Mass spectrometry-based metabolomic profiling identifies alterations in salivary redox status and fatty acid metabolism in response to inflammation and oxidative stress in periodontal disease

Huang, Yijing; Zhu, Mingyang; Li, Zi; Sa, Rina; Chu, Qianli; Zhang, Qingli; Zhang, Haifeng; Tang, Wenqi; Zhang, Meifang; Yin, Huiyong

doi:10.1016/j.freeradbiomed.2014.02.024

Cited by 74 publications

(71 citation statements)

References 48 publications

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“…FAMEs were separated by gas chromatography (Agilent 6890 GC; SP-2560 capillary column: 100 m × 0.25 mm internal diameter × 0.2 μm film; Supelco). Individual FAMEs were identified by positive chemical ionization with the use of methane as the reagent gas (Agilent 5975B) [38,39]. …”

Section: Methodsmentioning

confidence: 99%

Regulation of fatty acid composition and lipid storage by thyroid hormone in mouse liver

et al. 2014

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BackgroundThyroid hormones (THs) are potent hormones modulating liver lipid homeostasis. The perturbation of lipid homeostasis is a hallmark of non-alcoholic fatty liver disease (NAFLD), a very common liver disorder. It was reported that NAFLD patients were associated with higher incidence of hypothyroidism. However, whether abnormal thyroid function contributes to the pathogenesis of NAFLD remains unclear.ResultsWe used in vivo models to investigate the influence of hypothyroidism and TH on hepatic lipid homeostasis. We did not observe hepatic triglyceride accumulation in the liver of hypothyroid mice, although the liver was enlarged. We then characterized the hepatic fatty acid composition with gas chromatography–mass spectrometry in mice under different thyroid states. We found that hypothyroidism decreased saturated fatty acid (SFA) content while TH treatment restored the level of SFA. In agreement with this finding, we observed that the expression of acetyl-CoA carboxylase 1 and fatty acid synthase, the rate-limit enzymes for de novo lipogenesis (DNL), decreased in hypothyroid mice while increased after TH treatment. We also found that the ratio of C18:1n-9/C18:0 and C16:1n-7/C16:0 was decreased by TH treatment, suggesting the activity of stearoyl-CoA desaturase-1 was suppressed. This finding indicated that TH is able to suppress triglyceride accumulation by reducing fatty acid desaturation. Additionally, we found that hepatic glycogen content was substantially influenced by TH status, which was associated with glycogen synthase expression. The increased glycogen storage might explain the enlarged liver we observed in hypothyroid mice.ConclusionsTaken together, our study here suggested that hypothyroidism in mice might not lead to the development of NAFLD although the liver became enlarged. However, disturbed TH levels led to altered hepatic fatty acid composition and glycogen accumulation.

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Section: Methodsmentioning

confidence: 99%

Regulation of fatty acid composition and lipid storage by thyroid hormone in mouse liver

et al. 2014

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“…A recent study examined the oxylipins from human periodontitis samples and found inflammatory markers including increased prostaglandins and leukotrienes (Huang, et al, 2014). EETs and diols were also measured in this study but did not exhibit as much change.…”

Section: Seh As a Target For Inflammatory Diseasesmentioning

confidence: 99%

Soluble epoxide hydrolase as a therapeutic target for pain, inflammatory and neurodegenerative diseases

Wagner

McReynolds

Schmidt

et al. 2017

Pharmacology & Therapeutics

201

192

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Eicosanoids are biologically active lipid signaling molecules derived from polyunsaturated fatty acids. Many of the actions of eicosanoid metabolites formed by cyclooxygenase and lipoxygenase enzymes have been characterized, however, the epoxy-fatty acids (EpFAs) formed by cytochrome P450 enzymes are newly described by comparison. The EpFA metabolites modulate a diverse set of physiologic functions that include inflammation and nociception among others. Regulation of EpFAs occurs primarily via release, biosynthesis and enzymatic transformation by the soluble epoxide hydrolase (sEH). Targeting sEH with small molecule inhibitors has enabled observation of the biological activity of the EpFAs in vivo in animal models, greatly contributing to the overall understanding of their role in the inflammatory response. Their role in modulating inflammation has been demonstrated in disease models including cardiovascular pathology and inflammatory pain, but extends to neuroinflammation and neuroinflammatory disease. Moreover, while the EpFA demonstrate activity against inflammatory pain, interestingly, this action extends to blocking chronic neuropathic pain as well. This review outlines the role of modulating sEH and the biological action of EpFA in models of pain and inflammatory diseases.

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“…Both short-term [74] and long-term follow-up of metabolite profiles show that 'metabolic individuality' is preserved in a significant proportion of people [75]. Measurement of metabolic profiles of urine [76], blood serum/plasma [77,78], faecal [79] and saliva samples using high-throughput proton nuclear magnetic resonance spectroscopy ( 1 H NMR) [80,81] or mass spectrometry (MS) [82][83][84] are untargeted (requiring no knowledge of metabolites present) or targeted [85]. Large amounts of data are produced requiring sophisticated statistical analysis, but the end result is either a 'metabolic footprint' or lists of metabolites and relative abundances and allowing for metabolic phenotyping in health and disease [86,87].…”

Section: Metabolomics In Ramentioning

confidence: 99%

Lipid and Metabolic Changes in Rheumatoid Arthritis

McGrath

Young

2015

Curr Rheumatol Rep

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While the most obvious manifestations of rheumatoid arthritis (RA) involve inflammation and damage in the synovial joints, the systemic effects of the condition are widespread and life-threatening. Of particular interest is the 'lipid paradox' of RA, where patients with a numerically equivocal starting lipid profile have a significantly raised risk of cardiovascular (CV) events and response to therapy results in a 'normalization' of lipid levels and reduction in events. Changes in lipids can be seen before overt disease manifestations which suggest that they are closely linked to the more widespread inflammation-driven metabolic changes associated with tumour necrosis factor (TNF). Cachexia involves a shift in body mass from muscle to fat, which may or may not directly increase the cardiovascular risk. However, since TNF inhibition is associated with reduction in cardiovascular events, it does suggest that these widespread metabolic changes involving lipids are of importance. Analysis of single lipids or metabolites have been used to identify some of the key changes, but more recently, metabolomic and lipidomic approaches have been applied to identify a broad spectrum of small molecule changes and identify potentially altered metabolic pathways. Further work is needed to understand fully the metabolic changes in lipid profiles and identify novel ways of targeting desired profile changes, but work so far does suggest that a better understanding may allow management of patients to downregulate the systemic effects of their disease that puts them at risk of cardiovascular complications.

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Mass spectrometry-based metabolomic profiling identifies alterations in salivary redox status and fatty acid metabolism in response to inflammation and oxidative stress in periodontal disease

Cited by 74 publications

References 48 publications

Regulation of fatty acid composition and lipid storage by thyroid hormone in mouse liver

Regulation of fatty acid composition and lipid storage by thyroid hormone in mouse liver

Soluble epoxide hydrolase as a therapeutic target for pain, inflammatory and neurodegenerative diseases

Lipid and Metabolic Changes in Rheumatoid Arthritis

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