Polyunsaturated fatty acids, inflammation, and metabolic syndrome in South Asian Americans in Maryland

Khan, Saira; Jackson, Robert T.

doi:10.1002/fsn3.698

Cited by 9 publications

(9 citation statements)

References 32 publications

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“…Generally, the quantitative accuracy of DR or 24-h recall is thought to be superior to that of the food frequency questionnaire (FFQ). Most of the other studies using DR or 24-h recall with smaller numbers of participants also reported that ARA intakes were around 100 mg/day or more, although there are some exceptions (Table 4) [28,[42][43][44][45][46][47][48]. These studies suggest that ARA intake, at least in advanced countries, is 100-250 mg/day for normal healthy adults.…”

Section: Dietary Intake Of Aramentioning

confidence: 95%

Intake of arachidonic acid-containing lipids in adult humans: dietary surveys and clinical trials

Kawashima

2019

Lipids Health Dis

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Long-chain polyunsaturated fatty acids (LCPUFAs) have important roles in physiological homeostasis. Numerous studies have provided extensive information about the roles of n-3 LCPUFA, such as docosahexaenoic acid and eicosapentaenoic acid. Arachidonic acid (ARA) is one of the major n-6 LCPUFAs and its biological aspects have been well studied. However, nutritional information for ARA is limited, especially in adult humans. This review presents a framework of dietary ARA intake and the effects of ARA supplementation on LCPUFA metabolism in adult humans, and the nutritional significance of ARA and LCPUFA is discussed.

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Section: Dietary Intake Of Aramentioning

confidence: 95%

Intake of arachidonic acid-containing lipids in adult humans: dietary surveys and clinical trials

Kawashima

2019

Lipids Health Dis

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“…Changes in the fatty acid metabolism of COPD may be related to energy limitation and anoxia [ 22 ]; a condition similar to emphysema has been reported in the lungs of rats with diet restrictions [ 23 ]. Polyunsaturated fatty acids (PUFAs) have also been reported to play an important role in COPD and various other inflammatory diseases [ 24 ]. In this study, the levels of arachidonic acid, docosapentaenoic acid, and eicosapentaenoic acid were significantly increased in both COPD1 and COPD2 groups; “sphingolipid metabolism”, “fatty acid biosynthesis”, “biosynthesis of unsaturated fatty acids”, “arachidonic acid metabolism” were evaluated as important in metabolic pathway analysis.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Targeted Metabolomic Study in the Lung, Plasma, and Urine of PPE/LPS-Induced COPD Mice Model

Kim

Lee

Kim

et al. 2022

IJMS

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(1) Background: Progression of chronic obstructive pulmonary disease (COPD) leads to irreversible lung damage and inflammatory responses; however, biomarker discovery for monitoring of COPD progression remains challenging. (2) Methods: This study evaluated the metabolic mechanisms and potential biomarkers of COPD through the integrated analysis and receiver operating characteristic (ROC) analysis of metabolic changes in lung, plasma, and urine, and changes in morphological characteristics and pulmonary function in a model of PPE/LPS-induced COPD exacerbation. (3) Results: Metabolic changes in the lungs were evaluated as metabolic reprogramming to counteract the changes caused by the onset of COPD. In plasma, several combinations of phenylalanine, 3-methylhistidine, and polyunsaturated fatty acids have been proposed as potential biomarkers; the α-aminobutyric acid/histidine ratio has also been reported, which is a novel candidate biomarker for COPD. In urine, a combination of succinic acid, isocitric acid, and pyruvic acid has been proposed as a potential biomarker. (4) Conclusions: This study proposed potential biomarkers in plasma and urine that reflect altered lung metabolism in COPD, concurrently with the evaluation of the COPD exacerbation model induced by PPE plus LPS administration. Therefore, understanding these integrative mechanisms provides new insights into the diagnosis, treatment, and severity assessment of COPD.

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“…The ER-resident CYB5R3 serves to maintain ER oxidation/reduction balance necessary for such eicosanoids synthesis as microsomal metabolism, or directly participate the metabolic reactions. When MVA pathway is inhibited, CYB5R3 prenylation was ablated and the bioactive intermediate metabolites or substrates of eicosanoid metabolism were accumulated, resulting in metaflammation and death (31,(33)(34)(35).…”

Section: Discussionmentioning

confidence: 99%

“…S4). As eicosanoids are closely related to inflammatory responses (31)(32)(33)(34)(35)(36), the metaflammation occurring in the mutant cells may be primarily contributed by the abnormal eicosanoids production.…”

Section: Ggpps-deficient Vascular Smooth Muscle Displays Inflammationmentioning

confidence: 99%

GGPP depletion initiates metaflammation through disequilibrating CYB5R3-dependent eicosanoid metabolism

Wei¹,

Zheng²,

Sun

et al. 2020

Journal of Biological Chemistry

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Metaflammation is a primary inflammatory complication of metabolic disorders characterized by altered production of many inflammatory cytokines, adipokines and lipid mediators. While multiple inflammation networks have been identified, the mechanisms by which metaflammation is initiated have long been controversial. As mevalonate pathway (MVA) produces abundant bioactive isoprenoids and abnormal MVA has a phenotypic association with inflammation/immunity, we speculate that isoprenoids from the MVA may provide a causal link between metaflammation and metabolic disorders. Using a line with the MVA isoprenoids producer geranygeranyldiphosphate synthase (GGPPS) deleted, we find that GGPP depletion causes an apparent metaflammation as evidenced by abnormal accumulation of fatty acids, eicosanoid intermediates and proinflammatory cytokines. We also find that GGPP prenylate cytochrome b5 reductase 3 (CYB5R3) and the prenylated CYB5R3 then translocate from the mitochondrial to ER pool. As CYB5R3 is a critical NADH-dependent reductase necessary for eicosanoids metabolism in ER, we thus suggests that GGPP-mediated CYB5R3 prenylation is necessary for eicosanoid metabolism. In addition, we observe that pharmacological inhibition of MVA pathway by simvastatin is sufficient to inhibit CYB5R3 translocation and induces smooth muscle death. Therefore, we conclude that the dysregulation of MVA intermediates is an essential mechanism for metaflammation initiation, in which the imbalanced production of eicosanoid intermediates in ER serve as an important pathogenic factor. Moreover, the interplay of MVA and eicosanoids metabolism as we reported here illustrates a model for the coordinating regulation among metabolite pathways.

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Polyunsaturated fatty acids, inflammation, and metabolic syndrome in South Asian Americans in Maryland

Cited by 9 publications

References 32 publications

Intake of arachidonic acid-containing lipids in adult humans: dietary surveys and clinical trials

Intake of arachidonic acid-containing lipids in adult humans: dietary surveys and clinical trials

Comprehensive Targeted Metabolomic Study in the Lung, Plasma, and Urine of PPE/LPS-Induced COPD Mice Model

GGPP depletion initiates metaflammation through disequilibrating CYB5R3-dependent eicosanoid metabolism

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