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2-Ketoglutaric acid Sale

(Synonyms: α-酮戊二酸; Alpha-Ketoglutaric acid) 目录号 : GC30136

An intermediate in the citric acid cycle

2-Ketoglutaric acid Chemical Structure

Cas No.:328-50-7

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10mM (in 1mL Water)
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1g
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产品描述

α-Ketoglutaric acid is an α-keto acid and a rate-determining metabolic intermediate in the citric acid cycle in its conjugate base form, α-ketoglutarate.1,2 It is formed via oxidative decarboxylation of isocitrate by isocitrate dehydrogenase (IDH), oxidative deamination of glutamate by glutamate dehydrogenase, or by pyridoxal phosphate-dependent transamination.2 α-Ketoglutaric acid is decarboxylated to succinyl-CoA by α-ketoglutarate dehydrogenase, a rate limiting step in the citric acid cycle. It is a precursor of glutamine and glutamate, energy sources for enterocytes and various immune cells, and an antioxidant with roles in immune homeostasis, aging, protein synthesis, and bone development.2,3

1.Krebs, H.A., Salvin, E., and Johnson, W.A.The formation of citric and α-ketoglutaric acids in the mammalian bodyBiochem. J.32(1)113-117(1938) 2.Wu, N., Yang, M., Gaur, U., et al.Alpha-ketoglutarate: Physiological functions and applicationsBiomol. Ther. (Seoul)24(1)1-8(2016) 3.Liu, S., He, L., and Yao, K.The antioxidative function of alpha-ketoglutarate and its applicationsBiomed. Res. Int.3408467(2018)

Chemical Properties

Cas No. 328-50-7 SDF
别名 α-酮戊二酸; Alpha-Ketoglutaric acid
Canonical SMILES OC(=O)CCC(=O)C(O)=O
分子式 C5H6O5 分子量 146.1
溶解度 Water : 50 mg/mL (342.23 mM) 储存条件 Store at -20°C
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1 mM 6.8446 mL 34.2231 mL 68.4463 mL
5 mM 1.3689 mL 6.8446 mL 13.6893 mL
10 mM 0.6845 mL 3.4223 mL 6.8446 mL
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Research Update

α-Ketoglutaric acid ameliorates hyperglycemia in diabetes by inhibiting hepatic gluconeogenesis via serpina1e signaling

Previously, we found that α-ketoglutaric acid (AKG) stimulates muscle hypertrophy and fat loss through 2-oxoglutarate receptor 1 (OXGR1). Here, we demonstrated the beneficial effects of AKG on glucose homeostasis in a diet-induced obesity (DIO) mouse model, which are independent of OXGR1. We also showed that AKG effectively decreased blood glucose and hepatic gluconeogenesis in DIO mice. By using transcriptomic and liver-specific serpina1e deletion mouse model, we further demonstrated that liver serpina1e is required for the inhibitory effects of AKG on hepatic gluconeogenesis. Mechanistically, we supported that extracellular AKG binds with a purinergic receptor, P2RX4, to initiate the solute carrier family 25 member 11 (SLC25A11)-dependent nucleus translocation of intracellular AKG and subsequently induces demethylation of lysine 27 on histone 3 (H3K27) in the seprina1e promoter region to decrease hepatic gluconeogenesis. Collectively, these findings reveal an unexpected mechanism for control of hepatic gluconeogenesis using circulating AKG as a signal molecule.

Alpha-Ketoglutarate, an Endogenous Metabolite, Extends Lifespan and Compresses Morbidity in Aging Mice

Metabolism and aging are tightly connected. Alpha-ketoglutarate is a key metabolite in the tricarboxylic acid (TCA) cycle, and its levels change upon fasting, exercise, and aging. Here, we investigate the effect of alpha-ketoglutarate (delivered in the form of a calcium salt, CaAKG) on healthspan and lifespan in C57BL/6 mice. To probe the relationship between healthspan and lifespan extension in mammals, we performed a series of longitudinal, clinically relevant measurements. We find that CaAKG promotes a longer, healthier life associated with a decrease in levels of systemic inflammatory cytokines. We propose that induction of IL-10 by dietary AKG suppresses chronic inflammation, leading to health benefits. By simultaneously reducing frailty and enhancing longevity, AKG, at least in the murine model, results in a compression of morbidity.

Alpha-Ketoglutarate dietary supplementation to improve health in humans

Alpha-ketoglutarate (AKG) is an intermediate in the Krebs cycle involved in various metabolic and cellular pathways. As an antioxidant, AKG interferes in nitrogen and ammonia balance, and affects epigenetic and immune regulation. These pleiotropic functions of AKG suggest it may also extend human healthspan. Recent studies in worms and mice support this concept. A few studies published in the 1980s and 1990s in humans suggested the potential benefits of AKG in muscle growth, wound healing, and in promoting faster recovery after surgery. So far there are no recently published studies demonstrating the role of AKG in treating aging and age-related diseases; hence, further clinical studies are required to better understand the role of AKG in humans. This review will discuss the regulatory role of AKG in aging, as well as its potential therapeutic use in humans to treat age-related diseases.

α-Ketoglutarate inhibits autophagy

The metabolite α-ketoglutarate is membrane-impermeable, meaning that it is usually added to cells in the form of esters such as dimethyl -ketoglutarate (DMKG), trifluoromethylbenzyl α-ketoglutarate (TFMKG) and octyl α-ketoglutarate (O-KG). Once these compounds cross the plasma membrane, they are hydrolyzed by esterases to generate α-ketoglutarate, which remains trapped within cells. Here, we systematically compared DMKG, TFMKG and O-KG for their metabolic and functional effects. All three compounds similarly increased the intracellular levels of α-ketoglutarate, yet each of them had multiple effects on other metabolites that were not shared among the three agents, as determined by mass spectrometric metabolomics. While all three compounds reduced autophagy induced by culture in nutrient-free conditions, TFMKG and O-KG (but not DMKG) caused an increase in baseline autophagy in cells cultured in complete medium. O-KG (but neither DMKG nor TFMK) inhibited oxidative phosphorylation and exhibited cellular toxicity. Altogether, these results support the idea that intracellular α-ketoglutarate inhibits starvation-induced autophagy and that it has no direct respiration-inhibitory effect.

Cytokine-like Roles for Metabolites in Immunity

Metabolites have functions in the immune system independent of their conventional roles as sources or intermediates in biosynthesis and bioenergetics. We are still in the pioneering phase of gathering information about the functions of specific metabolites in immunoregulation. In this review, we cover succinate, itaconate, α-ketoglutarate, and lactate as examples. Each of these metabolites has a different story of how their immunoregulatory functions were discovered and how their roles in the complex process of inflammation were revealed. Parallels and interactions are emerging between metabolites and cytokines, well-known immunoregulators. We depict molecular mechanisms by which metabolites prime cellular and often physiological changes focusing on intra- and extra-cellular activities and signaling pathways. Possible therapeutic opportunities for immune and inflammatory diseases are emerging.