同: glucose 6-phosphate

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the 7th letter of the Roman alphabet (同)g

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/05/08 11:52:49」(JST)

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グルコース-6-リン酸（グルコース-6-リンさん、Glucose-6-phosphate、G6P）とは、6位の炭素がリン酸化したグルコース分子のことである。ロビソンエステルとも言う。細胞中には多量に存在し、細胞に取り込まれたグルコースのほとんどがリン酸化を受けてG6Pになる。

細胞化学の中心的な化合物の一つであるため、G6Pはその後様々な運命をたどる。その始めに、まずは次のどちらかの代謝系に入る。

解糖系
ペントースリン酸経路

またこの他に、G6Pは直接グリコーゲンやデンプンなどの貯蔵多糖に変換されることもある。多細胞動物ではグリコーゲンとして肝臓や筋肉に蓄えられ、その他の多くの生物ではデンプンかグリコーゲン顆粒として細胞間組織に蓄えられる。

G6Pの生産

グルコースから

細胞中ではG6Pはグルコースの6位の炭素をリン酸化することにより作られる。これは多くの生物ではヘキソキナーゼの、高等動物では肝臓中のグルコキナーゼの酵素機能によって触媒される。この反応では1分子のATPが消費される。

グルコースが細胞に取り込まれると直ちにリン酸化が起こるのは、これが拡散してしまうのを防ぐためである。リン酸化により電荷が導入されるので、G6Pは容易に細胞膜を通過することができない。

グリコーゲンから

G6Pは、グリコーゲンの初期分解産物であるグルコース-1-リン酸から、グルコホスホムターゼでリン酸基を転移させることによっても作られる。

運命1:ペントースリン酸経路

NADP⁺ : NADPHの比率が上昇すると、体はNADPHを増産しようとする。この過程でG6Pはデヒドロゲナーゼにより脱水素化される。この可逆過程はペントースリン酸経路の最初の反応であり、この反応によりNADPHとリブロース-5-リン酸が作られ、多くの分子の合成に供される。またDNAの材料であるヌクレオチドが必要になった時にも、G6Pはペントースリン酸経路に回される。

運命2:解糖系

エネルギーや炭素骨格が必要となった場合には、G6Pは解糖系に入れられる。G6Pはまずグルコースリン酸イソメラーゼにより、フルクトース-6-リン酸に変換される。

G6Pから作られたフルクトース-6-リン酸はその後もう1つのリン酸基が付加され、フルクトース-1,6-ビスリン酸になる。2つ目のリン酸基の付加反応は不可逆反応である。そのためこの反応ではG6Pが不可逆的に分解され、解糖系を通じてATP生産のためのエネルギーを作り出す。

運命3:グリコーゲンとして貯蔵

血中糖濃度が高くなると、余分なグルコースは貯蔵されるようになる。グルコースから生成されたG6Pは、引き続いてホスホグルコースムターゼによりG1Pに変換される。G1Pはウリジン三リン酸（UTP）と結合してリン酸基が外れ、UDP-グルコースとなる。この反応は、この反応の過程で生成されるピロリン酸の加水分解に伴って進む。こうして活性化されたUDP-グルコースは、グリコーゲンシンターゼによってグリコーゲン分子の一部となる。これは、グルコース1分子を貯蔵するのに1分子のATPしか消費しないという意味で、非常に効率の良い貯蔵システムである。グリコーゲン合成は、高いストレスがかかるか血中糖濃度が低下するかして、キナーゼによりリン酸化されると停止する。

エネルギーが必要になると、グリコーゲンホスホリラーゼがグリコーゲン鎖から必要なだけ切り出すことができる。切り出された分子はG1Pであるが、ホスホグルコムターゼによってG6Pに変換され、G6Pホスファターゼによってリン酸基が外されてグルコースとなる。グルコースは細胞膜を通り抜け、血流に乗って必要な場所まで運ばれる。

運命4:脱リン酸化され血液中へ放出

肝臓はグルコース-6-ホスファターゼを持ち、解糖系や糖新生でできたグルコース-6-リン酸のリン酸基を外すことができる。こうしてできたグルコースは血液中に放出され、他の細胞に運ばれる。

参考文献

Berg, Jeremy M.; Tymoczko, Stryer (2002). Biochemistry (5th ed.). New York: W.H. Freeman and Company. ISBN 0-7167-3051-0.

Production of glucose 6-phosphate

From glucose

Within a cell, glucose 6-phosphate is produced by phosphorylation of glucose on the sixth carbon. This is catalyzed by the enzyme hexokinase in most cells, and, in higher animals, glucokinase in certain cells, most notably liver cells. One molecule of ATP is consumed in this reaction.

D-Glucose	Hexokinase		α-D-Glucose 6-phosphate

	ATP	ADP

	PO3- 4	H₂O

	Glucose 6-phosphatase

Compound C00031 at KEGG Pathway Database. Enzyme 2.7.1.1 at KEGG Pathway Database. Compound C00668 at KEGG Pathway Database. Reaction R01786 at KEGG Pathway Database.

The major reason for the immediate phosphorylation of glucose is to prevent diffusion out of the cell. The phosphorylation adds a charged phosphate group so the glucose 6-phosphate cannot easily cross the cell membrane.

From glycogen

Glucose-6-phosphate is also produced during glycogenolysis from glucose-1-phosphate, the first product of the breakdown of glycogen polymers.

Pentose phosphate pathway

When the ratio of NADP⁺ : NADPH increases, the body realizes it needs to produce more NADPH (a reducing agent for several reactions like fatty acid synthesis and glutathione reduction in erythrocytes). This will cause the G6P to be dehydrogenated by glucose 6-phosphate dehydrogenase. This reversible reaction is the initial step of the pentose phosphate pathway, which generates the useful cofactor NADPH as well as ribulose-5-phosphate, a carbon source for the synthesis of other molecules. Also, if the body needs nucleotide precursors of DNA for growth and synthesis, G6P will also be dehydrogenated and enter the pentose phosphate pathway.

Glycolysis

If the cell needs energy or carbon skeletons for synthesis then glucose 6-phosphate is targeted for glycolysis. Glucose 6-phosphate is first isomerized to fructose 6-phosphate by phosphoglucose isomerase.

α-D-Glucose 6-phosphate	Phosphoglucose isomerase	β-D-Fructose 6-phosphate





	Phosphoglucose isomerase

Compound C00668 at KEGG Pathway Database. Enzyme 5.3.1.9 at KEGG Pathway Database. Compound C05345 at KEGG Pathway Database. Reaction R00771 at KEGG Pathway Database.

This reaction converts glucose 6-phosphate to fructose 6-phosphate in preparation for phosphorylation to Fructose-1,6-bisphosphate. The addition of the 2nd phosphoryl group to produce Fructose-1,6-bisphosphate is an irreversible step, and so is used to irreversibly target the glucose 6-phosphate breakdown to provide energy for ATP production via glycolysis.

Click on genes, proteins and metabolites below to link to respective articles. ^{[§ 1]}

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|{{{bSize}}}px|alt=Glycolysis and Gluconeogenesis edit|]]

File:WP534.png

Glycolysis and Gluconeogenesis edit

^ The interactive pathway map can be edited at WikiPathways: "GlycolysisGluconeogenesis_WP534".

Storage as glycogen

If blood glucose levels are high, the body needs a way to store the excess glucose. After being converted to G6P, the molecule can be turned into glucose-1-phosphate by phosphoglucomutase. Glucose-1-phosphate can then be combined with uridine triphosphate (UTP) to form UDP-glucose, driven by the hydrolysis of UTP, releasing phosphate. Now, the activated UDP-glucose can add to a growing glycogen molecule with the help of glycogen synthase. This is a very efficient storage mechanism for glucose since it costs the body only 1 ATP to store the 1 glucose molecule and virtually no energy to remove it from storage. It is important to note that glucose-6-phosphate is an allosteric activator of glycogen synthase, which makes sense because when the level of glucose is high the body should store the excess glucose as glycogen. On the other hand, glycogen synthase is inhibited when it is phosphorylated by protein kinase during times of high stress or low levels of blood glucose, via hormone induction by glucagon or adrenaline.

When the body needs glucose for energy, glycogen phosphorylase, with the help of an orthophosphate, can cleave away a molecule from the glycogen chain. The cleaved molecule is in the form of glucose-1-phosphate, which can be converted into G6P by phosphoglucomutase. Next, the phosphoryl group on G6P can be cleaved by glucose-6-phosphatase so that a free glucose can be formed. This free glucose can pass through membranes and can enter the bloodstream to travel to other places in the body.

Dephosphorylation and release into bloodstream

Liver cells express the transmembrane enzyme glucose-6-phosphatase in the endoplasmic reticulum. The catalytic site is found on the lumenal face of the membrane, and removes the phosphate group from glucose-6-phosphate produced during glycogenolysis or gluconeogenesis. Free glucose is transported out of the endoplasmic reticulum via GLUT7 and released into the bloodstream via GLUT2 for uptake by other cells. Muscle cells lack this enzyme, so myofibers use glucose-6-phosphate in their own metabolic pathways such as glycolysis. Importantly, this prevents myocytes from releasing glycogen stores they have obtained into the blood.

References

Berg, Jeremy M.; Tymoczko, Stryer (2002). Biochemistry (5th ed.). New York: W.H. Freeman and Company. ISBN 0-7167-3051-0.

UpToDate Contents

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1. グルコース-6-ホスファターゼ欠損症（糖原病I型、フォンギールケ病） glucose 6 phosphatase deficiency glycogen storage disease i von gierke disease
2. 先天性好中球減少症 congenital neutropenia

English Journal

Galactosylated collagen matrix enhanced in vitro maturation of human embryonic stem cell-derived hepatocyte-like cells.

Ghodsizadeh A1, Hosseinkhani H, Piryaei A, Pournasr B, Najarasl M, Hiraoka Y, Baharvand H.Author information 1Department of Stem Cells and Developmental Biology at the Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, P.O. Box 19395-4644, Tehran, Iran.AbstractDue to their important biomedical applications, functional human embryonic stem cell-derived hepatocyte-like cells (hESC-HLCs) are an attractive topic in the field of stem cell differentiation. Here, we have initially differentiated hESCs into functional hepatic endoderm (HE) and continued the differentiation by replating them onto galactosylated collagen (GC) and collagen matrices. The differentiation of hESC-HE cells into HLCs on GC substrate showed significant up-regulation of hepatic-specific genes such as ALB, HNF4α, CYP3A4, G6P, and ASGR1. There was more albumin secretion and urea synthesis, as well as more cytochrome p450 activity, in differentiated HLCs on GC compared to the collagen-coated substrate. These results suggested that GC substrate has the potential to be used for in vitro maturation of hESC-HLCs.
Biotechnology letters.Biotechnol Lett.2014 May;36(5):1095-106. doi: 10.1007/s10529-014-1454-0. Epub 2014 Feb 22.
Due to their important biomedical applications, functional human embryonic stem cell-derived hepatocyte-like cells (hESC-HLCs) are an attractive topic in the field of stem cell differentiation. Here, we have initially differentiated hESCs into functional hepatic endoderm (HE) and continued the diffe
PMID 24563289

Resolving futile glucose cycling and glycogenolytic contributions to plasma glucose levels following a glucose load.

Nunes PM1, Jarak I, Heerschap A, Jones JG.Author information 1Department of Radiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.AbstractPURPOSE: After a glucose load, futile glucose/glucose-6-phosphate (G6P) cycling (FGC) generates [2-(2) H]glucose from (2) H2 O thereby mimicking a paradoxical glycogenolytic contribution to plasma glucose levels. Contributions of load and G6P derived from gluconeogenesis, FGC, and glycogenolysis to plasma glucose levels need resolution. A simple methodology is proposed integrating the administration of (2) H2 O with a glucose load containing [1-(2) H, 1-(13) C]glucose and [2-(2) H, 2-(13) C]glucose.
Magnetic resonance in medicine : official journal of the Society of Magnetic Resonance in Medicine / Society of Magnetic Resonance in Medicine.Magn Reson Med.2014 Apr;71(4):1368-73. doi: 10.1002/mrm.24789. Epub 2013 May 28.
PURPOSE: After a glucose load, futile glucose/glucose-6-phosphate (G6P) cycling (FGC) generates [2-(2) H]glucose from (2) H2 O thereby mimicking a paradoxical glycogenolytic contribution to plasma glucose levels. Contributions of load and G6P derived from gluconeogenesis, FGC, and glycogenolysis to
PMID 23716355

β-Phosphoglucomutase contributes to aciduricity in Streptococcus mutans.

Buckley AA1, Faustoferri RC, Quivey RG Jr.Author information 1Department of Microbiology & Immunology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.AbstractStreptococcus mutans encounters an array of sugar moieties within the oral cavity due to a varied human diet. One such sugar is β-d-glucose 1-phosphate (βDG1P), which must be converted to glucose 6-phosphate (G6P) before further metabolism to lactic acid. The conversion of βDG1P to G6P is mediated by β-phosphoglucomutase, which has not been previously observed in any oral streptococci, but has been extensively characterized and the gene designated pgmB in Lactococcus lactis. An orthologue was identified in S. mutans, SMU.1747c, and deletion of the gene resulted in the inability of the deletion strain to convert βDG1P to G6P, indicating that SMU.1747c is a β-phosphoglucomutase and should be designated pgmB. In this study, we sought to characterize how deletion of pgmB affected known virulence factors of S. mutans, specifically acid tolerance. The ΔpgmB strain showed a decreased ability to survive acid challenge. Additionally, the strain lacking β-phosphoglucomutase had a diminished glycolytic profile compared with the parental strain. Deletion of pgmB had a negative impact on the virulence of S. mutans in the Galleria mellonella (greater wax worm) animal model. Our results indicate that pgmB plays a role at the juncture of carbohydrate metabolism and virulence.
Microbiology (Reading, England).Microbiology.2014 Apr;160(Pt 4):818-27. doi: 10.1099/mic.0.075754-0. Epub 2014 Feb 7.
Streptococcus mutans encounters an array of sugar moieties within the oral cavity due to a varied human diet. One such sugar is β-d-glucose 1-phosphate (βDG1P), which must be converted to glucose 6-phosphate (G6P) before further metabolism to lactic acid. The conversion of βDG1P to G6P is mediate
PMID 24509501

Japanese Journal

Altered levels of primary metabolites in response to exogenous indole-3-acetic acid in wild type and auxin signaling mutants of Arabidopsis thaliana: A capillary electrophoresis-mass spectrometry analysis

Anegawa Aya,Ohnishi Miwa,Takagi Daisuke [他],Miyake Chikahiro,Shichijo Chizuko,Ishizaki Kimitsune,Fukaki Hidehiro,Mimura Tetsuro
Plant Biotechnology 32(1), 65-79, 2015
… Levels of G6P from the glycolic pathway were altered in WT roots and those of 2PG, 3PG were altered in tir1 shoots in response to IAA treatments. …
NAID 130005061610

Altered levels of primary metabolites in response to exogenous indole-3-acetic acid in wild type and auxin signaling mutants of Arabidopsis thaliana: A capillary electrophoresis-mass spectrometry analysis

Anegawa Aya,Ohnishi Miwa,Takagi Daisuke,Miyake Chikahiro,Shichijo Chizuko,Ishizaki Kimitsune,Fukaki Hidehiro,Mimura Tetsuro
Plant Biotechnology advpub(0), 2015
… Levels of G6P from the glycolic pathway were altered in WT roots and those of 2PG, 3PG were altered in tir1 shoots in response to IAA treatments. …
NAID 130004834262

酵素電極触媒型NADPH酸化反広を共役したペントースリン酸経路の再構成

酒井秀樹,戸木田裕一,辻村清也 [他],白井理,加納健司
電気化学および工業物理化学 : denki kagaku 81(12), 981-984, 2013-12-05
… We re-constructed in vitro pentose phosphate pathway for 24-e oxidation of glucose-6-phosphate (G6P) into CO2 and linked it to mediated bioelectrocatalytic NADPH oxidation system in order to improve the energy density of biofuel cells. … The electrolysis efficiency reached to 40% in the G6P oxidation by adjusting the composition of the enzymes in the pathway. …
NAID 10031203747

Related Pictures

★リンクテーブル★

リンク元	「グルコース6-リン酸」「glucose-6-phosphate」
拡張検索	「G6PD」「G6PD欠損症」
関連記事	「G」

「グルコース6-リン酸」

Glucose 6-phosphate
Names
	IUPAC name D-Glucopyranose 6-phosphate
Identifiers
CAS Registry Number	56-73-5
ChEBI	CHEBI:4170
ChemSpider	17216117
	InChI InChI=1S/C6H11O9P/c7-3-2(1-14-16(11,12)13)15-6(10)5(9)4(3)8/h2-10H,1H2,(H2,11,12,13)/t2-,3-,4+,5-,6?/m1/s1 ; Key: NBSCHQHZLSJFNQ-GASJEMHNSA-N ; InChI=1/C6H11O9P/c7-3-2(1-14-16(11,12)13)15-6(10)5(9)4(3)8/h2-10H,1H2,(H2,11,12,13)/t2-,3-,4+,5-,6u/m1/s1; Key: NBSCHQHZLSJFNQ-SEZHTIIRBF ;
Jmol-3D images	Image
MeSH	Glucose-6-phosphate
PubChem	208
	SMILES O[C@H]1[C@H](O)[C@@H](COP(O)(O)=O)OC(O)[C@@H]1O ;
Properties
Chemical formula	C6H13O9P
Molar mass	260.136
	Except where noted otherwise, data is given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
	verify (what is: /?)
	Infobox references

グルコース-6-リン酸
	IUPAC名 D-Glucopyranose 6-phosphate
	別称ロビソンエステル
識別情報
CAS登録番号	56-73-5
PubChem	208
ChemSpider	17216117
日化辞番号	J40.066A
KEGG	C00092
MeSH	Glucose-6-phosphate
ChEBI	CHEBI:4170
	SMILES O[C@H]1[C@H](O)[C@@H](COP(O)(O)=O)OC(O)[C@@H]1O;
	InChI InChI=1S/C6H13O9P/c7-3-2(1-14-16(11,12)13)15-6(10)5(9)4(3)8/h2-10H,1H2,(H2,11,12,13)/t2-,3-,4+,5-,6?/m1/s1; Key: NBSCHQHZLSJFNQ-GASJEMHNSA-N InChI=1/C6H13O9P/c7-3-2(1-14-16(11,12)13)15-6(10)5(9)4(3)8/h2-10H,1H2,(H2,11,12,13)/t2-,3-,4+,5-,6u/m1/s1; Key: NBSCHQHZLSJFNQ-SEZHTIIRBF;
特性
化学式	C6H13O9P
モル質量	260.136
	特記なき場合、データは常温 (25 °C)・常圧 (100 kPa) におけるものである。

　　[★]

英: glucose 6-phosphate, G6P, G-6-P
同: グルコース-6-リン酸 glucose-6-phosphate
関: グルコース1-リン酸、グルコース、解糖系、糖新生