Metabolic Profiling Analysis of Liver in Landes Geese During the Formation of Fatty Liver via GC-TOF/MS

Fatty liver production results from the process of overfeeding geese, inducing a dramatic increase in de novo liver lipogenesis. To investigate the alteration of liver metabolites by overfeeding, especially lipid metabolites, and the potential pathways causing these changes, 60 Landes geese at 65 days old were raised in three groups with 20 geese per group, namely, the D0 group (free from gavage), D7 group (overfeeding for 7 days), and D25 group (overfeeding for 25 days). At 90 days old, segments of liver tissue were collected from 10 geese of each group for gas chromatography time-of-flight/mass spectrometry (GC-TOF/MS) analysis. A large number of endogenous molecules in the livers of geese were altered dramatically by overfeeding. In the livers of overfed geese, the level of oleic acid was observed to continuously increase, while the levels of phenylalanine, methyl phosphate, sulfuric acid, and 3-hydroxybenzaldehyde were decreased. The most significantly different metabolites were enriched in amino acid, lipid, and nucleotide metabolism pathways. The present study further supports the idea that Landes geese efficiently produce fatty liver, and potential biomarkers and disturbed metabolic pathways during the process of forming fatty liver were identified. In conclusion, this study might provide some insights into the underlying mechanisms of fatty liver formation.

A Metabolic Profiling Analysis Revealed a Primary Metabolism Reprogramming in Arabidopsis glyI4 Loss-of-Function Mutant

Methylglyoxal (MG) is a cytotoxic compound often produced as a side product of metabolic processes such as glycolysis, lipid peroxidation, and photosynthesis. MG is mainly scavenged by the glyoxalase system, a two-step pathway, in which the coordinate activity of GLYI and GLYII transforms it into D-lactate, releasing GSH. In Arabidopsis thaliana, a member of the GLYI family named GLYI4 has been recently characterized. In glyI4 mutant plants, a general stress phenotype characterized by compromised MG scavenging, accumulation of reactive oxygen species (ROS), stomatal closure, and reduced fitness was observed. In order to shed some light on the impact of gly4 loss-of-function on plant metabolism, we applied a high resolution mass spectrometry-based metabolomic approach to Arabidopsis Col-8 wild type and glyI4 mutant plants. A compound library containing a total of 70 metabolites, differentially synthesized in glyI4 compared to Col-8, was obtained. Pathway analysis of the identified compounds showed that the upregulated pathways are mainly involved in redox reactions and cellular energy maintenance, and those downregulated in plant defense and growth. These results improved our understanding of the impacts of glyI4 loss-of-function on the general reprogramming of the plant’s metabolic landscape as a strategy for surviving under adverse physiological conditions.

A metabolic profiling analysis of degenerative intervertebral disc disease in a rabbit model via GC/TOF-MS

The authors have withdrawn this preprint due to author disagreement.

A Serum Metabolic Profiling Analysis During the Formation of Fatty Liver in Landes Geese via Gc-tof/ms

Background:During the process of fatty liver production by overfeeding, the levels of endogenous metabolites in the serumof geese would change dramatically. This study investigated the effects of overfeeding on serum metabolism of Landes geese and the underlying mechanisms using a metabolomics approach.Results:Sixty Landes geese of the same age were randomly divided into the following 3 groups: D0 group (free from gavage); D7 group (overfeeding for 7 days); D25 group (overfeeding for 25 days). The results showed that overfeeding significantly increased the body weight and the liver weight of geese. Serum enzymatic activities and serum lipid levels were significantly enhanced following overfeeding.Gas chromatography time-of-flight/massspectrometry (GC-TOF/MS) was employed to explore the serum metabolic patterns, and to identify potential contributors to the formation of fatty liver and the correlatedmetabolic pathways. A large number of endogenous molecules in serum were altered, especially at the late stage of overfeeding (7 days to 25 days). Continuous elevated levels of pyruvic acid, alanine, proline and beta-glycerophosphoric acid and reduced lactic acid level were observed in the serum of overfed geese. Pathway exploration found that the most of significantly different metabolites were involved in various amino acids metabolism, carbohydrate metabolismand lipid metabolism.Conclusions: These findings pinpoint specific metabolite changes and identify potential biomarkers for early diagnosis of fatty liver disease, as well as provide insights into the perturbation of metabolic pathways involved in fatty liver formation.

Serum biomarkers of the calcium-deficient rats identified by metabolomics based on UPLC/Q-TOF MS/MS

Background: We previously identified the urinary biomarkers to diagnose calcium deficiency and nutritional rickets by ultra-performance liquid chromatography/quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF MS/MS).To further confirm these biomarkers in vivo, we performed serum metabolomics analysis of calcium deficiency.Methods: A calcium-deficient rat model was established with a low-calcium diet for 12 weeks. Serum-metabolomics-based UPLC/Q-TOF MS/MS and multivariate statistical analysis was performed to identify the alterations in metabolites associated with calcium deficiency in rats.Results: Bone mineral density, serum parathyroid hormone and alkaline phosphatase were significantly decreased in the low-calcium diet group (LCG) compared to the normal calcium diet group (NCG). Serum metabolic-profiling analysis could definitively distinguish between the LCG and NCG andidentified25 calcium-deficient biomarkers. Three metabolites (indoxyl sulfate, phosphate, and taurine) of the 25 biomarkers were found in our previous urinary metabolomics study of rats with a calcium deficiency and nutritional rickets. The areas under the curve (AUCs) of these three biomarkers were greater than 0.8, and the combination of any two biomarkers was higher than 0.95.Conclusion: Dietary calcium deficiency induced the alterations of metabolites in the serum of rats, and the three identified biomarkers had relatively high diagnostic values for calcium deficiency in rats.hatase were significantly decreased in the low-calcium diet group (LCG) compared to the normal calcium diet group (NCG). Serum metabolic-profiling analysis could definitively distinguish between the LCG and NCG andidentified25 calcium-deficient biomarkers. Three metabolites (indoxyl sulfate, phosphate, and taurine) of the 25 biomarkers were found in our previous urinary metabolomics study of rats with a calcium deficiency and nutritional rickets. The areas under the curve (AUCs) of these three biomarkers were greater than 0.8, and the combination of any two biomarkers was higher than 0.95. Conclusion Dietary calcium deficiency induced the alterations of metabolites in the serum of rats, and the three identified biomarkers had relatively high diagnostic values for calcium deficiency in rats.