Energy Metabolism

Energy metabolism is the process of generating energy (ATP) from nutrients such as glucose and fatty acids through pathways such as the glycolysis pathway, the tricarboxylic acid cycle, and the pentose phosphate pathway. Metware Biotechnology’s Energy Metabolism Targeted Metabolomics obtains absolute quantitative results on 68 energy related metabolites from various fluid and tissue samples.

Technology Introduction

Energy metabolism is the process of anaerobic glycolysis and aerobic respiration from nutrients such as glucose and fatty acids for the production of energy (ATP). It is one of the most basic characteristics of life and maintains the basis of cellular function. Energy metabolism, also known as central carbon metabolism (CCM), mainly includes glycolysis pathway (EMP), tricarboxylic acid cycle (TCA), and pentose phosphate pathway (PPP). These pathways cycle through many intermediate compounds to generate energy. Metware Biotechnology uses QTRAP, a triple-quad LC-MS technology, to obtain absolute quantification of 68 metabolites associated with these pathways. One no longer have to guess how the cells or organism is doing, since our assay will help quantifiy their energy uses.

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Technology Features of Energy Targeted Metabolomics Service

Absolute quantification
68 standard curves, r > 0.99;
Wide coverage
the panel covers 68 compounds in the three major pathways;
High sensitivity
AB QTRAP® 6500+ LC-MS/MS,ng/ml concentration can be detected.

Applications of Energy Targeted Metabolomics Service

Applications: Biomarker Screening
Applications: Functional Studies

Reveal metabolic changes associated with the observed phenotype.

Applications: Mechanism Study

Validate mechanism of energy metabolism from your biological system.

List of Metabolites
Index Compounds Class
1 Pyruvic acid Organic acid And Its derivatives
2 Serine Amino acids
3 L-Glutamic acid Amino acids
4 Threonine Amino acids
5 Lysine Amino acids
6 Tyrosine Amino acids
7 Arginine Amino acids
8 Ornithine Amino acids
9 L-Leucine Amino acids
10 Glutamine Amino acid derivatives
11 L-Alanine Amino acids
12 Succinic Acid Organic acid And Its derivatives
13 Alpha-Ketoglutaric Acid Organic acid And Its derivatives
14 L-Asparagine Amino acids
15 Adenine Nucleotide and Its metabolomics
16 Inosine Nucleotide and Its metabolomics
17 3-phenyllactic acid Organic acid And Its derivatives
18 Citric acid Organic acid And Its derivatives
19 Lactate Organic acid And Its derivatives
20 ADP Nucleotide and Its metabolomics

Project Workflow of Energy Targeted Metabolomics Service e

Energy Targeted Metabolism Services Case Study

1) Article Spotlight: S1P defects cause a new entity of cataract, alopecia, oral mucosal disorder, and psoriasis-like syndrome


In this report, the authors discovered a new entity named cataract, alopecia,oral mucosal disorder, and psoriasis-like (CAOP) syndrome in two unrelated and ethnically diverse patients. Furthermore, patient 1 failed to respond to regular treatment. The authors found that CAOP syndrome was caused by an autosomal recessive defect in the mitochondrial membrane-bound transcription factor peptidase/site-1 protease (MBTPS1, S1P). Mitochondrial abnormalities were observed in patient 1 with CAOP syndrome. Furthermore, the authors found that S1P is a novel mitochondrial protein that forms a trimeric complex with ETFA/ETFB. S1P enhances ETFA/ETFB flavination and maintains its stability. Patient S1P variants destabilize ETFA/ETFB, impair mitochondrial respiration, decrease fatty acid b-oxidation activity, and shift mitochondrial oxidative phosphorylation (OXPHOS) to glycolysis. Mitochondrial dysfunction and inflammatory lesions in patient 1 were significantly ameliorated by riboflavin supplementation, which restored the stability of ETFA/ETFB. Our study discovered that mutations in MBTPS1 resulted in a new entity of CAOP syndrome and elucidated the mechanism of the mutations in the new disease.

2) Article Spotlight: Non-oxidative pentose phosphate pathway controls regulatory T cell function by integrating metabolism and epigenetics


Regulatory T (Treg) cells are critical for maintaining immune homeostasis and preventing autoimmunity. Here, the authors show that the non-oxidative pentose phosphate pathway (PPP) regulates Treg function to prevent autoimmunity. Deletion of transketolase (TKT), an indispensable enzyme of non-oxidative PPP, in Treg cells causes a fatal autoimmune disease in mice, with impaired Treg suppressive capability despite regular Treg numbers and normal Foxp3 expression levels. Mechanistically, reduced glycolysis and enhanced oxidative stress induced by TKT deficiency triggers excessive fatty acid and amino acid catabolism,resulting in uncontrolled oxidative phosphorylation and impaired mitochondrial fitness. Reduced α-KG levels as a result of reductive TCA cycle activity leads to DNA hypermethylation, thereby limiting functional gene expression and suppressive activity of TKT-deficient Treg cells. The authors also find that TKT levels are frequently downregulated in Treg cells of people with autoimmune disorders. Our study identifies the non-oxidative PPP as an integrator of metabolic and epigenetic processes that control Treg function.

3) Article Spotlight: Effect of heat and hypoxia stress on mitochondrion and energy metabolism in the gill of hard clam


Aquatic animals suffer from heat and hypoxia stress more frequently due to global climate change and other anthropogenic activities. Heat and hypoxia stress can significantly affect mitochondrial function and energy metabolism. Here, the response and adaptation characteristics of mitochondria and energy metabolism in the gill of the hard clam Mercenaria mercenaria under heat (35 ◦C), hypoxia (0.2 mg/L), and heat plus hypoxia stress (35 ◦C, 0.2 mg/L) after 48 h exposure were investigated. Mitochondrial membrane potentials were depolarized under environmental stress. Mitochondrial fusion, fission and mitophagy played a key role in maintain mitochondrion function. The AMPK subunits showed different expression under environmental stress. Acceleration of  enzyme activities (phosphofructokinase, pyruvate kinase and lactic dehydrogenase) and accumulation of anaerobic metabolites in glycolysis and TCA cycle implied that the anaerobic metabolism might play a key role in providing energy. Accumulation of amino acids might help to increase tolerance under heat and heat combined hypoxia stress. In addition, urea cycle played a key role in amino acid metabolism to prevent ammonia/nitrogen toxicity. This study improved our understanding of the mitochondrial and energy metabolism responses of marine bivalves exposed to environmental stress.


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