biology of Human Vitamins, 40–70. The Royal Society of Chemistry, 2018. http://dx.doi.org/10.1039/bk9781788014649-00040.
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The controlled flux of small molecules in cells constitutes metabolism. The catabolic/degradative arm oxidizes molecules such as glucose, amino acids and fatty acids to CO2, while the electrons removed are stored in chemically useful molecules such as the coenzyme forms of vitamins B2 and B3. The anabolic/biosynthetic arms of metabolism, utilize ATP, NADH (coenzyme form of B3) and acyl-CoAs (coenzyme form of vitamin B5) to power biosynthesis of proteins, nucleic acids, polysaccharides, steroids and membrane lipids. Each vitamin has unique chemical reactivity that enables one or more central transformations at nodal points in small molecule metabolism, including glycolysis, the tricarboxylate cycle, amino acid metabolism and one-carbon metabolism in purine and pyrimidine biosynthesis.
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Casaer, Michael P., and Greet Van den Berghe. "Nutrition support in acute cardiac care." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 360–72. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0030.
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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Full enteral feeding in vasopressor dependent patients recovering from hemodynamic shock increases the risk for bowel ischemia. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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"Cellular metabolism." In Oxford Assess and Progress: Medical Sciences, edited by Jade Chow, John Patterson, Kathy Boursicot, and David Sales. Oxford University Press, 2012. http://dx.doi.org/10.1093/oso/9780199605071.003.0014.
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Cellular metabolism is divided into catabolism — responsible for converting nutrients into the energy sources and smaller molecules required for the chemical reactions of the body — and anabolism, which is the interconversion and synthesis of the molecules that maintain the body’s structure and function. This chapter examines the control of metabolism and the central metabolic pathways. Such control includes compartmentalization of metabolic processes and the cooperation between the metabolic activities of different organs. Metabolic control is important because metabolism must match the availability of nutrients to the demand for the products of the metabolic processes and both will vary over time. The synthesis of adenosine triphosphate (ATP), with its high-energy phosphate bond, lies at the heart of these central metabolic pathways. Most of the ATP is produced by oxidative phosphorylation in the mitochondria, but glycolysis and the tricarboxylic acid cycle (also known as the citric acid cycle or Krebs cycle) provide additional amounts. Of the nutrients entering the body from the diet, fat, glucose, and amino acids are the main fuels for cellular metabolism. The utilization of lipids, fatty acids, and ketone bodies is important in metabolism in addition to the key role played by glucose. Glucose is the fuel for energy production in glycolysis. It is also manufactured by gluconeogenesis and stored as glycogen by glycogenesis. It is important to know how different organs utilize different fuels and how energy production alters between the fed state and starvation. Amino-acid metabolism and coenzymes in amino acid oxidation are also important although some details, including the urea cycle, have not been covered here. Energy balance and the relationship between food intake and energy expenditure lead to the concept of body mass index (BMI). The BMI offers a quick method of quantifying the nutritional status of a person, and BMI values may be helpful in assessing the risk of, for example, obesity-related diseases such as type II diabetes and coronary heart disease. Cellular metabolism not only contributes to the medical sciences background to clinical reasoning, but there are also a number of identifiable, inborn errors of metabolism. While individually rare (with incidences of approx. 1–25 per 100,000 births), collectively they present a considerable number of new cases each year.
Reports on the topic "Lipid anabolism"
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Corscadden, Louise, and Anjali Singh. Metabolism And Measurable Metabolic Parameters. ConductScience, December 2022. http://dx.doi.org/10.55157/me20221213.
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Metabolism is the sum of chemical reactions involved in sustaining the life of organisms.[1] It constantly provides your body with the energy to perform essential functions. The process is categorized into two groups:[2] Catabolism: It’s the process of breaking down molecules to obtain energy. For example, converting glucose to pyruvate by cellular respiration. Anabolism: It’s the process of synthesis of compounds required to run the metabolic process of the organisms. For example, carbohydrates, proteins, lipids, and nucleic acids.[2] Metabolism is affected by a range of factors, such as age, sex, muscle mass, body size, and physical activity affect metabolism or BMR (the basal metabolic rate). By definition, BMR is the minimum amount of calories your body requires to function at rest.[2] Now, you have a rough idea about the concept. But, you might wonder why you need to study it. What and how metabolic parameters are measured to determine the metabolism of the organism? Find the answer to all these questions in this article.