Глюкоза

Источники

1. Справочное издание

   Ragueneau E, Gong C, Sinquin P, Sevilla C, Beavers D, Grentner A, et al. The Reactome Knowledgebase 2026 Nucleic Acids Research, 2026.

   doi:10.1093/nar/gkaf1223PubMed 41251150

   Финансирование и результат

   Финансирование

   The development of Reactome is supported by grants from the National Institutes of Health (U24HG012198 and U24HG012198-02S1 for Core Trust Seal development; U24HG011851), European Bioinformatics Institute (EMBL-EBI), Open Targets (The Target Validation Platform), and Connected Minds Prototyping (York University). Funding to pay the Open Access publication charges for this article was provided by the National Institutes of Health (U24HG012198). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

   Результат

   Human pathway and reaction summations of release 97, read through reactome.org/ContentService on 2026-10-21. Digestion of dietary carbohydrate (R-HSA-189085): salivary and intestinal amylases convert starch to maltotriose, maltose, limit dextrins and some glucose; enzymes on the luminal surface of enterocytes digest limit dextrins and disaccharides to glucose, galactose and fructose; lactose yields glucose and galactose, sucrose glucose and fructose. Intestinal hexose absorption (R-HSA-8981373): SGLT1 co-transports Na+ with glucose and galactose, and basolateral GLUT2 releases hexoses into the blood. Glycolysis (R-HSA-70171): entirely cytosolic; two NAD+ are reduced to NADH per glucose; under anaerobic conditions or in cells lacking mitochondria NAD+ is regenerated by reducing pyruvate to lactate. Hexokinase reaction (R-HSA-70420): glucokinase and the three hexokinases catalyse an irreversible reaction; glucokinase occurs only in hepatocytes and pancreatic beta cells, has a higher Km than the hexokinases, is less readily inhibited by its product and is thought to act as a glucose sensor coupled to insulin release; glucokinase mutations are associated with MODY2. Phosphofructokinase 1 (R-HSA-70467): irreversible under physiological conditions, allosterically regulated by ATP, citrate and fructose 2,6-bisphosphate. Fructose 2,6-bisphosphate (R-HSA-9634600): its levels rise with insulin and fall with glucagon signalling; PKA phosphorylates PFKFB1. Pyruvate kinase (R-HSA-71670): essentially irreversible; isozymes L (liver) and R (red cells) come from PKLR, and PKLR mutations are associated with haemolytic anaemias. Pyruvate metabolism (R-HSA-70268): when oxygen is limiting, as in exercising muscle, or mitochondria are absent, as in red blood cells, NADH is reoxidised by reducing pyruvate to lactate, which is released into the blood, taken up mainly by the liver, oxidised to pyruvate and used for gluconeogenesis. Gluconeogenesis (R-HSA-70263): glucose synthesis from pyruvate consumes six high-energy phosphates, four from ATP and two from GTP. PDH complex (R-HSA-9861559): the mitochondrial complex converts pyruvate, CoA and NAD+ to acetyl-CoA, CO2 and NADH. PDH regulation (R-HSA-204174): PDK1 to PDK4 inactivate the complex by phosphorylation and PDP1 and PDP2 reactivate it. Vitamin B1 metabolism (R-HSA-196819): Wernicke-Korsakoff syndrome is associated with thiamin deficiency in alcoholism. Citric acid cycle (R-HSA-71403): all reactions are mitochondrial; the acetyl group of acetyl-CoA is completely oxidised to CO2, yielding one GTP or ATP, three NADH and one FADH2. Citrate synthase (R-HSA-70975) and IDH3 (R-HSA-70967) are irreversible; IDH3 releases CO2, is activated by ADP and inhibited by NADH and high ATP; the OGDH reaction (R-HSA-71401) releases CO2; aconitase, succinyl-CoA ligase, fumarate hydratase and MDH2 are reversible, MDH2 being highly endergonic but pulled forward by the cycle; succinate dehydrogenase (R-HSA-70994) reduces ubiquinone, with FAD covalently bound to His-99 of SDHA. Respiratory electron transport (R-HSA-611105): energy is largely released in mitochondria; oxygen consumption depends on ADP availability; 2.5 ATP form per NADH electron pair and 1.5 per FADH2 pair; 10 NADH give 25 and 2 FADH2 give 3, 28 in all, plus 2 from the Krebs cycle and 2 from glycolysis, 32 per glucose in theory; the actual yield probably does not reach 32; the glycerol phosphate shuttle bypasses complex I, so 1.5 ATP form per cytosolic NADH, while malate-aspartate shuttle NADH enters at complex I. Statements not used, because they conflict with UniProt or with the arithmetic: R-HSA-611105 assigns 3 ATP to malate-aspartate shuttle NADH and swaps the overall equations of the two shuttles; R-HSA-71401 states that ATP and NADH enhance and Ca2+ and ADP decrease OGDH activity, the reverse of UniProt Q02218; R-HSA-204174 states that dichloroacetic acid inhibits PDH, whereas UniProt records it as an inhibitor of PDK1 to PDK3.

2. Справочное издание

   UniProt Consortium. UniProt: the Universal Protein Knowledgebase in 2025 Nucleic Acids Research, 2025.

   doi:10.1093/nar/gkae1010PubMed 39552041

   Финансирование и результат

   Финансирование

   National Human Genome Research Institute (NHGRI) [HG002273]; Office of the Director, NIH OD [U24HG007822]; National Institute of Allergy and Infectious Diseases (NIAID); National Institute on Aging (NIA); National Institute of General Medical Sciences (NIGMS) [R35GM141873]; National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); National Eye Institute (NEI); National Cancer Institute (NCI); National Heart, Lung, and Blood Institute (NHLBI); Biotechnology and Biological Sciences Research Council (BBSRC) [BB/T015608/1]; National Science Foundation's Directorate for Biological Sciences [BB/X002179/1]; Open Targets; Horizon 2020 - Research and Innovation Framework Programme [825575]; State Secretariat for Education, Research and Innovation (SERI); European Molecular Biology Laboratory (EMBL) Australia. Funding for open access charge: National Institutes of Health.

   Результат

   Reviewed human UniProtKB entries, release 2026_03, read through rest.uniprot.org on 2026-10-21. SLC5A1 (P13866, SGLT1): Na+-coupled symporter of D-glucose or D-galactose with a Na+ to sugar ratio of 2:1, absorbing them across the apical brush-border membrane of enterocytes, with basolateral exit through GLUT2. SLC2A2 (P11168, GLUT2): facilitative transporter of glucose, fructose and galactose; likely mediates bidirectional glucose transfer across the hepatocyte membrane and glucose uptake by beta cells; expressed in liver, beta cells, small intestine and kidney. SLC2A1 (P11166, GLUT1): basal glucose uptake; present at the blood-brain barrier, where it carries glucose into the brain; detected in erythrocytes. SLC2A3 (P11169, GLUT3): highly expressed in brain. SLC2A4 (P14672, GLUT4): insulin-regulated; retained intracellularly in muscle and fat cells and translocated to the cell surface upon insulin stimulation. HK1 (P19367) and HK3 (P52790): allosteric enzymes inhibited by their product, glucose 6-phosphate. GCK (P35557): weak affinity for glucose, mainly expressed in pancreatic beta cells and liver, acts as the glucose sensor of the beta cell; at low glucose the inactive GCK-GCKR complex is recruited to the hepatocyte nucleus; variants cause maturity-onset diabetes of the young 2 and familial hyperinsulinaemic hypoglycaemia 3. PFKL (P17858), PFKM (P08237) and PFKP (Q01813): catalyse the first committing step of glycolysis, need Mg2+, are allosterically activated by ADP, AMP or fructose 2,6-bisphosphate and inhibited by ATP or citrate. PFKFB1 (P16118): makes and degrades fructose 2,6-bisphosphate; phosphorylation at Ser-33 inhibits the kinase and activates the bisphosphatase; liver. GPI (P06744), ALDOA (P04075), ALDOB (P05062), ALDOC (P09972), TPI1 (P60174), GAPDH (P04406, with phosphate and NAD+), PGK1 (P00558, Mg2+), PGAM1 (P18669) and PGAM2 (P15259, with 2,3-bisphosphoglycerate as primer) and ENO1 (P06733), ENO2 (P09104) and ENO3 (P13929, Mg2+) catalyse reactions that run in both directions in glycolysis and gluconeogenesis. PKLR (P30613): allosterically activated by fructose 1,6-bisphosphate, needs Mg2+ or Mn2+ and K+; variants cause congenital non-spherocytic haemolytic anaemia 2 with decreased red-cell pyruvate kinase activity. PKM (P14618): isoform M1 is active without fructose 1,6-bisphosphate, isoform M2 requires it. LDHA (P00338) and LDHB (P07195) interconvert pyruvate and lactate with NADH and NAD+. PDHA1 (P08559): with PDHB forms E1, which catalyses thiamine pyrophosphate-dependent decarboxylation of pyruvate and reductive acetylation of the lipoyl groups of E2; phosphorylation by PDK family kinases inactivates it and dephosphorylation reactivates it. PDK1 (Q15118), PDK2 (Q15119) and PDK3 (Q15120): inhibited by dichloroacetate. PDK4 (Q16654): up-regulated by prolonged fasting, down-regulated by insulin. CS (O75390): forms citrate from acetyl-CoA and oxaloacetate. ACO2 (Q99798): isomerises citrate to isocitrate via cis-aconitate, with a [4Fe-4S] cluster. IDH3A (P50213): with IDH3B and IDH3G decarboxylates isocitrate to 2-oxoglutarate with NAD+; activated by citrate and ADP; high ATP inhibits. OGDH (Q02218): thiamine diphosphate-dependent, irreversible decarboxylation of 2-oxoglutarate; Ca2+ and ADP stimulate, ATP and NADH reduce its activity. SUCLG1 (P53597) with SUCLG2 (Q96I99) or SUCLA2 (Q9P2R7): couples succinyl-CoA hydrolysis to GTP or ATP synthesis, the only substrate-level phosphorylation of the cycle. SDHA (P31040): FAD-containing flavoprotein of complex II in the inner membrane, transfers electrons from succinate to ubiquinone. FH (P07954): reversible interconversion of fumarate and L-malate. MDH2 (P40926): reversible conversion of malate to oxaloacetate with NAD+.

3. Регуляторное

   US Food and Drug Administration. GLUCOPHAGE (metformin hydrochloride) tablets and GLUCOPHAGE XR extended-release tablets: full prescribing information US Food and Drug Administration, Drugs@FDA, NDA 020357 and NDA 021202, label revised May 2018, 2018.

   https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/020357s034,021202s018lbl.pdf

   Финансирование и результат

   Финансирование

   US Food and Drug Administration

   Результат

   Indicated as an adjunct to diet and exercise to improve glycaemic control in adults and, for the immediate-release tablet, children of 10 years and older with type 2 diabetes. Mechanism of action: decreases hepatic glucose production, decreases intestinal absorption of glucose and improves insulin sensitivity by increasing peripheral glucose uptake and utilisation; insulin secretion remains unchanged. Pharmacokinetics: absolute bioavailability of a 500 mg tablet under fasting conditions about 50 to 60%; steady-state plasma concentrations generally below 1 µg/mL; apparent volume of distribution 654 ± 358 L after 850 mg; negligible plasma protein binding; excreted unchanged in urine with no hepatic metabolism, no identified human metabolites and no biliary excretion; about 90% of absorbed drug eliminated renally within 24 hours; plasma elimination half-life about 6.2 hours and blood half-life about 17.6 hours; renal clearance about 3.5 times creatinine clearance, so tubular secretion is the major route. Single 850 mg dose: peak concentration 1.86 ± 0.52 µg/mL and renal clearance 384 ± 122 mL/min with creatinine clearance 61 to 90 mL/min, against 4.12 ± 1.83 µg/mL and 108 ± 57 mL/min at 31 to 60 mL/min and 3.93 ± 0.92 µg/mL and 130 ± 90 mL/min at 10 to 30 mL/min. Contraindicated at eGFR below 30 mL/min/1.73 m2; initiation not recommended at 30 to 45; benefit and risk assessed if eGFR falls below 45; discontinue below 30. Discontinue at or before iodinated contrast imaging when eGFR is 30 to 60 mL/min/1.73 m2, in liver disease, alcoholism or heart failure, or with intra-arterial contrast, and re-evaluate eGFR after 48 hours. Boxed warning: postmarketing metformin-associated lactic acidosis, characterised by blood lactate above 5 mmol/L, anion gap acidosis without ketonuria or ketonaemia, raised lactate to pyruvate ratio and plasma metformin generally above 5 µg/mL; metformin decreases liver uptake of lactate, raising blood lactate; prompt haemodialysis recommended, metformin being dialysable with a clearance up to 170 mL/min. Lactic acidosis reported in about 32% of overdose cases. Vitamin B12: in 29-week trials a decrease to subnormal levels of previously normal serum vitamin B12 occurred in about 7% of patients, possibly through interference with B12 absorption from the B12-intrinsic factor complex, may be associated with anaemia, and appears rapidly reversible on discontinuation or B12 supplementation; measure haematological parameters annually and B12 every 2 to 3 years. Drug interactions: inhibitors of organic cation transporter 2 (OCT2) and multidrug and toxin extrusion (MATE), among them ranolazine, vandetanib, dolutegravir and cimetidine, may increase systemic exposure; single-dose cimetidine 400 mg with metformin 850 mg gave geometric mean ratios of 1.40 for AUC and 1.61 for peak concentration; carbonic anhydrase inhibitors such as topiramate may increase the risk of lactic acidosis. No clinical study has established conclusive evidence of macrovascular risk reduction. In a 29-week double-blind placebo-controlled US trial in obese patients with type 2 diabetes, fasting plasma glucose changed by −53.0 mg/dL with metformin up to 2550 mg daily (n = 141) and +6.3 mg/dL with placebo (n = 145), and HbA1c by −1.4% and +0.4% (both P = 0.001); mean weight change was −1.4 lb and −2.4 lb. Adverse reactions with metformin against placebo: diarrhoea 53% against 12%, nausea or vomiting 26% against 8%, flatulence 12% against 6%; diarrhoea led to discontinuation in 6%.

4. Независимое

   Patel MS, Nemeria NS, Furey W, Jordan F. The Pyruvate Dehydrogenase Complexes: Structure-based Function and Regulation Journal of Biological Chemistry, 2014.

   doi:10.1074/jbc.R114.563148PubMed 24798336

   Финансирование и результат

   Финансирование

   Supported, in whole or in part, by National Institutes of Health grants DK 20478 (to M.S.P.), GM050380 (to F.J.) and GM061791 (to W.F.) and by the Veterans Affairs Merit Review (W.F.).

   Результат

   Review. The pyruvate dehydrogenase complex links glycolysis to the tricarboxylic acid cycle and comprises pyruvate dehydrogenase (E1), dihydrolipoamide acetyltransferase (E2) and dihydrolipoamide dehydrogenase (E3), which work sequentially. E1, a thiamin diphosphate-dependent enzyme, decarboxylates pyruvate and reductively acetylates the lipoyl groups covalently attached to E2; E2 transfers the acetyl group to CoA, forming acetyl-CoA; E3 transfers electrons from the dihydrolipoyl groups of E2 to FAD and then to NAD+.

5. Регуляторное

   EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA), Turck D, Bresson JL, Burlingame B, Dean T, Fairweather-Tait S, et al. Dietary reference values for thiamin EFSA Journal, 2016.

   doi:10.2903/j.efsa.2016.4653PubMed 42006014

   Финансирование и результат

   Финансирование

   European Food Safety Authority, on request from the European Commission (question EFSA-Q-2011-01225).

   Результат

   Free thiamin is the precursor of thiamin diphosphate (TDP, thiamin pyrophosphate), the coenzyme of pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and branched-chain alpha-keto acid dehydrogenase and of transketolase in the pentose phosphate pathway; the three dehydrogenases also require cofactors derived from pantothenic acid, riboflavin and niacin. Thiamin deficiency causes several forms of beriberi, dry (sensory and motor peripheral neuropathy) and wet (with congestive heart failure), and Wernicke's encephalopathy and Korsakoff's syndrome.

6. Независимое

   Judge A, Dodd MS. Metabolism Essays in Biochemistry, 2020.

   doi:10.1042/EBC20190041PubMed 32830223

   Финансирование и результат

   Финансирование

   Ayesha Judge is funded by a PhD studentship from Coventry University with additional funding and support from the University Alliance Doctoral Training Alliance. Michael Dodd is funded by Coventry University and the Centre for Sport, Exercise and Life Sciences.

   Результат

   Educational review. Insulin, released after eating, binds the insulin receptor, a tyrosine kinase that autophosphorylates and recruits insulin receptor substrate, leading to phosphorylation of AKT; in skeletal muscle, heart and adipose tissue insulin signalling translocates GLUT4 from internal vesicles to the plasma membrane; insulin inhibits hormone-sensitive lipase in adipose tissue; glucagon, released as blood glucose falls, acts mainly on the liver through a G-protein-coupled receptor that raises cAMP. Gluconeogenesis bypasses the irreversible steps of glycolysis with pyruvate carboxylase, activated by acetyl-CoA, phosphoenolpyruvate carboxykinase, fructose-1,6-bisphosphatase and glucose-6-phosphatase. Because pyruvate dehydrogenase is irreversible and the carbon entering the citric acid cycle as acetyl-CoA is lost in its decarboxylation steps, fats cannot produce glucose at a net rate; the glyoxylate cycle, which bypasses these steps in plants, bacteria, fungi, algae and protozoa, is stated not to exist in animals.

7. Справочное издание

   UniProt Consortium. UniProt: the Universal Protein Knowledgebase in 2025 Nucleic Acids Research, 2025.

   doi:10.1093/nar/gkae1010PubMed 39552041

   Финансирование и результат

   Финансирование

   National Human Genome Research Institute (NHGRI) [HG002273]; Office of the Director, NIH OD [U24HG007822]; National Institute of Allergy and Infectious Diseases (NIAID); National Institute on Aging (NIA); National Institute of General Medical Sciences (NIGMS) [R35GM141873]; National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); National Eye Institute (NEI); National Cancer Institute (NCI); National Heart, Lung, and Blood Institute (NHLBI); Biotechnology and Biological Sciences Research Council (BBSRC) [BB/T015608/1]; National Science Foundation's Directorate for Biological Sciences [BB/X002179/1]; Open Targets; Horizon 2020 - Research and Innovation Framework Programme [825575]; State Secretariat for Education, Research and Innovation (SERI); European Molecular Biology Laboratory (EMBL) Australia. Funding for open access charge: National Institutes of Health.

   Результат

   Reviewed human UniProtKB entries, release 2026_03, read through rest.uniprot.org on 2026-10-21. NAMPT (P43490) condenses nicotinamide with 5-phosphoribosyl-1-pyrophosphate to nicotinamide mononucleotide, the rate-limiting step of mammalian NAD biosynthesis, and NMNAT1 (Q9HAN9) forms NAD+ from nicotinamide mononucleotide and ATP. RFK (Q969G6) phosphorylates riboflavin (vitamin B2) to FMN, the rate-limiting step of FAD synthesis, and FLAD1 (Q8NFF5) adenylates FMN to FAD. SDHA (P31040), the flavoprotein of succinate dehydrogenase (complex II), binds FAD through tele-8alpha-FAD histidine 99 and transfers electrons from succinate to ubiquinone. NDUFV1 (P49821) of complex I accepts electrons from NADH on FMN and passes them along iron-sulfur clusters to ubiquinone; complex I reaction: ubiquinone + NADH + 5 H+(in) = ubiquinol + NAD+ + 4 H+(out). In the Q cycle of complex III, which contains the two haem b groups of MT-CYB (P00156), the [2Fe-2S] cluster of UQCRFS1 (P47985) and the covalent haem c of CYC1 (P08574), 2 protons are consumed from the matrix, 4 are released into the intermembrane space and 2 electrons pass to cytochrome c. CYCS (P99999), in the intermembrane space, carries electrons from cytochrome c1 to cytochrome oxidase. In complex IV, electrons pass through CuA of MT-CO2 (P00403) and haem a of MT-CO1 (P00395) to the haem a3-CuB centre; 4 Fe(II)-cytochrome c + O2 + 8 H+(in) = 4 Fe(III)-cytochrome c + 2 H2O + 4 H+(out). The respiratory chain creates an electrochemical gradient over the inner membrane that drives the ATP synthase, which couples ATP synthesis by rotation of its central stalk to proton translocation (ATP5F1B, P06576); its c-ring consists of eight c subunits (ATP5MC1, P05496).

8. Независимое

   Watt IN, Montgomery MG, Runswick MJ, Leslie AG, Walker JE. Bioenergetic cost of making an adenosine triphosphate molecule in animal mitochondria Proceedings of the National Academy of Sciences of the United States of America, 2010.

   doi:10.1073/pnas.1011099107PubMed 20847295

   Финансирование и результат

   Финансирование

   This work was funded by the Medical Research Council.

   Результат

   In the 3.5 Å crystal structure of the bovine F1-c-ring complex (PDB 2xnd), the c-ring has eight c subunits, so eight protons are translocated per 360° rotation, which produces three ATP: 2.7 protons per ATP. c-Subunit sequences are identical in almost all vertebrates. For each two electrons transferred to oxygen from NADH or succinate, ten or six protons are thought to be pumped out of the matrix; ADP/ATP exchange and phosphate-proton symport add one proton, a cost of 3.7 protons per ATP supplied to the cytoplasm, predicting P/O ratios of 2.7 and 1.6, close to experimental values of 2.5 and 1.5. The proton-motive force generated by respiration drives ATP synthesis.

9. Справочное издание

   Milo R, Phillips R. Cell Biology by the Numbers Garland Science, 2015.

   doi:10.1201/9780429258770

   Финансирование и результат

   Финансирование

   not stated

   Результат

   Textbook, online edition read 2026-10-21 at book.bionumbers.org, vignette 'What is the free energy released upon combustion of sugar?'. The free energy released in oxidising glucose by oxygen is about -3000 kJ/mol (about -700 kcal/mol). Glycolysis, the TCA cycle and the electron transfer chain couple the combustion of one glucose molecule to the production of roughly 30 ATP molecules (BNID 101778).

10. Финансирование не установлено

    Rolfe DF, Brown GC. Cellular energy utilization and molecular origin of standard metabolic rate in mammals Physiological Reviews, 1997.

    doi:10.1152/physrev.1997.77.3.731PubMed 9234964

    Финансирование и результат

    Финансирование

    Not read: the publisher's HTML and PDF full text returned HTTP 403 on 2026-10-21; the PubMed, Europe PMC and Crossref records list no funder, and Semantic Scholar lists no open-access copy.

    Результат

    Review with quantitative estimates for mammals in the standard state, read in the abstract. About 90% of oxygen consumption is mitochondrial, of which about 20% is uncoupled by the mitochondrial proton leak and 80% is coupled to ATP synthesis. Of the 80% coupled to ATP synthesis, about 25-30% is used by protein synthesis, 19-28% by the Na+-K+-ATPase, 4-8% by the Ca2+-ATPase, 2-8% by the actinomyosin ATPase, 7-10% by gluconeogenesis and 3% by ureagenesis.

11. Финансирование не установлено

    Kellett GL, Helliwell PA. The diffusive component of intestinal glucose absorption is mediated by the glucose-induced recruitment of GLUT2 to the brush-border membrane Biochemical Journal, 2000.

    doi:10.1042/bj3500155PubMed 10926839

    Финансирование и результат

    Финансирование

    Not read: the Portland Press PDF returned HTTP 403, the PubMed Central copy is PDF-only behind a browser check, and the PubMed and Crossref records list no funder.

    Результат

    Read in the abstract. In perfused rat jejunum in vivo, phloretin, a GLUT2 inhibitor, strongly inhibited absorption; brush-border GLUT2 rose about 2-fold when luminal glucose was raised from 0 to 100 mM. The phloretin-sensitive component was carrier-mediated and co-operative (n = 1.6, half-maximal at 56 mM glucose), and paracellular flow was negligible; the SGLT1-mediated component was half-maximal at 27 mM. The authors conclude that GLUT2-mediated facilitated diffusion across the brush-border membrane is the principal route of glucose absorption, up to 3-fold greater than that by SGLT1.

12. Независимое

    Röder PV, Geillinger KE, Zietek TS, Thorens B, Koepsell H, Daniel H. The role of SGLT1 and GLUT2 in intestinal glucose transport and sensing PLoS One, 2014.

    doi:10.1371/journal.pone.0089977PubMed 24587162

    Финансирование и результат

    Финансирование

    The work was supported by the Deutsche Forschungsgemeinschaft (GZ DA 190/10-1, Nutra2Sense). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

    Результат

    After a 4 g/kg intragastric glucose bolus, giving about 160 mM luminal glucose, SGLT1-deficient mice retained 80% less glucose tracer in intestinal tissue and had 73% less tracer in plasma than wild-type mice (4 to 5 mice per group), and their GIP and GLP-1 responses were abolished. Immunostaining showed GLUT2 in the basolateral but not the apical membrane; GLUT2 in brush-border membrane fractions was attributed mainly to basolateral contamination and did not change after the bolus (3 mice per group). The authors find no evidence for apical GLUT2 in glucose influx and expect the controversy to continue.