Sex Dependency of Human Metabolic Profiles Revisited

Siegert, Sabine

doi:10.4172/2153-0769.1000115

Cited by 5 publications

(5 citation statements)

References 22 publications

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“…Among obtained metabotypes, it is interesting to note that the level of all acylcarnitines was higher in castrated males than in intact gilts. This result already has been observed comparing plasma and serum concentration of acylcarnitines in men and women (Slupsky et al, 2007;Reuter et al, 2008;Mittelstrass et al, 2011;Siegert et al, 2012). Mihalik et al (2010) reported that increased levels of several acylcarnitines were pres-ent in the plasma of obese individuals and in men and women with type 2 diabetes.…”

Section: Discussionsupporting

confidence: 57%

“…A total of 132 out of 186 analyzed metabolites (71%) passed the quality control step. It is worth mentioning that the CV% threshold that was used in our study (CV% = 20) is more stringent than that was used by previous studies performed with the same AbsoluteIDQ metabolomic platform in human plasma or serum (CV% = 25 or 30; Mittelstrass et al, 2011;Siegert et al, 2012). In this way, we wanted to be very conservative and prefiltered the data set to maximize the potentials of the statistical pipelines that rely only on the metabolites less affected by analytical or technical factors that could increase the variability in the quantification.…”

Section: Metabolomic Datamentioning

confidence: 98%

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Deconstructing the pig sex metabolome: Targeted metabolomics in heavy pigs revealed sexual dimorphisms in plasma biomarkers and metabolic pathways1

Bovo

Mazzoni

Calò

et al. 2015

Journal of Animal Science

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Metabolomics has opened new possibilities to investigate metabolic differences among animals. In this study, we applied a targeted metabolomic approach to deconstruct the pig sex metabolome as defined by castrated males and entire gilts. Plasma from 545 performance-tested Italian Large White pigs (172 castrated males and 373 females) sampled at about 160 kg live weight were analyzed for 186 metabolites using the Biocrates AbsoluteIDQ p180 Kit. After filtering, 132 metabolites (20 AA, 11 biogenic amines, 1 hexose, 13 acylcarnitines, 11 sphingomyelins, 67 phosphatidylcholines, and 9 lysophosphatidylcholines) were retained for further analyses. The multivariate approach of the sparse partial least squares discriminant analysis was applied, together with a specifically designed statistical pipeline, that included a permutation test and a 10 cross-fold validation procedure that produced stability and effect size statistics for each metabolite. Using this approach, we identified 85 biomarkers (with metabolites from all analyzed chemical families) that contributed to the differences between the 2 groups of pigs ( < 0.05 at the stability statistic test). All acylcarnitines and almost all biogenic amines were higher in castrated males than in gilts. Metabolites involved in tryptophan catabolism had the largest differences (i.e., delta = 20% for serotonin) between castrated males (higher) and gilts (lower). The level of several AA (Ala, Arg, Gly, His, Lys, Ser, Thr, and Trp) was higher in gilts (delta was from approximately 1.0 to approximately 4.8%) whereas products of AA catabolism (taurine, 2-aminoadipic acid, and methionine sulfoxide) were higher in castrated males (delta was approximately 5.0-6.0%), suggesting a metabolic shift in castrated males toward energy storage and lipid production. Similar general patterns were observed for most sphingomyelins, phosphatidylcholines, and lysophosphatidylcholines. Metabolomic pathway analysis and pathway enrichment identified several differences between the 2 sexes. This metabolomic overview opened new clues on the biochemical mechanisms underlying sexual dimorphism that, on one hand, might explain differences in terms of economic traits between castrated male pigs and entire gilts and, on the other hand, could strengthen the pig as a model to define metabolic mechanisms related to fat deposition.

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Section: Discussionsupporting

confidence: 57%

Section: Metabolomic Datamentioning

confidence: 98%

Deconstructing the pig sex metabolome: Targeted metabolomics in heavy pigs revealed sexual dimorphisms in plasma biomarkers and metabolic pathways1

Bovo

Mazzoni

Calò

et al. 2015

Journal of Animal Science

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“…Strengths of this study include the biochemical analyses in a relatively large cohort of male and female mice, which enabled us to analyse the effects of genotype, sex and their interaction. Sexual dimorphism in plasma acylcarnitine concentrations have been reported, [30][31][32] but effects of sex on tissue (acyl)carnitine levels are unexplored. We observed sexual dimorphism for the levels of many acylcarnitines in particular in the kidney, an organ known to have high degree of sexually dimorphic gene expression.…”

Section: Discussionmentioning

confidence: 99%

Slc22a5 haploinsufficiency does not aggravate the phenotype of the long‐chain acyl‐CoA dehydrogenase KO mouse

Ranea-Robles

Vlies

et al. 2019

J of Inher Metab Disea

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Secondary carnitine deficiency is commonly observed in inherited metabolic diseases characterised by the accumulation of acylcarnitines such as mitochondrial fatty acid oxidation (FAO) disorders. It is currently unclear if carnitine deficiency and/or acylcarnitine accumulation play a role in the pathophysiology of FAO disorders. The long-chain acyl-CoA dehydrogenase (LCAD) KO mouse is a model for long-chain FAO disorders and is characterised by decreased levels of tissue and plasma free carnitine. Tissue levels of carnitine are controlled by SLC22A5, the plasmalemmal carnitine transporter. Here, we have further decreased carnitine availability in the LCAD KO mouse through a genetic intervention by introducing one defective Slc22a5 allele (jvs). Slc22a5 haploinsufficiency decreased free carnitine levels in liver, kidney, and heart of LCAD KO animals. The resulting decrease in the tissue long-chain acylcarnitines levels had a similar magnitude as the decrease in free carnitine.Levels of cardiac deoxycarnitine, a carnitine biosynthesis intermediate, were elevated due to Slc22a5 haploinsufficiency in LCAD KO mice. A similar increase in heart and muscle deoxycarnitine was observed in an independent experiment using Slc22a5 jvs/jvs mice. Cardiac hypertrophy, fasting-induced hypoglycemia and increased liver weight, the major phenotypes of the LCAD KO mouse, were not affected by Slc22a5 haploinsufficiency. This may suggest that secondary carnitine deficiency does not play a major role in the pathophysiology of these phenotypes. Similarly, our data do not support a major role for toxicity of longchain acylcarnitines in the phenotype of the LCAD KO mouse. K E Y W O R D S biosynthesis, carnitine, fatty acid oxidation disorders, haploinsufficiency, modifier

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“…We analysed the association of age with metabolites by linear regression, in which the metabolite concentration was extrapolated to age zero years and was set to 100%. In addition, the interaction of age with sex was checked due to indications of sexual dimorphism in the metabolome [20]. This was done by adding an interaction term between age and sex.…”

Section: Statistical Analysesmentioning

confidence: 99%

The Association of Acylcarnitines and Amino Acids With Age in Dutch and South-Asian Surinamese Living in Amsterdam

Muilwijk

Vaz

Celis‐Morales

et al. 2018

The Journal of Clinical Endocrinology &Amp; Metabolism

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Sex Dependency of Human Metabolic Profiles Revisited

Cited by 5 publications

References 22 publications

Deconstructing the pig sex metabolome: Targeted metabolomics in heavy pigs revealed sexual dimorphisms in plasma biomarkers and metabolic pathways1

Deconstructing the pig sex metabolome: Targeted metabolomics in heavy pigs revealed sexual dimorphisms in plasma biomarkers and metabolic pathways1

Slc22a5 haploinsufficiency does not aggravate the phenotype of the long‐chain acyl‐CoA dehydrogenase KO mouse

The Association of Acylcarnitines and Amino Acids With Age in Dutch and South-Asian Surinamese Living in Amsterdam

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