Age-related distributions of nine fasting plasma free fatty acids in a population of Chinese adults

Shen, Fan; Qi, Jia-Hui; Xu, Fei; Ning, Leping; Pang, Roberta; Zhou, Xin; Liu, Song-Mei

doi:10.1016/j.cca.2012.10.001

Cited by 5 publications

(4 citation statements)

References 33 publications

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“…Statistic analysis indicated that gender-specific difference was observed neither in the levels of twelve serum TFAs in each physiopathological state nor between three physiopathological states ( Supplementary Table S3 ). It is worth noting that age-specific differences were only detected in the levels of some TFAs including C 18:2 , C 20:2 , C 20:3 , C 20:4 , C 20:5 , and C 22:6 in HCs and C 18:3 in BLD patients ( Supplementary Tables S4 and S5 ), while for LC patients, no age-specific differences was observed, which are in line with previous reports 19 34 . Our findings indicate that different metabolic mechanisms between HC, BLDs, and LC might exist.…”

Section: Discussionsupporting

confidence: 91%

Simultaneous Quantification of Serum Nonesterified and Esterified Fatty Acids as Potential Biomarkers to Differentiate Benign Lung Diseases from Lung Cancer

Ren

Zhang

Liu

et al. 2016

Sci Rep

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In this study, we have employed graphene oxide as a matrix to simultaneously and directly quantify serum nonesterified and esterified fatty acids (FAs) using matrix-assisted laser/desorption ionization-Fourier transform ion cyclotron resonance mass spectrometry (MALDI-FTICR MS). Twelve serum nonesterified FAs combined with their individual esterified FAs (i.e., C16:0, C16:1, C18:0, C18:1, C18:2, C18:3, C20:2, C20:3, C20:4, C20:5, C22:5, and C22:6) were quantified based on their calibration curves with the correlation coefficients of >0.99, along with the analytical time of <1 min each sample. As a result, serum levels of twelve total FAs (TFAs) in 1440 serum samples from 487 healthy controls (HCs), 479 patients with benign lung diseases (BLDs) and 474 patients with lung cancer (LC) were determined. Statistical analysis indicated that significantly increased levels of C16:0, C16:1, C18:0, C18:1, C18:3, C20:3, and C22:6 and decreased levels of C20:5 were observed in LC patients compared with BLDs. Receiver operating characteristic (ROC) analysis revealed that panel a (C18:2, C20:3, C20:4, C20:5, C22:5, and C22:6), panel b (C18:0, C20:4, C20:5, and C22:6), and panel c (C16:1, C18:0, C18:1, C20:3, and C22:6) have exhibited good diagnostic ability to differentiate BLDs from LC relative to clinical uses of tumor markers (CEA and Cyfra 21-1).

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Section: Discussionsupporting

confidence: 91%

Simultaneous Quantification of Serum Nonesterified and Esterified Fatty Acids as Potential Biomarkers to Differentiate Benign Lung Diseases from Lung Cancer

Ren

Zhang

Liu

et al. 2016

Sci Rep

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“…However, it is unclear whether similar glucolipotoxic threshold levels are attained in vivo. There is a wide range of plasma PA levels in healthy individuals and the levels are altered significantly in various diseases but barely reach the in vitro threshold levels reported here [42][43][44]. Therefore, clinical and population-based studies are needed to ascertain the relevant in vivo glucolipotoxic threshold levels in relation to beta cell pathophysiology.…”

Section: Discussionmentioning

confidence: 99%

Beta cell response to nutrient overload involves phospholipid remodelling and lipid peroxidation

et al. 2015

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Aims/hypothesis Membrane phospholipids are the major intracellular source for fatty acid-derived mediators, which regulate myriad cell functions. We showed previously that high glucose levels triggered the hydrolysis of polyunsaturated fatty acids from beta cell phospholipids. These fatty acids were subjected to free radical-catalysed peroxidation to generate the bioactive aldehyde 4-hydroxy-2E-nonenal (4-HNE). The latter activated the nuclear peroxisome proliferator-activated receptor-δ (PPARδ), which in turn augmented glucosestimulated insulin secretion. The present study aimed at investigating the combined effects of glucose and fatty acid overload on phospholipid turnover and the subsequent generation of lipid mediators, which affect insulin secretion and beta cell viability. Methods INS-1E cells were incubated with increasing glucose concentrations (5-25 mmol/l) without or with palmitic acid (PA; 50-500 μmol/l) and taken for fatty acid-based lipidomic analysis and functional assays. Rat isolated islets of Langerhans were used similarly. Results PA was incorporated into membrane phospholipids in a concentration-and time-dependent manner; incorporation was highest at 25 mmol/l glucose. This was coupled to a rapid exchange with saturated, mono-unsaturated and polyunsaturated fatty acids. Importantly, released arachidonic acid and linoleic acid were subjected to peroxidation, resulting in the generation of 4-HNE, which further augmented insulin secretion by activating PPARδ in beta cells. However, this adaptive increase in insulin secretion was abolished at high glucose and PA levels, which induced endoplasmic reticulum stress, apoptosis and cell death. Conclusions/interpretation These findings highlight a key role for phospholipid remodelling and fatty acid peroxidation in mediating adaptive and cytotoxic interactions induced by nutrient overload in beta cells.

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“…Thus, it is important to explore risk factors of T2D, CAD and T2D&CAD: these factors include obesity, metabolic syndrome, family history of T2D or CAD, impaired glucose tolerance, low physical activity, increased plasma triglycerides (TG), and decreased HDL-cholesterol [ 5 – 7 ]. Of these risk factors, plasma fatty acid composition is of particular interest because of the role of plasma fatty acids in normal and pathophysiologic responses [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in FADS1 and FADS2 alter plasma fatty acids and desaturase levels in type 2 diabetic patients with coronary artery disease

Wang

Yang

et al. 2016

J Transl Med

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BackgroundTo explore whether plasma fatty acids and SNPs in the fatty acid desaturase (FADS) gene associated with type 2 diabetes (T2D) and coronary artery disease (CAD).MethodsIn this cross-sectional study, we utilized gas chromatography–mass spectrometric analysis and the high-resolution melting method to detect plasma fatty acids and SNPs respectively (rs174537G>T, rs174616C>T, rs174460T>C, and rs174450A>C) in 234 T2D, 200 CAD, 185 T2D&CAD patients, and 253 healthy controls.ResultsWe found that T2D&CAD patients had the highest plasma arachidonic acid, dihomo-gamma-linolenic acid and delta-6 desaturase, and the lowest stearic acid, linolenic acid, and saturated fatty acids; plasma eicosapentaenoic acid and docosahexaenoic acid elevated in T2D patients, but significantly reduced in CAD patients. Moreover, T2D patients with rs174537 GG genotype were at risk of developing T2D&CAD (odds ratio (OR) 1.763; 95 % CI 1.143–2.718; p = 0.010), with elevated plasma LDL-cholesterol, arachidonic acid, and delta-6 desaturase.ConclusionsOur results show that SNPs in FADS gene (particularly rs174537) associate with plasma fatty acids and desaturase levels in patients with both T2D and CAD, which maybe increases the risk of CAD in diabetic patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-0834-8) contains supplementary material, which is available to authorized users.

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Age-related distributions of nine fasting plasma free fatty acids in a population of Chinese adults

Cited by 5 publications

References 33 publications

Simultaneous Quantification of Serum Nonesterified and Esterified Fatty Acids as Potential Biomarkers to Differentiate Benign Lung Diseases from Lung Cancer

Simultaneous Quantification of Serum Nonesterified and Esterified Fatty Acids as Potential Biomarkers to Differentiate Benign Lung Diseases from Lung Cancer

Beta cell response to nutrient overload involves phospholipid remodelling and lipid peroxidation

Polymorphisms in FADS1 and FADS2 alter plasma fatty acids and desaturase levels in type 2 diabetic patients with coronary artery disease

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