Journal articles: 'Fatty acid metabolism'

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Harwood, J. L. "Fatty Acid Metabolism." Annual Review of Plant Physiology and Plant Molecular Biology 39, no. 1 (June 1988): 101–38. http://dx.doi.org/10.1146/annurev.pp.39.060188.000533.

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de las Fuentes, Lisa, Pilar Herrero, Linda R. Peterson, Daniel P. Kelly, Robert J. Gropler, and Víctor G. Dávila-Román. "Myocardial Fatty Acid Metabolism." Hypertension 41, no. 1 (January 2003): 83–87. http://dx.doi.org/10.1161/01.hyp.0000047668.48494.39.

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SPIECKERMANN, P., J. HUTTER, and C. ALVES. "Myocardial fatty acid metabolism." Journal of Molecular and Cellular Cardiology 18 (1986): 68. http://dx.doi.org/10.1016/s0022-2828(86)80233-4.

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Yamamoto, Tsunehisa, and Motoaki Sano. "Deranged Myocardial Fatty Acid Metabolism in Heart Failure." International Journal of Molecular Sciences 23, no. 2 (January 17, 2022): 996. http://dx.doi.org/10.3390/ijms23020996.

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The heart requires fatty acids to maintain its activity. Various mechanisms regulate myocardial fatty acid metabolism, such as energy production using fatty acids as fuel, for which it is known that coordinated control of fatty acid uptake, β-oxidation, and mitochondrial oxidative phosphorylation steps are important for efficient adenosine triphosphate (ATP) production without unwanted side effects. The fatty acids taken up by cardiomyocytes are not only used as substrates for energy production but also for the synthesis of triglycerides and the replacement reaction of fatty acid chains in cell membrane phospholipids. Alterations in fatty acid metabolism affect the structure and function of the heart. Recently, breakthrough studies have focused on the key transcription factors that regulate fatty acid metabolism in cardiomyocytes and the signaling systems that modify their functions. In this article, we reviewed the latest research on the role of fatty acid metabolism in the pathogenesis of heart failure and provide an outlook on future challenges.

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Lopaschuk, Gary D., John R. Ussher, Clifford D. L. Folmes, Jagdip S. Jaswal, and William C. Stanley. "Myocardial Fatty Acid Metabolism in Health and Disease." Physiological Reviews 90, no. 1 (January 2010): 207–58. http://dx.doi.org/10.1152/physrev.00015.2009.

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There is a constant high demand for energy to sustain the continuous contractile activity of the heart, which is met primarily by the β-oxidation of long-chain fatty acids. The control of fatty acid β-oxidation is complex and is aimed at ensuring that the supply and oxidation of the fatty acids is sufficient to meet the energy demands of the heart. The metabolism of fatty acids via β-oxidation is not regulated in isolation; rather, it occurs in response to alterations in contractile work, the presence of competing substrates (i.e., glucose, lactate, ketones, amino acids), changes in hormonal milieu, and limitations in oxygen supply. Alterations in fatty acid metabolism can contribute to cardiac pathology. For instance, the excessive uptake and β-oxidation of fatty acids in obesity and diabetes can compromise cardiac function. Furthermore, alterations in fatty acid β-oxidation both during and after ischemia and in the failing heart can also contribute to cardiac pathology. This paper reviews the regulation of myocardial fatty acid β-oxidation and how alterations in fatty acid β-oxidation can contribute to heart disease. The implications of inhibiting fatty acid β-oxidation as a potential novel therapeutic approach for the treatment of various forms of heart disease are also discussed.

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Koundouros, Nikos, and George Poulogiannis. "Reprogramming of fatty acid metabolism in cancer." British Journal of Cancer 122, no. 1 (December 10, 2019): 4–22. http://dx.doi.org/10.1038/s41416-019-0650-z.

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AbstractA common feature of cancer cells is their ability to rewire their metabolism to sustain the production of ATP and macromolecules needed for cell growth, division and survival. In particular, the importance of altered fatty acid metabolism in cancer has received renewed interest as, aside their principal role as structural components of the membrane matrix, they are important secondary messengers, and can also serve as fuel sources for energy production. In this review, we will examine the mechanisms through which cancer cells rewire their fatty acid metabolism with a focus on four main areas of research. (1) The role of de novo synthesis and exogenous uptake in the cellular pool of fatty acids. (2) The mechanisms through which molecular heterogeneity and oncogenic signal transduction pathways, such as PI3K–AKT–mTOR signalling, regulate fatty acid metabolism. (3) The role of fatty acids as essential mediators of cancer progression and metastasis, through remodelling of the tumour microenvironment. (4) Therapeutic strategies and considerations for successfully targeting fatty acid metabolism in cancer. Further research focusing on the complex interplay between oncogenic signalling and dysregulated fatty acid metabolism holds great promise to uncover novel metabolic vulnerabilities and improve the efficacy of targeted therapies.

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Strandberg, Ursula, Jussi Vesterinen, Timo Ilo, Jarkko Akkanen, Miina Melanen, and Paula Kankaala. "Fatty acid metabolism and modifications in Chironomus riparius." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1804 (June 15, 2020): 20190643. http://dx.doi.org/10.1098/rstb.2019.0643.

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A priori knowledge of fatty acid modifications in consumers is essential for studies using fatty acids as biomarkers. We investigated fatty acid metabolism and possible modification pathways in benthic invertebrate Chironomus riparius larvae (Diptera). We conducted diet manipulation experiments using natural food sources (two chlorophyte algae, a diatom and a non-toxic cyanobacterium). We also did a diet-switch experiment on two different resources, fish food flakes TetraMin ® and cyanobacterium Spirulina , to study fatty acid turnover in Chironomus . Results of the diet manipulation experiments indicate that Chironomus larvae have a strong tendency to biosynthesize 20:5n-3 and 20:4n-6 from precursor fatty acids, and that the dietary availability of polyunsaturated fatty acids (PUFA) does not control larval growth. Fatty acid modifications explain why low dietary availability of PUFA did not significantly limit growth. This has ecologically relevant implications on the role of benthic chironomids in conveying energy to upper trophic level consumers. A diet-switch experiment showed that the turnover rate of fatty acids in Chironomus is relatively fast––a few days. The compositional differences of algal diets were large enough to separate Chironomus larvae into distinct groups even if significant modification of PUFA was observed. In summary, fatty acids are excellent dietary biomarkers for Chironomus , if modifications of PUFA are considered, and will provide high-resolution data on resource use. This article is part of the theme issue ‘The next horizons for lipids as ‘trophic biomarkers': evidence and significance of consumer modification of dietary fatty acids'.

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Yoon, Hyunho, and Sanghoon Lee. "Fatty Acid Metabolism in Ovarian Cancer: Therapeutic Implications." International Journal of Molecular Sciences 23, no. 4 (February 16, 2022): 2170. http://dx.doi.org/10.3390/ijms23042170.

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Ovarian cancer is the most malignant gynecological tumor. Previous studies have reported that metabolic alterations resulting from deregulated lipid metabolism promote ovarian cancer aggressiveness. Lipid metabolism involves the oxidation of fatty acids, which leads to energy generation or new lipid metabolite synthesis. The upregulation of fatty acid synthesis and related signaling promote tumor cell proliferation and migration, and, consequently, lead to poor prognosis. Fatty acid-mediated lipid metabolism in the tumor microenvironment (TME) modulates tumor cell immunity by regulating immune cells, including T cells, B cells, macrophages, and natural killer cells, which play essential roles in ovarian cancer cell survival. Here, the types and sources of fatty acids and their interactions with the TME of ovarian cancer have been reviewed. Additionally, this review focuses on the role of fatty acid metabolism in tumor immunity and suggests that fatty acid and related lipid metabolic pathways are potential therapeutic targets for ovarian cancer.

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Xu, Huan, Yanbo Chen, Meng Gu, Chong Liu, Qi Chen, Ming Zhan, and Zhong Wang. "Fatty Acid Metabolism Reprogramming in Advanced Prostate Cancer." Metabolites 11, no. 11 (November 9, 2021): 765. http://dx.doi.org/10.3390/metabo11110765.

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Prostate cancer (PCa) is a carcinoma in which fatty acids are abundant. Fatty acid metabolism is rewired during PCa development. Although PCa can be treated with hormone therapy, after prolonged treatment, castration-resistant prostate cancer can develop and can lead to increased mortality. Changes to fatty acid metabolism occur systemically and locally in prostate cancer patients, and understanding these changes may lead to individualized treatments, especially in advanced, castration-resistant prostate cancers. The fatty acid metabolic changes are not merely reflective of oncogenic activity, but in many cases, these represent a critical factor in cancer initiation and development. In this review, we analyzed the literature regarding systemic changes to fatty acid metabolism in PCa patients and how these changes relate to obesity, diet, circulating metabolites, and peri-prostatic adipose tissue. We also analyzed cellular fatty acid metabolism in prostate cancer, including fatty acid uptake, de novo lipogenesis, fatty acid elongation, and oxidation. This review broadens our view of fatty acid switches in PCa and presents potential candidates for PCa treatment and diagnosis.

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Dikalov, Sergey, Alexander Panov, and Anna Dikalova. "Critical Role of Mitochondrial Fatty Acid Metabolism in Normal Cell Function and Pathological Conditions." International Journal of Molecular Sciences 25, no. 12 (June 12, 2024): 6498. http://dx.doi.org/10.3390/ijms25126498.

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Abstract: There is a “popular” belief that a fat-free diet is beneficial, supported by the scientific dogma indicating that high levels of fatty acids promote many pathological metabolic, cardiovascular, and neurodegenerative conditions. This dogma pressured scientists not to recognize the essential role of fatty acids in cellular metabolism and focus on the detrimental effects of fatty acids. In this work, we critically review several decades of studies and recent publications supporting the critical role of mitochondrial fatty acid metabolism in cellular homeostasis and many pathological conditions. Fatty acids are the primary fuel source and essential cell membrane building blocks from the origin of life. The essential cell membranes phospholipids were evolutionarily preserved from the earlier bacteria in human subjects. In the past century, the discovery of fatty acid metabolism was superseded by the epidemic growth of metabolic conditions and cardiovascular diseases. The association of fatty acids and pathological conditions is not due to their “harmful” effects but rather the result of impaired fatty acid metabolism and abnormal lifestyle. Mitochondrial dysfunction is linked to impaired metabolism and drives multiple pathological conditions. Despite metabolic flexibility, the loss of mitochondrial fatty acid oxidation cannot be fully compensated for by other sources of mitochondrial substrates, such as carbohydrates and amino acids, resulting in a pathogenic accumulation of long-chain fatty acids and a deficiency of medium-chain fatty acids. Despite popular belief, mitochondrial fatty acid oxidation is essential not only for energy-demanding organs such as the heart, skeletal muscle, and kidneys but also for metabolically “inactive” organs such as endothelial and epithelial cells. Recent studies indicate that the accumulation of long-chain fatty acids in specific organs and tissues support the impaired fatty acid oxidation in cell- and tissue-specific fashion. This work, therefore, provides a basis to challenge these established dogmas and articulate the need for a paradigm shift from the “pathogenic” role of fatty acids to the critical role of fatty acid oxidation. This is important to define the causative role of impaired mitochondrial fatty acid oxidation in specific pathological conditions and develop novel therapeutic approaches targeting mitochondrial fatty acid metabolism.

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Li, Xiaoting, and Xukun Bi. "Integrated Control of Fatty Acid Metabolism in Heart Failure." Metabolites 13, no. 5 (April 29, 2023): 615. http://dx.doi.org/10.3390/metabo13050615.

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Disrupted fatty acid metabolism is one of the most important metabolic features in heart failure. The heart obtains energy from fatty acids via oxidation. However, heart failure results in markedly decreased fatty acid oxidation and is accompanied by the accumulation of excess lipid moieties that lead to cardiac lipotoxicity. Herein, we summarized and discussed the current understanding of the integrated regulation of fatty acid metabolism (including fatty acid uptake, lipogenesis, lipolysis, and fatty acid oxidation) in the pathogenesis of heart failure. The functions of many enzymes and regulatory factors in fatty acid homeostasis were characterized. We reviewed their contributions to the development of heart failure and highlighted potential targets that may serve as promising new therapeutic strategies.

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Katafuchi, Takeshi, and Makoto Makishima. "Fatty Acid Metabolism during Exercise." Journal of Nihon University Medical Association 80, no. 1 (February 1, 2021): 15–19. http://dx.doi.org/10.4264/numa.80.1_15.

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SATO, Ryuichiro. "Fatty Acid Metabolism and SREBP." Oleoscience 1, no. 11 (2001): 1065–72. http://dx.doi.org/10.5650/oleoscience.1.1065.

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LONDON, BARRY. "Fatty Acid Metabolism and Arrhythmias." Journal of Cardiovascular Electrophysiology 15, no. 11 (November 2004): 1317–18. http://dx.doi.org/10.1046/j.1540-8167.2004.04576.x.

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Giovannini, M., C. Agostoni, G. Biasucci, A. Rottoli, D. Luotti, S. Trojan, and E. Riva. "Fatty acid metabolism in phenylketonuria." European Journal of Pediatrics 155, S1 (January 1996): S132—S135. http://dx.doi.org/10.1007/pl00014230.

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Innis, Sheila M., Howard Sprecher, David Hachey, John Edmond, and Robert E. Anderson. "Neonatal polyunsaturated fatty acid metabolism." Lipids 34, no. 2 (February 1999): 139–49. http://dx.doi.org/10.1007/s11745-999-0348-x.

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Handler, Jeffrey A., and Ronald G. Thurman. "Fatty acid-dependent ethanol metabolism." Biochemical and Biophysical Research Communications 133, no. 1 (November 1985): 44–51. http://dx.doi.org/10.1016/0006-291x(85)91839-x.

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Vieira, Andre F. C., Mark A. Xatse, Sofi Y. Murray, and Carissa Perez Olsen. "Oleic Acid Metabolism in Response to Glucose in C. elegans." Metabolites 13, no. 12 (December 6, 2023): 1185. http://dx.doi.org/10.3390/metabo13121185.

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A key response to glucose stress is an increased production of unsaturated fatty acids to balance the increase in saturated fatty acids in the membrane. The C. elegans homolog of stearoyl-CoA desaturase, FAT-7, introduces the first double bond into saturated C18 fatty acids yielding oleic acid, and is a critical regulatory point for surviving cold and glucose stress. Here, we incorporated 13C stable isotopes into the diet of nematodes and quantified the 13C-labelled fatty acid using GC-MS and HPLC/MS-MS to track its metabolic response to various concentrations of glucose. Previous work has analyzed the membrane composition of C. elegans when responding to mild glucose stress and showed few alterations in the overall fatty acid composition in the membrane. Here, in nematodes exposed to higher concentrations of glucose, a specific reduction in oleic acid and linoleic acid was observed. Using time courses and stable isotope tracing, the response of fatty acid metabolism to increasing levels of glucose stress is characterized, revealing the funneling of monounsaturated fatty acids to preserve the abundance of polyunsaturated fatty acids. Taken together, higher levels of glucose unveil a specific reduction in oleic and linolenic acid in the metabolic rewiring required to survive glucose stress.

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Olmedo, Patricio, Juan Vidal, Excequel Ponce, Bruno G. Defilippi, Alonso G. Pérez-Donoso, Claudio Meneses, Sebastien Carpentier, Romina Pedreschi, and Reinaldo Campos-Vargas. "Proteomic and Low-Polar Metabolite Profiling Reveal Unique Dynamics in Fatty Acid Metabolism during Flower and Berry Development of Table Grapes." International Journal of Molecular Sciences 24, no. 20 (October 19, 2023): 15360. http://dx.doi.org/10.3390/ijms242015360.

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Grapevine development and ripening are complex processes that involve several biochemical pathways, including fatty acid and lipid metabolism. Fatty acids are essential components of lipids, which play crucial roles in fruit maturation and flavor development. However, the dynamics of fatty acid metabolism in grape flowers and berries are poorly understood. In this study, we present those dynamics and investigate the mechanisms of fatty acid homeostasis on ‘Thompson Seedless’ berries using metabolomic and proteomic analyses. Low-polar metabolite profiling indicated a higher abundance of fatty acids at the pre-flowering and pre-veraison stages. Proteomic analyses revealed that grape flowers and berries display unique profiles of proteins involved in fatty acid biosynthesis, triacylglycerol assembly, fatty acid β-oxidation, and lipid signaling. These findings show, for the first time, that fatty acid metabolism also plays an important role in the development of non-oil-rich tissues, opening new perspectives about lipid function and its relation to berry quality.

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Bommiasamy, Hemamalini, Rungtawan Sriburi, Suzanne Jackowski, and Joseph W. Brewer. "Plasma cell differentiation and lipid metabolism (83.18)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S115. http://dx.doi.org/10.4049/jimmunol.178.supp.83.18.

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Abstract Plasma cells are terminally differentiated B cells that produce and secrete profuse amounts of antibodies. Plasma cell differentiation involves an increase in exocytic pathway components and expansion of the endoplasmic reticulum (ER) in order to accommodate high-rate immunoglobulin synthesis. ER expansion requires membrane biogenesis, a process that requires phospholipids. Increased phospholipid synthesis is dependent upon a sufficient supply of fatty acids. We have found that de novo fatty acid biosynthesis increases in CH12 B cells differentiating in response to lipopolysaccharide (LPS). Increased fatty acid biosynthesis correlates with upregulation of acetyl CoA carboxylase (ACC) and fatty acid synthase (FAS), enzymes that catalyze the formation of fatty acids. Further investigation will shed light into mechanisms that regulate lipid synthesis and ER expansion in differentiating plasma cells. Supported by NIH-GM61970 and NIH-T32 A1007508

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Cheng, Qiang, Zhongxuan Li, Jing Zhang, Henan Guo, Marhaba Ahmat, Junhao Cheng, Zaheer Abbas, et al. "Soybean Oil Regulates the Fatty Acid Synthesis Ⅱ System of Bacillus amyloliquefaciens LFB112 by Activating Acetyl-CoA Levels." Microorganisms 11, no. 5 (April 29, 2023): 1164. http://dx.doi.org/10.3390/microorganisms11051164.

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[Background] Bacillus LFB112 is a strain of Bacillus amyloliquefaciens screened in our laboratory. Previous studies found that it has a strong ability for fatty acid metabolism and can improve the lipid metabolism of broilers when used as feed additives. [Methods] This study aimed to confirm the fatty acid metabolism of Bacillus LFB112. Sterilized soybean oil (SSO) was added to the Beef Peptone Yeast (BPY) medium, and its effect on fatty acid content in the supernatant and bacteria, as well as expression levels of genes related to fatty acid metabolism, were studied. The control group was the original culture medium without oil. [Results] Acetic acid produced by the SSO group of Bacillus LFB112 decreased, but the content of unsaturated fatty acids increased. The 1.6% SSO group significantly increased the contents of pyruvate and acetyl-CoA in the pellets. Furthermore, the mRNA levels of enzymes involved in the type II fatty acid synthesis pathway of FabD, FabH, FabG, FabZ, FabI, and FabF were up-regulated. [Conclusions] Soybean oil increased the content of acetyl-CoA in Bacillus LFB112, activated its type II fatty acid synthesis pathway, and improved the fatty acid metabolism level of Bacillus LFB112. These intriguing results pave the way for further investigations into the intricate interplay between Bacillus LFB112 and fatty acid metabolism, with potential applications in animal nutrition and feed additive development.

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BRUCE, Jennifer S., and Andrew M. SALTER. "Metabolic fate of oleic acid, palmitic acid and stearic acid in cultured hamster hepatocytes." Biochemical Journal 316, no. 3 (June 15, 1996): 847–52. http://dx.doi.org/10.1042/bj3160847.

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Unlike other saturated fatty acids, dietary stearic acid does not appear to raise plasma cholesterol. The reason for this remains to be established, although it appears that it must be related to inherent differences in the metabolism of the fatty acid. In the present study, we have looked at the metabolism of palmitic acid and stearic acid, in comparison with oleic acid, by cultured hamster hepatocytes. Stearic acid was taken up more slowly and was poorly incorporated into both cellular and secreted triacylglycerol. Despite this, stearic acid stimulated the synthesis and secretion of triacylglycerol to the same extent as the other fatty acids. Incorporation into cellular phospholipid was lower for oleic acid than for palmitic acid and stearic acid. Desaturation of stearic acid, to monounsaturated fatty acid, was found to be greater than that of palmitic acid. Oleic acid produced from stearic acid was incorporated into both triacylglycerol and phospholipid, representing 13% and 6% respectively of the total after a 4 h incubation. Significant proportions of all of the fatty acids were oxidized, primarily to form ketone bodies, but by 8 h more oleic acid had been oxidized compared with palmitic acid and stearic acid.

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Guo, Zengkui, and Michael D. Jensen. "Intramuscular fatty acid metabolism evaluated with stable isotopic tracers." Journal of Applied Physiology 84, no. 5 (May 1, 1998): 1674–79. http://dx.doi.org/10.1152/jappl.1998.84.5.1674.

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We evaluated the applicability of stable isotopic tracers to the study of intramuscular fatty acid metabolism by infusing both [U-13C]palmitate and [1-13C]oleate intravenously for 4 h into fasted conscious rats. Skeletal muscles were sequentially biopsied, and the concentration and13C enrichment of fatty acids were measured by gas chromatography/combustion/isotope ratio mass spectrometry. Throughout the study, the13C enrichment of plasma palmitate and oleate remained substantially greater than intramuscular nonesterified palmitate and oleate enrichment, which in turn was greater than intramuscular triglyceride palmitate and oleate enrichment. Fractional synthesis rates of intramuscular triglycerides in gastrocnemius and soleus were 0.267 ± 0.075 and 0.100 ± 0.030/h ( P = 0.04), respectively, as determined by using [U-13C]palmitate, and were 0.278 ± 0.049 and 0.075 ± 0.013/h ( P = 0.02), respectively, by using [1-13C]oleate. We conclude that plasma free fatty acids are a source for intramuscular triglycerides and nonesterified fatty acids; the latter are likely the synthetic precursors of the former. Uniformly and singly labeled [13C]fatty acid tracers will provide an important tool to study intramuscular fatty acid and triglyceride metabolism.

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Calles-Escandon, J., and P. Driscoll. "Free fatty acid metabolism in aerobically fit individuals." Journal of Applied Physiology 77, no. 5 (November 1, 1994): 2374–79. http://dx.doi.org/10.1152/jappl.1994.77.5.2374.

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The impact of aerobic fitness level on the production and disposal of serum free fatty acids was investigated in 26 normal young volunteers. The fitness level was ascertained by history and confirmed by determination of maximal aerobic capacity. Energy expenditure and substrate oxidation at rest were measured with indirect calorimetry. Free fatty acid turnover was measured with an infusion of [14C]palmitic acid. All tests were done > or = 48 h after the last bout of exercise. The sedentary (SED) volunteers had higher rates of systemic delivery of fatty acids than aerobically fit (FIT) individuals (532 +/- 53.4 vs. 353 +/- 62.3 mumol/min; P = 0.05). This difference was accentuated when the values were normalized to fat-free mass (9.2 +/- 0.8 and 5.9 +/- 0.98 mumol.kg-1.min-1 for SED and FIT, respectively). Fatty acid oxidation was similar between FIT and SED volunteers in absolute numbers (209 +/- 25 vs. 202 +/- 21 mumol/min, respectively; NS) as well as when normalized to fat-free mass (3.8 +/- 0.9 vs. 3.6 +/- 1.4 mumol.kg-1.min-1, respectively; NS). In contrast, the nonoxidative disposal of serum fatty acids was higher in SED (330 +/- 46.1 mumol/min) than in FIT individuals (144 +/- 52 mumol/min; P = 0.026). Thus, the ratio of nonoxidative to oxidative disposal rates of fatty acids was higher in SED than in FIT individuals (1.65 +/- 0.29 vs. 0.75 +/- 0.17; P = 0.021). The data support the hypothesis that high aerobic fitness level is associated with a low rate of systemic delivery of fatty acids at rest. Nevertheless, subjects with high aerobic fitness levels have fat oxidation at the same rate as unfit individuals.

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Gallagher, Patricia A., Steven A. Warner, and Aristotle J. Domnas. "Presqualene metabolism in two species of Lagenidium." Canadian Journal of Microbiology 40, no. 10 (October 1, 1994): 858–64. http://dx.doi.org/10.1139/m94-136.

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The fate of precursors of the isoprenoid pathway was studied in the sterol auxotroph Lagenidium giganteum and in the positive control organism Lagenidium callinectes. Acetate derived from glucose and mevalonic acid was converted to sterols and fatty acids in L. callinectes. Lagenidium giganteum converted mevalonic acid to sterols and fatty acids, but glucose-derived acetate was not utilized for sterol synthesis. The results showed that the defect in the isoprenoid pathway of L. giganteum occurs at the level of the β-hydroxy-β-methylglutarylcoenzyme A reductase–synthase complex. Various aspects of this defect are discussed relative to metabolism of the organism.Key words: Lagenidium giganteum, Lagenidium callinectes, glucose, mevalonic acid utilization, fatty acids, sterol production.

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Black, Irene L., Helen M. Roche, Anne-Marie Tully, and Michael J. Gibney. "Acute-on-chronic effects of fatty acids on intestinal triacylglycerol-rich lipoprotein metabolism." British Journal of Nutrition 88, no. 6 (December 2002): 661–69. http://dx.doi.org/10.1079/bjn2002738.

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Postprandial triacylglycerol (TAG) metabolism is an important metabolic state that has been associated with cardiovascular disease. The magnitude of the postprandial TAG response is determined by dietary fat composition, which alters intestinal and hepatic TAG-rich lipoprotein (TRL) metabolism. Caco-2 cell monolayers are morphologically and physiologically similar to the human intestinal enterocytes, hence they are a good model to study intestinal lipoprotein metabolism. To date only the acute effect of fatty acid composition on intestinal TRL metabolism in Caco-2 cells has been investigated. Little is known of the effect of habitual, or chronic, dietary fat composition on intestinal TRL metabolism. Using the Caco-2 cell model, the present study investigated the acute-on-chronic effect of fatty acid composition on TRL metabolism. Caco-2 cells were grown in the presence of 0·05 mM-PALMITIC ACID (PA; 16 : 0), -OLEIC ACID (OA; 18 : 1N-9),-EICOSAPENTAENOIC ACID (EPA; 20 : 5N-3) OR NO FATTY ACID (CONTROL) FOR 19 D, THEN ONE OF FOUR ACUTE TREATMENTS (CONTROL (BOVINE SERUM ALBUMIN (BSA; 5 G/L)) OR BSA (5 G/L) PLUS 0·5 Mm-PA, -OA or -EPA) were administered for 22 h. Significant acute×chronic interactions for the effect of fatty acid composition on cellular TAG:secretedde novoTAG, and cellularde novoTAG:de novophospholipid were observed. Thus the effect of a fatty acid was determined by the duration of exposure to the fatty acid intervention. Acute PA treatment increasedde novoTAG synthesis, but chronic PA supplementation did not. Acute and chronic OA treatments increasedde novoTAG secretion. For EPA, chronic supplementation had the greatest effect on TAG synthesis and secretion. The acute-on-chronic effects of fatty acids on apolipoprotein B metabolism were relatively minor compared with the changes noted for TRL lipid composition. The present study shows that the Caco-2 cell model is valuable for studying intestinal TRL metabolism and that fatty acids modulate this process, the nature of which can be determined by the length of exposure of the cell to the fatty acid.

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Stinkens, R., G. H. Goossens, J. W. E. Jocken, and E. E. Blaak. "Targeting fatty acid metabolism to improve glucose metabolism." Obesity Reviews 16, no. 9 (July 16, 2015): 715–57. http://dx.doi.org/10.1111/obr.12298.

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Frayn, K. N. "The glucose–fatty acid cycle: a physiological perspective." Biochemical Society Transactions 31, no. 6 (December 1, 2003): 1115–19. http://dx.doi.org/10.1042/bst0311115.

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Glucose and fatty acids are the major fuels for mammalian metabolism and it is clearly essential that mechanisms exist for mutual co-ordination of their utilization. The glucose–fatty acid cycle, as it was proposed in 1963, describes one set of mechanisms by which carbohydrate and fat metabolism interact. Since that time, the importance of the glucose–fatty acid cycle has been confirmed repeatedly, in particular by elevation of plasma non-esterified fatty acid concentrations and demonstration of an impairment of glucose utilization. Since 1963 further means have been elucidated by which glucose and fatty acids interact. These include stimulation of hepatic glucose output by fatty acids, potentiation of glucose-stimulated insulin secretion by fatty acids, and the cellular mechanism whereby high glucose and insulin concentrations inhibit fatty acid oxidation via malonyl-CoA regulation of carnitine palmitoyltransferase-1. The last of these mechanisms, discovered by Denis McGarry and Daniel Foster in 1977, provides an almost exact complement to the mechanism described in the glucose–fatty acid cycle whereby high concentrations of fatty acids inhibit glucose utilization. These additional discoveries have not detracted from the important of the glucose–fatty acid cycle: rather, they have reinforced the importance of mechanisms whereby glucose and fat can interact.

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Nickerson, James G., Hakam Alkhateeb, Carley R. Benton, James Lally, Jennifer Nickerson, Xiao-Xia Han, Meredith H. Wilson, et al. "Greater Transport Efficiencies of the Membrane Fatty Acid Transporters FAT/CD36 and FATP4 Compared with FABPpm and FATP1 and Differential Effects on Fatty Acid Esterification and Oxidation in Rat Skeletal Muscle." Journal of Biological Chemistry 284, no. 24 (April 20, 2009): 16522–30. http://dx.doi.org/10.1074/jbc.m109.004788.

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In selected mammalian tissues, long chain fatty acid transporters (FABPpm, FAT/CD36, FATP1, and FATP4) are co-expressed. There is controversy as to whether they all function as membrane-bound transporters and whether they channel fatty acids to oxidation and/or esterification. Among skeletal muscles, the protein expression of FABPpm, FAT/CD36, and FATP4, but not FATP1, correlated highly with the capacities for oxidative metabolism (r ≥ 0.94), fatty acid oxidation (r ≥ 0.88), and triacylglycerol esterification (r ≥ 0.87). We overexpressed independently FABPpm, FAT/CD36, FATP1, and FATP4, within a normal physiologic range, in rat skeletal muscle, to determine the effects on fatty acid transport and metabolism. Independent overexpression of each fatty acid transporter occurred without altering either the expression or plasmalemmal content of other fatty acid transporters. All transporters increased fatty acid transport, but FAT/CD36 and FATP4 were 2.3- and 1.7-fold more effective than FABPpm and FATP1, respectively. Fatty acid transporters failed to alter the rates of fatty acid esterification into triacylglycerols. In contrast, all transporters increased the rates of long chain fatty acid oxidation, but the effects of FABPpm and FAT/CD36 were 3-fold greater than for FATP1 and FATP4. Thus, fatty acid transporters exhibit different capacities for fatty acid transport and metabolism. In vivo, FAT/CD36 and FATP4 are the most effective fatty acid transporters, whereas FABPpm and FAT/CD36 are key for stimulating fatty acid oxidation.

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Reibel, D. K., B. O'Rourke, K. A. Foster, H. Hutchinson, C. E. Uboh, and R. L. Kent. "Altered phospholipid metabolism in pressure-overload hypertrophied hearts." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 1 (January 1, 1986): H1—H6. http://dx.doi.org/10.1152/ajpheart.1986.250.1.h1.

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The content and fatty acyl composition of phospholipids were examined in pressure-overload hypertrophied hearts. Cardiac hypertrophy was induced in rats by abdominal aortic constriction. Twenty-one days postconstriction the content of myocardial phosphatidylcholine (PC), sphingomyelin, and phosphatidylinositol (PI) was significantly elevated by 10, 10, and 20%, respectively. The essential fatty acid, linoleic acid, was markedly reduced in PC, phosphatidylethanolamine (PE), PI, and cardiolipin (CL) of hypertrophied hearts. The associated changes in fatty acyl composition were specific for the individual phospholipid class as evidenced by a significant elevation of palmitic acid in PC, docosahexaenoic acid in PE and oleic acid in CL. Alterations in fatty acyl composition of phospholipids were associated with no change in the composition of cardiac triglycerides, cardiac free fatty acids or serum lipids. The fatty acyl composition of phospholipids was also altered in pressure-overload hypertrophied hearts of cats, as evidenced by a reduction of linoleic acid and an elevation of arachidonic acid in total phospholipids. These findings demonstrate that changes in phospholipid metabolism occur in the pressure-overloaded mammalian heart. Such alterations may contribute to altered membrane function in the hypertrophied myocardium.

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Bonen, Arend, G. Lynis Dohm, and Luc J. C. van Loon. "Lipid metabolism, exercise and insulin action." Essays in Biochemistry 42 (November 27, 2006): 47–59. http://dx.doi.org/10.1042/bse0420047.

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Skeletal muscle constitutes 40% of body mass and takes up 80% of a glucose load. Therefore, impaired glucose removal from the circulation, such as that which occurs in obesity and type 2 diabetes, is attributable in large part to the insulin resistance in muscle. Recent research has shown that fatty acids, derived from adipose tissue, can interfere with insulin signalling in muscle. Hence, insulin-stimulated GLUT4 translocation to the cell surface is impaired, and therefore, the rate of glucose removal from the circulation into muscle is delayed. The mechanisms provoking lipid-mediated insulin resistance are not completely understood. In sedentary individuals, excess intramyocellular accumulation of triacylglycerols is only modestly associated with insulin resistance. In contrast, endurance athletes, despite accumulating large amounts of intramyocellular triacylglycerols, are highly insulin sensitive. Thus it appears that lipid metabolites, other than triacylglycerols, interfere with insulin signalling. These metabolites, however, are not expected to accumulate in athletic muscles, as endurance training increases the capacity for fatty acid oxidation by muscle. These observations, and others in severely obese individuals and type 2 diabetes patients, suggest that impaired rates of fatty acid oxidation are associated with insulin resistance. In addition, in obesity and type 2 diabetes, the rates of fatty acid transport into muscle are also increased. Thus, excess intracellular lipid metabolite accumulation, which interferes with insulin signalling, can occur as a result of impaired rates of fatty acid oxidation and/or increased rates of fatty acid transport into muscle. Accumulation of excess intramyocellular lipid can be avoided by exercise, which improves the capacity for fatty acid oxidation.

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Parsons, H. G., and V. C. Dias. "Intramitochondrial fatty acid metabolism: riboflavin deficiency and energy production." Biochemistry and Cell Biology 69, no. 7 (July 1, 1991): 490–97. http://dx.doi.org/10.1139/o91-073.

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Inborn errors of fatty acid β-oxidation have contributed significantly to our understanding of intracellular fatty acid metabolism. The first intramitochondrial step in β-oxidation of fatty acyl-CoA of different chain lengths is catalyzed by the three chain length specific acyl-CoA dehydrogenases. Inherited deficiency of these enzymes has been reported. Some are riboflavin responsive. The first step of fatty acid oxidation is reviewed with specific emphasis on β-oxidation in newborn infants, rendered riboflavin deficient by phototherapy. Given that medium chain fatty acids are not stored as triacylglycerols and undergo rapid β-oxidation, they have been proposed as superior substrates compared with long chain triglycerides in times of metabolic stress. This review also examines medium chain triglycerides as an alternate energy source. When medium chain triglycerides were fed as 50% of total energy, glucose sparing was present with little loss of energy as dicarboxylic acids.Key words: β-oxidation, acyl-CoA dehydrogenase, riboflavin, medium chain triglycerides, dicarboxylic acids.

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Armbruster, Julia, Mostafa A. Aboouf, Max Gassmann, Angela Egert, Hubert Schorle, Veit Hornung, Tobias Schmidt, et al. "Myoglobin regulates fatty acid trafficking and lipid metabolism in mammary epithelial cells." PLOS ONE 17, no. 10 (October 12, 2022): e0275725. http://dx.doi.org/10.1371/journal.pone.0275725.

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Myoglobin (MB) is known to bind and deliver oxygen in striated muscles at high expression levels. MB is also expressed at much reduced levels in mammary epithelial cells, where the protein´s function is unclear. In this study, we aim to determine whether MB impacts fatty acid trafficking and facilitates aerobic fatty acid ß-oxidation in mammary epithelial cells. We utilized MB-wildtype versus MB-knockout mice and human breast cancer cells to examine the impact of MB and its oxygenation status on fatty acid metabolism in mouse milk and mammary epithelia. MB deficient cells were generated through CRISPR/Cas9 and TALEN approaches and exposed to various oxygen tensions. Fatty acid profiling of milk and cell extracts were performed along with cell labelling and immunocytochemistry. Our findings show that MB expression in mammary epithelial cells promoted fatty acid oxidation while reducing stearyl-CoA desaturase activity for lipogenesis. In cells and milk product, presence of oxygenated MB significantly elevated indices of limited fatty acid ß-oxidation, i.e., the organelle-bound removal of a C2 moiety from long-chain saturated or monounsaturated fatty acids, thus shifting the composition toward more saturated and shorter fatty acid species. Presence of the globin also increased cytoplasmic fatty acid solubility under normoxia and fatty acid deposition to lipid droplets under severe hypoxia. We conclude that MB can function in mammary epithelia as intracellular O2-dependent shuttle of oxidizable fatty acid substrates. MB’s impact on limited oxidation of fatty acids could generate inflammatory mediator lipokines, such as 7-hexadecenoate. Thus, the novel functions of MB in breast epithelia described herein range from controlling fatty acid turnover and homeostasis to influencing inflammatory signalling cascade. Future work is needed to analyse to what extent these novel roles of MB also apply to myocytic cell physiology and malignant cell behaviour, respectively.

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Jensen, Michael D., Karin Ekberg, and Bernard R. Landau. "Lipid metabolism during fasting." American Journal of Physiology-Endocrinology and Metabolism 281, no. 4 (October 1, 2001): E789—E793. http://dx.doi.org/10.1152/ajpendo.2001.281.4.e789.

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These studies were conducted to understand the relationship between measures of systemic free fatty acid (FFA) reesterification and regional FFA, glycerol, and triglyceride metabolism during fasting. Indirect calorimetry was used to measure fatty acid oxidation in six men after a 60-h fast. Systemic and regional (splanchnic, renal, and leg) FFA ([3H]palmitate) and glycerol ([3H]glycerol) kinetics, as well as splanchnic triglyceride release, were measured. The rate of systemic FFA reesterification was 366 ± 93 μmol/min, which was greater ( P < 0.05) than splanchnic triglyceride fatty acid output (64 ± 6 μmol/min), a measure of VLDL triglyceride fatty acid export. The majority of glycerol uptake occurred in the splanchnic and renal beds, although some leg glycerol uptake was detected. Systemic FFA release was approximately double that usually present in overnight postabsorptive men, yet the regional FFA release rates were of the same proportions previously observed in overnight postabsorptive men. In conclusion, FFA reesterification at rest during fasting far exceeds splanchnic triglyceride fatty acid output. This indicates that nonhepatic sites of FFA reesterification are important, and that peripheral reesterification of FFA exceeds the rate of simultaneous intracellular triglyceride fatty acid oxidation.

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Ferreira, Raphael, Paulo Gonçalves Teixeira, Verena Siewers, and Jens Nielsen. "Redirection of lipid flux toward phospholipids in yeast increases fatty acid turnover and secretion." Proceedings of the National Academy of Sciences 115, no. 6 (January 22, 2018): 1262–67. http://dx.doi.org/10.1073/pnas.1715282115.

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Bio-based production of fatty acids and fatty acid-derived products can enable sustainable substitution of petroleum-derived fuels and chemicals. However, developing new microbial cell factories for producing high levels of fatty acids requires extensive engineering of lipid metabolism, a complex and tightly regulated metabolic network. Here we generated a Saccharomyces cerevisiae platform strain with a simplified lipid metabolism network with high-level production of free fatty acids (FFAs) due to redirected fatty acid metabolism and reduced feedback regulation. Deletion of the main fatty acid activation genes (the first step in β-oxidation), main storage lipid formation genes, and phosphatidate phosphatase genes resulted in a constrained lipid metabolic network in which fatty acid flux was directed to a large extent toward phospholipids. This resulted in simultaneous increases of phospholipids by up to 2.8-fold and of FFAs by up to 40-fold compared with wild-type levels. Further deletion of phospholipase genes PLB1 and PLB2 resulted in a 46% decrease in FFA levels and 105% increase in phospholipid levels, suggesting that phospholipid hydrolysis plays an important role in FFA production when phospholipid levels are increased. The multiple deletion mutant generated allowed for a study of fatty acid dynamics in lipid metabolism and represents a platform strain with interesting properties that provide insight into the future development of lipid-related cell factories.

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KISHINO, Shigenobu, and Jun OGAWA. "Novel Fatty Acid Metabolism of Lactic Acid Bacteria:Application to Functional Fatty Acid Production and Gut Lipid Metabolism Control." KAGAKU TO SEIBUTSU 51, no. 11 (2013): 738–44. http://dx.doi.org/10.1271/kagakutoseibutsu.51.738.

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Childs, Caroline E. "Sex hormones and n-3 fatty acid metabolism." Proceedings of the Nutrition Society 79, no. 2 (August 16, 2019): 219–24. http://dx.doi.org/10.1017/s0029665119001071.

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α-Linolenic acid (ALA) is an n-3 fatty acid found in plant-derived foods such as linseeds and linseed oil. Mammals can convert this essential fatty acid into longer-chain fatty acids including EPA, docosapentaenoic acid (DPA) and DHA. Women demonstrate greater increases in the EPA status after ALA supplementation than men, and a growing body of animal model research identifies mechanisms by which sex hormones such as oestrogen and progesterone interact with the synthesis of EPA and DHA. Alternatively, EPA, DPA and DHA can be consumed directly, with oily fish being a rich dietary source of these nutrients. However, current National Diet and Nutrition Data reveals a median oily fish intake of 0 g daily across all age ranges and in both sexes. As longer-chain n-3 fatty acids have a crucial role in fetal and neonatal brain development, advice to consume dietary ALA could prove to be a pragmatic and acceptable alternative to advice to consume fish during pregnancy, if benefits upon tissue composition and functional outcomes can be demonstrated. Further research is required to understand the effects of increasing dietary ALA during pregnancy, and will need to simultaneously address conflicts with current dietary advice to only eat ‘small amounts’ of vegetable oils during pregnancy. Improving our understanding of sex-specific differences in fatty acid metabolism and interactions with pregnancy has the potential to inform both personalised nutrition advice and public health policy.

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Rudzite, Vera, Edite Jurika, Gabriele Baier-Bitterlich, Bernhard Widner, Gilbert Reibnegger, and Dietmar Fuchs. "Pteridines and Lipid Metabolism." Pteridines 9, no. 2 (May 1998): 103–12. http://dx.doi.org/10.1515/pteridines.1998.9.2.103.

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Summary The effect of 9 different pteridines on fatty acid incorporation into phospholipids as well as on cholesterol and phospholipid content was compared in vitro using rat liver homogenate, Krebs-Ringer phosphate buffer containing 0.3 % albumin (pH=7.4), fatty acid mixture and glycerol. D-neopterin (5-30 pmol/g) induced an increase of saturated, a decrease of unsaturated fatty acids incorporation into phospholipids and elevated the cholesterol content in samples. The phospholipid amount in samples remained unchanged. Sepiapterin, 7,8-dihydrobiopterin, 5,6,7,8-tetrahydrobiopterin, biopterin, monapterin and 7,8-dihydroneopterin addition to samples induced an inverse relationship: a decrease of saturated, an increase of unsaturated fatty acid, especially arachidonic acid, incorporation into phospholipids and the decrease of cholesterol content in samples. The phospholipid amount in samples remained unchanged or increased. Lipid metabolism was not altered after addition of xanthopterin and isoxanthopterin to samples. It was suggested that neopterin decreased membrane fluidity, prevented cell cycle, induced cell dystrophy and apoptosis, and promoted the cholesterol precipitation while tetrahydrobiopterin, its precursors, biopterin, monapterin and dihydroneopterin increased membrane fluidity, stimulated cell cycle, prevented cholesterol precipitation. The data point to a potential role of increased neopterin concentrations in vivo to support atherosclerosis development and progression whereas the other pteridines may have a protective effect. Moreover, these pteridines can also promote cell transformation.

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Calder, P. C., P. Yaqoob, and E. A. Newsholme. "Triacylglycerol metabolism by lymphocytes and the effect of triacylglycerols on lymphocyte proliferation." Biochemical Journal 298, no. 3 (March 15, 1994): 605–11. http://dx.doi.org/10.1042/bj2980605.

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This study investigates the ability of lymphocytes to utilize fatty acids originating from triacylglycerols and the effect of triacylglycerols upon mitogen-stimulated lymphocyte proliferation. Lymphocytes isolated from rat lymph nodes, spleen, thymus and lymphatic duct had a lipoprotein lipase activity of approx. 10 units/mg of protein, indicating that the fatty acids of circulating triacylglycerols are accessible to these cells. In culture lymph node lymphocytes hydrolysed triacylglycerols added to the medium as emulsions. Both non-esterified fatty acids and free glycerol appeared in the cell culture medium, but their concentrations indicated that a high proportion of each (65-90% of fatty acids and 60-80% of glycerol) was taken up by the cells. The incorporation and fate of triacylglycerol-fatty acids was studied by culturing the cells in the presence of tri[3H]oleoylglycerol or tri[14C]inoleoylglycerol. Both fatty acids were incorporated into lymphocyte lipids in a time-dependent manner; linoleic acid was incorporated at a significantly greater rate than oleic acid. The majority of oleic acid (greater than 70%) was incorporated into cellular triacylglycerol, while less than 10% was incorporated into phospholipids. In contrast, linoleic acid incorporation into cellular triacylglycerol never exceeded 25%, while up to 45% was incorporated into phospholipids. Triacylglycerols containing polyunsaturated fatty acids inhibited concanavalin A-stimulated lymphocyte proliferation in a concentration- and time-dependent manner; triacylglycerols containing saturated fatty acids or oleic acid were not inhibitory. Such direct effects of certain triacylglycerols on lymphocyte function may explain why some clinical trials of polyunsaturated fatty acid-rich diets have been successful in improving the condition of patients suffering from inflammatory diseases.

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Guo, Wen, Nasi Huang, Jun Cai, Weisheng Xie, and James A. Hamilton. "Fatty acid transport and metabolism in HepG2 cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 3 (March 2006): G528—G534. http://dx.doi.org/10.1152/ajpgi.00386.2005.

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The mechanism(s) of fatty acid uptake by liver cells is not fully understood. We applied new approaches to address long-standing controversies of fatty acid uptake and to distinguish diffusion and protein-based mechanisms. Using HepG2 cells containing an entrapped pH-sensing fluorescence dye, we showed that the addition of oleate (unbound or bound to cyclodextrin) to the external buffer caused a rapid (seconds) and dose-dependent decrease in intracellular pH (pHin), indicating diffusion of fatty acids across the plasma membrane. pHin returned to its initial value with a time course (in min) that paralleled the metabolism of radiolabeled oleate. Preincubation of cells with the inhibitors phloretin or triacsin C had no effect on the rapid pHin drop after the addition of oleate but greatly suppressed pHin recovery. Using radiolabeled oleate, we showed that its esterification was almost completely inhibited by phloretin or triacsin C, supporting the correlation between pHin recovery and metabolism. We then used a dual-fluorescence assay to study the interaction between HepG2 cells and cis-parinaric acid (PA), a naturally fluorescent but slowly metabolized fatty acid. The fluorescence of PA increased rapidly upon its addition to cells, indicating rapid binding to the plasma membrane; pHin decreased rapidly and simultaneously but did not recover within 5 min. Phloretin had no effect on the PA-mediated pHin drop or its slow recovery but decreased the absolute fluorescence of membrane-bound PA. Our results show that natural fatty acids rapidly bind to, and diffuse through, the plasma membrane without hindrance by metabolic inhibitors or by an inhibitor of putative membrane-bound fatty acid transporters.

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Reithuber, Elisabeth, Priyanka Nannapaneni, Olena Rzhepishevska, Anders E. G. Lindgren, Oleksandr Ilchenko, Staffan Normark, Fredrik Almqvist, Birgitta Henriques-Normark, and Peter Mellroth. "The Bactericidal Fatty Acid Mimetic 2CCA-1 Selectively Targets Pneumococcal Extracellular Polyunsaturated Fatty Acid Metabolism." mBio 11, no. 6 (December 15, 2020): e03027-20. http://dx.doi.org/10.1128/mbio.03027-20.

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ABSTRACTStreptococcus pneumoniae, a major cause of pneumonia, sepsis, and meningitis worldwide, has the nasopharynges of small children as its main ecological niche. Depletion of pneumococci from this niche would reduce the disease burden and could be achieved using small molecules with narrow-spectrum antibacterial activity. We identified the alkylated dicyclohexyl carboxylic acid 2CCA-1 as a potent inducer of autolysin-mediated lysis of S. pneumoniae, while having low activity against Staphylococcus aureus. 2CCA-1-resistant strains were found to have inactivating mutations in fakB3, known to be required for uptake of host polyunsaturated fatty acids, as well as through inactivation of the transcriptional regulator gene fabT, vital for endogenous, de novo fatty acid synthesis regulation. Structure activity relationship exploration revealed that, besides the central dicyclohexyl group, the fatty acid-like structural features of 2CCA-1 were essential for its activity. The lysis-inducing activity of 2CCA-1 was considerably more potent than that of free fatty acids and required growing bacteria, suggesting that 2CCA-1 needs to be metabolized to exert its antimicrobial activity. Total lipid analysis of 2CCA-1 treated bacteria identified unique masses that were modeled to 2CCA-1 containing lysophosphatidic and phosphatidic acid in wild-type but not in fakB3 mutant bacteria. This suggests that 2CCA-1 is metabolized as a fatty acid via FakB3 and utilized as a phospholipid building block, leading to accumulation of toxic phospholipid species. Analysis of FabT-mediated fakB3 expression elucidates how the pneumococcus could ensure membrane homeostasis and concurrent economic use of host-derived fatty acids.IMPORTANCE Fatty acid biosynthesis is an attractive antibiotic target, as it affects the supply of membrane phospholipid building blocks. In Streptococcus pneumoniae, it is not sufficient to target only the endogenous fatty acid synthesis machinery, as uptake of host fatty acids may bypass this inhibition. Here, we describe a small-molecule compound, 2CCA-1, with potent bactericidal activity that upon interactions with the fatty acid binding protein FakB3, which is present in a limited number of Gram-positive species, becomes metabolized and incorporated as a toxic phospholipid species. Resistance to 2CCA-1 developed specifically in fakB3 and the regulatory gene fabT. These mutants reveal a regulatory connection between the extracellular polyunsaturated fatty acid metabolism and endogenous fatty acid synthesis in S. pneumoniae, which could ensure balance between efficient scavenging of host polyunsaturated fatty acids and membrane homeostasis. The data might be useful in the identification of narrow-spectrum treatment strategies to selectively target members of the Lactobacillales such as S. pneumoniae.

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Burdge, G. C. "Polyunsaturated fatty acid intakes and -linolenic acid metabolism." American Journal of Clinical Nutrition 93, no. 3 (December 29, 2010): 665–66. http://dx.doi.org/10.3945/ajcn.110.008169.

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Dunning, Kylie R., Darryl L. Russell, and Rebecca L. Robker. "Lipids and oocyte developmental competence: the role of fatty acids and β-oxidation." REPRODUCTION 148, no. 1 (July 2014): R15—R27. http://dx.doi.org/10.1530/rep-13-0251.

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Metabolism and ATP levels within the oocyte and adjacent cumulus cells are associated with quality of oocyte and optimal development of a healthy embryo. Lipid metabolism provides a potent source of energy and its importance during oocyte maturation is being increasingly recognised. The triglyceride and fatty acid composition of ovarian follicular fluid has been characterised for many species and is influenced by nutritional status (i.e. dietary fat, fasting, obesity and season) as well as lactation in cows. Lipid in oocytes is a primarily triglyceride of specific fatty acids which differ by species, stored in distinct droplet organelles that re-localise during oocyte maturation. The presence of lipids, particularly saturated vs unsaturated fatty acids, in in vitro maturation systems affects oocyte lipid content as well as developmental competence. Triglycerides are metabolised by lipases that have been localised to cumulus cells as well as oocytes. Fatty acids generated by lipolysis are further metabolised by β-oxidation in mitochondria for the production of ATP. β-oxidation is induced in cumulus–oocyte complexes (COCs) by the LH surge, and pharmacological inhibition of β-oxidation impairs oocyte maturation and embryo development. Promoting β-oxidation with l-carnitine improves embryo development in many species. Thus, fatty acid metabolism in the mammalian COC is regulated by maternal physiological and in vitro environmental conditions; and is important for oocyte developmental competence.

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Ranea-Robles, Pablo, and Sander M. Houten. "The biochemistry and physiology of long-chain dicarboxylic acid metabolism." Biochemical Journal 480, no. 9 (May 4, 2023): 607–27. http://dx.doi.org/10.1042/bcj20230041.

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Mitochondrial β-oxidation is the most prominent pathway for fatty acid oxidation but alternative oxidative metabolism exists. Fatty acid ω-oxidation is one of these pathways and forms dicarboxylic acids as products. These dicarboxylic acids are metabolized through peroxisomal β-oxidation representing an alternative pathway, which could potentially limit the toxic effects of fatty acid accumulation. Although dicarboxylic acid metabolism is highly active in liver and kidney, its role in physiology has not been explored in depth. In this review, we summarize the biochemical mechanism of the formation and degradation of dicarboxylic acids through ω- and β-oxidation, respectively. We will discuss the role of dicarboxylic acids in different (patho)physiological states with a particular focus on the role of the intermediates and products generated through peroxisomal β-oxidation. This review is expected to increase the understanding of dicarboxylic acid metabolism and spark future research.

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Luo, Yuting, Hanbing Wang, Baorui Liu, and Jia Wei. "Fatty Acid Metabolism and Cancer Immunotherapy." Current Oncology Reports 24, no. 5 (March 1, 2022): 659–70. http://dx.doi.org/10.1007/s11912-022-01223-1.

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Strandvik, Birgitta. "Fatty Acid Metabolism in Cystic Fibrosis." New England Journal of Medicine 350, no. 6 (February 5, 2004): 605–7. http://dx.doi.org/10.1056/nejme038217.

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Muoio, Deborah M. "Metabolism and Vascular Fatty Acid Transport." New England Journal of Medicine 363, no. 3 (July 15, 2010): 291–93. http://dx.doi.org/10.1056/nejmcibr1005397.

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Eckardt, Nancy A. "Tocopherols and ER Fatty Acid Metabolism." Plant Cell 20, no. 2 (February 2008): 246. http://dx.doi.org/10.1105/tpc.108.200212.

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Buchan, Gregory J., Gustavo Bonacci, Marco Fazzari, Sonia R. Salvatore, and Stacy Gelhaus Wendell. "Nitro-fatty acid formation and metabolism." Nitric Oxide 79 (September 2018): 38–44. http://dx.doi.org/10.1016/j.niox.2018.07.003.

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Strandvik, Birgitta. "Fatty acid metabolism in cystic fibrosis." Prostaglandins, Leukotrienes and Essential Fatty Acids 83, no. 3 (September 2010): 121–29. http://dx.doi.org/10.1016/j.plefa.2010.07.002.

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Journal articles on the topic 'Fatty acid metabolism'

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