Abstract:AimOur aim was to perform an in‐depth analysis of the composition of fatty acids in milk from mothers delivering extremely preterm babies. We investigated longitudinal changes in milk fatty acid profiles and the relationship between several types of fatty acids, including omega‐3 and omega‐6.MethodsMilk samples were collected at three stages of lactation from 78 mothers who delivered at less than 28 weeks of pregnancy at the Sahlgrenska University Hospital, Gothenburg, Sweden, from April 2013 to September 2015… Show more
“…Total lipids were extracted from milk and FA methyl esters (FAMEs) prepared and analyzed by gas chromatography-mass spectrometry (GC-MS). 18 In accordance with previous studies, no effect of pasteurization on the FA composition was noted. 19,20 Venous blood samples were collected from the infants at birth (cord blood), on postnatal days 1, 7, 14, and 28, and postmenstrual age (PMA) weeks 32, 36, and 40.…”
Section: Methodssupporting
confidence: 92%
“…The results from this analysis are published elsewhere. 18 Frozen, anonymous donor milk samples from 6 mothers were obtained from Moder-smjölkcentralen at Queen Silvia Children’s Hospital. Total lipids were extracted from milk and FA methyl esters (FAMEs) prepared and analyzed by gas chromatography-mass spectrometry (GC-MS).…”
There appears to be no or low correlation between the amount of DHA administered parenterally and levels measured in serum. Whether this observation reflects serum phospholipid fraction only or truly represents the amount of accreted DHA needs to be investigated. None of the parenteral lipid emulsions satisfactorily maintained high levels of both ω-6 and ω-3 LC-PUFAs in infant serum.
“…Total lipids were extracted from milk and FA methyl esters (FAMEs) prepared and analyzed by gas chromatography-mass spectrometry (GC-MS). 18 In accordance with previous studies, no effect of pasteurization on the FA composition was noted. 19,20 Venous blood samples were collected from the infants at birth (cord blood), on postnatal days 1, 7, 14, and 28, and postmenstrual age (PMA) weeks 32, 36, and 40.…”
Section: Methodssupporting
confidence: 92%
“…The results from this analysis are published elsewhere. 18 Frozen, anonymous donor milk samples from 6 mothers were obtained from Moder-smjölkcentralen at Queen Silvia Children’s Hospital. Total lipids were extracted from milk and FA methyl esters (FAMEs) prepared and analyzed by gas chromatography-mass spectrometry (GC-MS).…”
There appears to be no or low correlation between the amount of DHA administered parenterally and levels measured in serum. Whether this observation reflects serum phospholipid fraction only or truly represents the amount of accreted DHA needs to be investigated. None of the parenteral lipid emulsions satisfactorily maintained high levels of both ω-6 and ω-3 LC-PUFAs in infant serum.
“…The more interesting finding was that GGPP depletion was specific detrimental to neonatal mice but not to adult mice. This phenomenon may be explained as that the adult smooth muscle cells of the inducible KO animals is not sensitive to the MVA dysfunction, while perinatal smooth muscle does not, because 1) the accumulated lipid acids from breast milk are toxic to the SMC when they are not metabolized properly (40) ; 2) the perinatal SMC requires a large amount of new membrane that is primarily synthesized by cholesterol or MVA pathway.…”
Section: Discussionmentioning
confidence: 99%
“…Given the accumulated eicosanoids are a pathogenic factor for the inflammation and apoptosis, the neonatal animals in a suckling period would be expected more sensitive to GGPPS deletion because abundant polyunsaturated fatty acids were existed in mother milk (40), whereas the adult animal would be resistant to GGPPS deletion. To validate this expectation, we crossed Ggps1 flox/flox mice with SM22-CreERT2 mice and then examined the phenotypes of adult (Ggps1 SM22KO ) mice.…”
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.
“…After analysis of CEs, the remaining sample was dried under N 2 and subjected to alkaline transesterification using sodium methoxide [27]. Fatty acid methyl esters (FAMEs) were analyzed by gas chromatography–mass spectrometry using an Agilent 7820 gas chromatograph coupled to an Agilent 5975 mass selective detector (Agilent Technologies, USA) [28]. FAMEs were identified by comparing retention time and mass spectra to authentic standards (FAME mixture ME 100, stearidonic acid, adrenic acid, osbond acid, and clupanodonic acid, all from Larodan AB, Solna, Sweden).…”
Background
Recent technical advances in the extraction of dermal interstitial fluid (ISF) have stimulated interest in using this rather unexploited biofluid as an alternative to blood for detection and prediction of disease. However, knowledge about the presence of useful biomarkers for health monitoring in ISF is still limited. In this study, we characterized the lipidome of human suction blister fluid (SBF) as a surrogate for pure ISF and compared it to that of plasma.
Methods
Plasma and SBF samples were obtained from 18 healthy human volunteers after an overnight fast. Total lipids were extracted and analyzed by liquid chromatography-tandem mass spectrometry. One hundred ninety-three lipid species covering 10 complex lipid classes were detected and quantified in both plasma and SBF using multiple reaction monitoring. A fraction of the lipid extract was subjected to alkaline transesterification and fatty acid methyl esters were analyzed by gas chromatography–mass spectrometry.
Results
The total concentration of lipids in SBF was 17% of the plasma lipid concentration. The molar fraction of lipid species within lipid classes, as well as total fatty acids, showed a generally high correlation between plasma and SBF. However, SBF had larger fractions of lysophospholipids and diglycerides relative to plasma, and consequently less diacylphospholipids and triglycerides. Principal component analysis revealed that the interindividual variation in SBF lipid profiles was considerably larger than the within-subject variation between plasma and SBF.
Conclusions
Plasma and SBF lipid profiles show high correlation and SBF could be used interchangeably with blood for the analysis of major lipids used in health monitoring.
Electronic supplementary material
The online version of this article (10.1186/s12944-019-1107-3) contains supplementary material, which is available to authorized users.
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