Amino acids serve as the building blocks of life, which are directly or indirectly linked to all human diseases and health conditions. Within the body, amino acid metabolism maintains a dynamic equilibrium, with blood amino acids acting as the central pivot and the liver playing a pivotal role in regulating their levels. The development and progression of various ailments, spanning cardiovascular, renal, diabetic, oncologic, geriatric, and neurologic disorders, can result in disturbances to amino acid metabolism and serum amino acid concentrations. Meanwhile, there are over 400 recognized diseases stem from compromised amino acid metabolism. Amino acid testing has evolved into an indispensable diagnostic and disease screening tool, concurrently serving as a reference standard for nutritional supplementation, overall nutritional well-being enhancement, and early disease prevention in all populations. At Metware Bio, we've established an LC-MS/MS-based platform designed for the comprehensive analysis of 94 amino acids and their metabolites, allowing precise targeting and quantification.
● Early diagnosis of disease
● Metabolic Disease: Type 2 Diabetes,Obesity
● Neuropathic Disease
● Cardiovascular Disorders(CVD)
● Gastrointestinal Disease
● Nutrition and Health
● Cancer
● Drug development
● Food scientific research
Amino Acid Compounds | ||
2-Aminoethanesulfonic Acid | Sarcosine | γ-Glutamate-Cysteine |
L-Cystine | L-Pipecolic Acid | Nα-Acetyl-L-glutamine |
1,3-Dimethyluric Acid | L-Theanine | N-Acetyl-L-Tyrosine |
N-Propionylglycine | Ethanolamine | γ-Aminobutyric Acid |
N-Isovaleroylglycine | 3-N-Methyl-L-Histidine | D-Alanyl-D-Alanine |
Succinic Acid | Homoserine | Guanidinoethyl Sulfonate |
5-Hydroxy-tryptophan | Creatine | Homo-L-arginine |
3,7-Dimethyluric Acid | Kinurenine | L-Tryptophyl-L-glutamic acid |
Glycine | L-Cystathionine | Nicotinuric Acid |
L-Alanine | 5-Aminovaleric Acid | N-Acetylneuraminic Acid |
L-Valine | N6-Acetyl-L-Lysine | N,N-Dimethylglycine |
L-Leucine | Phosphorylethanolamine | 4-Acetamidobutyric Acid |
L-Methionine | Anserine | L-Carnosine |
L-Isoleucine | Trans-4-Hydroxy-L-Proline | 6-Aminocaproic Acid |
L-Proline | D-Homocysteine | 3-Chloro-L-Tyrosine |
L-Serine | α-Aminoadipic acid | S-(5-Adenosy)-L-Homocysteine |
L-Tryptophan | L-Ornithine | Kynurenic Acid |
L-Phenylalanine | L-tyrosine methyl ester | N'-Formylkynurenine |
L-Tyrosine | 2-Aminobutyric acid | Urea |
L-Cysteine | (5-L-Glutamyl)-L-Amino Acid | argininosuccinic acid |
L-Glutamic acid | 3-Iodo-L-Tyrosine | 5-Hydroxylysine |
L-Aspartate | P-Aminohippuric Acid | O-Phospho-L-Serine |
L-Asparagine Anhydrous | Glycyl-L-Proline | N-Acetylaspartate |
L-Glutamine | Trimethylamine N-Oxide | L-Homocystine |
L-Lysine | 1,3,7-Trimethyluric Acid | 3-Aminoisobutanoic Acid |
L-Histidine | 3-Hydroxyhippuric Acid | Glutathione Oxidized |
L-Arginine | N8-Acetylspermidine | L-α-Aspartyl-L-phenylalanine |
L-Threonine | (S)-β-Aminoisobutyric Acid | N-Glycyl-L-Leucine |
L-Citrulline | S-Sulfo-L-Cysteine | Creatine Phosphate |
5-Hydroxy-Tryptamine | Methionine Sulfoxide | glycylphenylalanine |
L-Homocitrulline | Nα-Acetyl-L-Arginine | 1-Methylhistidine |
Beta-Alanine |
Abstract
Intracellular zinc ion (Zn2+) accumulation disrupts the Zn2+ homeostasis, providing an ion-overloading anticancer strategy with great potential. The self-adaptation of tumor cells to ion concentration, however, puts forward higher requirements for the design of ion-overloading strategy. Herein, “block and attack” antitumor strategy was applied through a composite nanomaterials (UHSsPZH NPs). The strategy demonstrated powerful ion interference ability through both “blocking” the efflux of excess Zn2+ via gene silencing and “attacking” tumor cells via target deliveryof ZnO2. After cellular internalization, ZnO2 was degraded to Zn2+ and hydrogen peroxide (H2O2), and the gene expression of zinc transporter 1 (ZnT1) was silenced by targeting of released siRNA, which together caused intracellular Zn2+-overload.Disorder of Zn2+ further interfered with intracellular Ca2+ homeostasis, inhibited the electron transport chain and promoted the production of endogenous reactive oxygen species (ROS), which assisted the “attack” to tumor cells together with the exogenous ROS generated by UHSsPZH NPs under 980 nm laser irradiation. In summary, this work supplies a “block and attack” strategy for the application of ion homeostasis interference in tumor therapy.
Abstract
Rearing silkworms (Bombyx mori) using formula feed has revolutionized traditional mulberry feed strategies. However, low silk production efficiencies persist and have caused bottlenecks, hindering the industrial application of formula feed sericulture. Here, we investigated the effects of formula feed amino acid composition on silk yields. We showed that imbalanced amino acids reduced DNA proliferation, decreased Fib-H, Fib-L, and P25 gene expression, and caused mild autophagy in the posterior silk gland, reducing cocoon shell weight and ratio. When compared with mulberry leaves, Gly, Ala, Ser, and Tyr percentages of total amino acids in formula feed were decreased by 5.26%, while Glu and Arg percentages increased by 9.56%. These changes increased uric acid and several amino acids levels in the hemolymph of silkworms on formula feed. Further analyses showed that Gly and Thr (important synthetic Gly sources) increased silk yields, with Gly increasing amino acid conversion efficiencies to silk protein, and reducing urea levels in hemolymph. Also, Gly promoted endomitotic DNA synthesis in silk gland cells via phosphoinositide 3-kinase (PI3K)/Akt/target of rapamycin (TOR) signaling. In this study, we highlighted the important role of Gly in regulating silk yields in silkworms.
Abstract
Extracellular vesicles (EVs) play an important role in human and bovine milk composition. According to excellent published studies, it also exerts various functions in the gut, bone, or immune system. However, the effects of milk-derived EVs on skeletal muscle growth and performance have yet to be fully explored. Firstly, the current study examined the amino acids profile in human milk EVs (HME) and bovine milk EVs (BME) using targeted metabolomics. Secondly, HME and BME were injected in the quadriceps of mice for four weeks (1 time/3 days). Then, related muscle performance, muscle growth markers/pathways, and amino acids profile were detected or measured by grip strength analysis, rotarod performance testing, Jenner-Giemsa/H&E staining, Western blotting, and targeted metabolomics, respectively. Finally, HME and BME were co-cultured with C2C12 cells to detect the above-related indexes and further testify relative phenomena. Our findings mainly demonstrated that HME and BME significantly increase the diameter of C2C12 myotubes. HME treatment demonstrates higher exercise performance and muscle fiber densities than BME treatment. Besides, after KEGG and correlation analyses with biological function after HME and BME treatment, results showed L-Ornithine acts as a "notable marker" after HME treatment to affect mouse skeletal muscle growth or functions. Otherwise, L-Ornithine also significantly positively correlates with the activation of the AKT/mTOR pathway and myogenic regulatory factors (MRFs) and can also be observed in muscle and C2C12 cells after HME treatment. Overall, our study not only provides a novel result for the amino acid composition of HME and BME, but the current study also indicates the advantage of human milk on skeletal muscle growth and performance.
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