Database : MEDLINE
Search on : Adenosine and Diphosphate [Words]
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[PMID]: 29523466
[Au] Autor:Wilkins B; Hullikunte S; Simmonds M; Sasse A; Larsen PD; Harding SA
[Ad] Address:Department of Cardiology, Wellington Hospital, Wellington, New Zealand.
[Ti] Title:Improving the Prescribing Gap For Guideline Recommended Medications Post Myocardial Infarction.
[So] Source:Heart Lung Circ;, 2017 Nov 14.
[Is] ISSN:1444-2892
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:BACKGROUND: We assessed the effect of a pre-discharge medication checklist on discharge prescription rates of guideline recommended medications following myocardial infarction. In addition, we assessed what proportion of the residual prescribing gap following implementation of the checklist was due to the presence of contraindications. METHODS: We examined baseline prescription rates of guideline recommended medications in 100 patients discharged from our institution following acute myocardial infarction. We then introduced a pre-discharge checklist and reassessed discharge medications and reasons for non-prescription of guideline recommended medications in 447 patients with acute myocardial infarction. RESULTS: We demonstrated a significant gap in the prescription of guideline recommended secondary prevention medications at the time of discharge in our pre-intervention cohort. Introduction of a pre-discharge checklist resulted in a significant improvement in the prescription rates of all guideline recommended secondary prevention medications, with aspirin increasing from 90% to 97% (p=0.004), Adenosine diphosphate (ADP) receptor antagonist from 84% to 96% (p=0.0001), B-blocker from 79% to 87% (p=0.03), statin from 88% to 96% (p=0.002) and angiotensin converting enzyme (ACE) inhibitor from 58% to 70% (p=0.03). The residual gap in prescribing was largely explained by the presence of contraindications or absence of an indication in the case of ACE-inhibitors. Once these were taken into account there was a residual gap of 0-4% which represents genuine non-adherence to the guidelines. CONCLUSIONS: Introduction of a pre-discharge checklist led to significant improvement in prescription rates of all five guideline recommended secondary prevention medications. The residual gap in medication prescription following introduction of the checklist was largely due to the presence of contraindications rather than non-adherence.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29338536
[Au] Autor:Kupka D; Sibbing D
[Ad] Address:a Department of Cardiology , LMU München , Munich , Germany.
[Ti] Title:P2Y receptor inhibitors: an evolution in drug design to prevent arterial thrombosis.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):303-315, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: P2Y12 inhibitors are a critical component of dual antiplatelet therapy (DAPT), which is the superior strategy to prevent arterialthrombosis in patients with acute coronary syndromes (ACS) and undergoing stent implantation.. Areas covered: Basic science articles, clinical studies, and reviews from 1992-2017 were searched using Pubmed library to collet impactful literature. After an introduction to the purinergic receptor biology, this review summarizes current knowledge on P2Y12 receptor inhibitors. Furthermore, we describe the subsequent improvements of next-generation P2Y12 receptor inhibitors facing the ambivalent problem of bleeding events versus prevention of arterial thrombosis in a variety of clinical settings. Therefore, we summarize data from relevant preclinical and clinical trials of currently approved P2Y12 receptor inhibitors (clopidogrel, prasugrel, ticagrelor, cangrelor) and provide strategies of drug switching and management of bleeding events. Expert opinion: An enormous amount of pharmacologic and clinical data is available for the application of P2Y12 receptor inhibitors. Today prasugrel, ticagrelor and clopidogrel are the standard of care drugs during dual antiplatelet therapy for ACS patients, but have considerable rates of bleeding. Recent and future clinical trials will provide evidence for subsequent escalation and de-escalation strategies of P2Y12 receptor inhibition. These data may pave the way for an evidence-based, individualized P2Y12 receptor inhibitor therapy.
[Mh] MeSH terms primary: Drug Design
Purinergic P2Y Receptor Antagonists/pharmacology
Thrombosis/prevention & control
[Mh] MeSH terms secundary: Acute Coronary Syndrome/complications
Acute Coronary Syndrome/drug therapy
Animals
Drug Therapy, Combination
Hemorrhage/chemically induced
Hemorrhage/epidemiology
Humans
Platelet Aggregation Inhibitors/administration & dosage
Platelet Aggregation Inhibitors/adverse effects
Platelet Aggregation Inhibitors/pharmacology
Purinergic P2Y Receptor Antagonists/administration & dosage
Purinergic P2Y Receptor Antagonists/adverse effects
Thrombosis/etiology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Platelet Aggregation Inhibitors); 0 (Purinergic P2Y Receptor Antagonists)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180118
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1428557

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[PMID]: 29519292
[Au] Autor:Fu H; Zhang Y
[Ad] Address:Department of Intensive Care Unit, the 309th Hospital of PLA, Beijing 100091, China. Corresponding author: Zhang Yuxiang, Email: 15810550308@163.com.
[Ti] Title:[Evaluation of platelet function in critically ill patients and its clinical significance].
[So] Source:Zhonghua Wei Zhong Bing Ji Jiu Yi Xue;30(3):284-288, 2018 Mar.
[Is] ISSN:2095-4352
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:OBJECTIVE: Platelets play a pivotal role in the thromboembolic, inflammatory, and immunomodulatory process. The alteration of platelet quality often affects the treatment and prognosis of critically ill patients, and has a significant correlation with mortality. With the further research on the function of the platelet, it is found that the abnormal platelet quality can present during the early stage of the illness of the critically ill patients. In order to evaluate the alterations of the platelet quality more accurately, the further studies of platelet parameters, including platelet counts (PLT), platelet hematocrit (PCT), platelet large cell ratio (PLCR), mean platelet volume (MPV), platelet distribution width (PDW), immature platelet fraction (IPF) and so on, are still be the focus of current researches in the field of critical illness. At the same time, the application of thromboelastography/thrombelastography-platelet mapping (TEG/TEG MP) to the measurement of platelet function, especially the researches on the inhibitory rate of adenosine diphosphate (ADP) and the inhibitory rate of arachidonic acid (AA), is the hot spot of current researches. With regard to the diagnosis, prognosis and early goal-directed therapy (EGDT) of the critically ill patients, it is important to comprehensively apply the methods of platelet function evaluation.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3760/cma.j.issn.2095-4352.2018.03.019

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[PMID]: 29484409
[Au] Autor:Liu H; Li G; Zhang B; Sun D; Wu J; Chen F; Kong F; Luan Y; Jiang W; Wang R; Xue X
[Ad] Address:Shandong Luye Pharmaceutical Co., Ltd., Yantai, Shandong 264000, P.R. China.
[Ti] Title:Suppression of the NF­κB signaling pathway in colon cancer cells by the natural compound Riccardin D from Dumortierahirsute.
[So] Source:Mol Med Rep;17(4):5837-5843, 2018 Apr.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Colorectal cancer (CRC) is a major cause of mortality and morbidity. Chronic inflammation is closely associated with the development, progression and prognosis of the majority of intestinal malignancies. In recent years, targeting the nuclear factor (NF)­κB signaling pathway for CRC therapy has become an attractive strategy. Riccardin D, a novel macrocyclicbis (bibenzyl) compound, was isolated from the Chinese liverwort plant. Previous studies have suggested that Riccardin D exerted chemo­preventative effects against the intestinal malignancy formation. In the present study, cell counting kit­8, Hochest 33258 staining, mitochondria membrane permeability assay, western blotting analysis, reverse transcription­polymerase chain reaction, luciferase reporter gene assay and molecular modeling analysis were performed to detect the effect and mechanisms of Riccardin D on human colon cancer cells. The results demonstrated that Riccardin D significantly inhibited the growth of HT­29 cells. In addition, the cDNA expression of cyclooxygenase­2, and the protein expression and activity of NF­κB and tumor necrosis factor­α were downregulated; however, the protein expression of cleaved caspase­3 and ­9, and cleaved poly (adenosine diphosphate­ribose) polymerase, and the B­cell lymphoma (Bcl)­2: Bcl­2­associated X protein ratio were upregulated. Furthermore, Auto Dock analysis identified binding sites between Riccardin D and NF­κB. These results indicated that Riccardin D may inhibit cell proliferation and induce apoptosis in HT­29 cells, which may be associated with the blocking of the NF­κB signaling pathway. Thus, Riccardin D should be investigated as an NF­κB inhibitor in cancer therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3892/mmr.2018.8617

  5 / 39168 MEDLINE  
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[PMID]: 29484394
[Au] Autor:Wang W; Xu B; Li Q; Jiang D; Yan S
[Ad] Address:Department of Pharmacy, Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.
[Ti] Title:Anti­cancer effects of a novel Pan­RAF inhibitor in a hepatocellular carcinoma cell line.
[So] Source:Mol Med Rep;17(4):6185-6193, 2018 Apr.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:The RAF/mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK (RAF/MEK/ERK) signaling cascade serves a prominent role in hepatocellular carcinoma (HCC) proliferation. Sorafenib (BAY 43­9006) is a potent multikinase inhibitor of RAF kinases and a few receptor tyrosine kinases. Additionally, sorafenib causes apoptosis in a number of human tumor cell lines such as leukemia cell lines. Sorafenib is the first targeted drug to prolong the overall survival of patients with advanced HCC. However, sorafenib activity is less favorable in certain cancers, including sarcomas and melanomas, due to patient insensitivity and drug resistance. In the present study, a novel bi­aryl urea, N­(3­trifluoromethylphenyl)­N'-(2-methyl-4-(6­cyclopropanecarboxamido-pyrimidin-4-yl) oxyphenyl) urea (CBI­5725), is shown to be a potential candidate for the treatment of liver cancer. In the present study, the in vitro activities of CBI­5725 and sorafenib in PLC/PRF/5 HCC cells were examined and the corresponding in vivo antitumor activities in PLC/PRF/5 human tumor xenografts. An alamar blue assay confirmed that CBI­5725 was more cytotoxic than sorafenib to PLC/PRF/5 cells, suggesting that CBI­5725 inhibited tumor cell proliferation more potently than sorafenib. CBI­5725 inhibited the RAF/MEK/ERK signaling pathway to the same extent as sorafenib. In addition, CBI­5725 elicited cell cycle arrest in the G2/M phase, while sorafenib did not markedly alter the cell cycle. Furthermore, CBI­5725 induced apoptosis more strongly than sorafenib in a dose­dependent manner, which may be attributed to greater caspase­3 and poly(adenosine 5'­diphosphate­ribose) polymerase activation by CBI­5725. In the PLC/PRF/5 xenograft model, 2 mg/kg CBI­5725 inhibited tumor growth by 73%. At doses ranging from 6 to 18 mg/kg, CBI­5725 nearly completely prevented tumor growth. These results imply that the antitumor efficacy of CBI­5725 in HCC models may result from the suppression of the RAF/MEK/ERK signaling pathway, the induction of cell cycle arrest in the G2/M phase, and the initiation of caspase­3­dependent apoptosis. These observations suggested that CBI­5725 may be a potent novel compound for the treatment of HCC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3892/mmr.2018.8615

  6 / 39168 MEDLINE  
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[PMID]: 29407168
[Au] Autor:Wang S; Jiang J; Wang Y; Jia Q; Dai S; Wang Y; Lv L; Wang J
[Ad] Address:Department of Pharmacology, Dalian Medical University, Dalian, Liaoning Province, 116044, China.
[Ti] Title:rLj-RGD3, a novel recombinant toxin protein from Lampetra japonica, prevents coronary thrombosis-induced acute myocardial infarction by inhibiting platelet functions in rats.
[So] Source:Biochem Biophys Res Commun;, 2018 Feb 03.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Recombinant Lampetra japonica RGD-peptide (rLj-RGD3), a soluble protein containing three RGD sequences, was acquired from the oral salivary glands of Lampetra japonica using recombinant DNA technology. The aim of this study was to investigate the protective effects of rLj-RGD3 against acute myocardial infarction (AMI) induced by coronary artery thrombosis, as well as the underlying mechanisms. A rat model of AMI caused by ferric chloride-induced thrombosis on the surface of the left anterior descending (LAD) coronary artery was successfully established. Rats were given various doses of rLj-RGD3 (12 µg/kg, 24 µg/kg and 48 µg/kg) via sublingual intravenous delivery 10 min before AMI. ST segment elevation was recorded by electrocardiogram (ECG) until the end of the model. Left ventricular Evans blue content and histopathological changes were examined. Blood samples were collected to determine 5-hydroxytryptamine (5-HT), ß-thromboglobulin (ß-TG), platelet factor 4 (PF4) and cAMP levels. The effects of rLj-RGD3 on platelet aggregation, adhesion and intracellular calcium concentrations were also measured. rLj-RGD3 significantly reduced ST segment elevation, prevented thrombus formation in the coronary artery and decreased Evans blue content in the left ventricular myocardium. Meanwhile, rLj-RGD3 exerted an inhibitory effect on adenosine diphosphate (ADP)-induced platelet aggregation and blocked platelet adhesion to collagen. Treatment with rLj-RGD3 prevented 5-HT, ß-TG and PF4 release and significantly elevated intracellular cAMP levels in a dose-dependent manner but decreased the level of cytosolic-free Ca , an aggregation-inducing molecule. These results show that rLj-RGD3 can effectively reduce coronary thrombosis in AMI rats by strongly inhibiting platelet function, indicating that the recombinant RGD toxin protein rLj-RGD3 may serve as a potent clinical therapeutic agent for AMI.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

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[PMID]: 29326162
[Au] Autor:Manav MC; Beljantseva J; Bojer MS; Tenson T; Ingmer H; Hauryliuk V; Brodersen DE
[Ad] Address:From the Department of Molecular Biology and Genetics, Centre for Bacterial Stress Response and Persistence, Gustav Wieds Vej 10c, DK-8000 Aarhus C, Denmark.
[Ti] Title:Structural basis for (p)ppGpp synthesis by the small alarmone synthetase RelP.
[So] Source:J Biol Chem;293(9):3254-3264, 2018 Mar 02.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The stringent response is a global reprogramming of bacterial physiology that renders cells more tolerant to antibiotics and induces virulence gene expression in pathogens in response to stress. This process is driven by accumulation of the intracellular alarmone guanosine-5'-di(tri)phosphate-3'-diphosphate ((p)ppGpp), which is produced by enzymes of the RelA SpoT homologue (RSH) family. The Gram-positive Firmicute pathogen, , encodes three RSH enzymes: a multidomain RSH (Rel) that senses amino acid starvation on the ribosome and two small alarmone synthetase (SAS) enzymes, RelQ (SAS1) and RelP (SAS2). In , RelQ (SAS1) was shown to form a tetramer that is activated by pppGpp and inhibited by single-stranded RNA, but the structural and functional regulation of RelP (SAS2) is unexplored. Here, we present crystal structures of RelP in two major functional states, pre-catalytic (bound to GTP and the non-hydrolyzable ATP analogue, adenosine 5'-(α,ß-methylene)triphosphate (AMP-CPP)), and post-catalytic (bound to pppGpp). We observed that RelP also forms a tetramer, but unlike RelQ (SAS1), it is strongly inhibited by both pppGpp and ppGpp and is insensitive to inhibition by RNA. We also identified putative metal ion-binding sites at the subunit interfaces that were consistent with the observed activation of the enzyme by Zn ions. The structures reported here reveal the details of the catalytic mechanism of SAS enzymes and provide a molecular basis for understanding differential regulation of SAS enzymes in Firmicute bacteria.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.RA117.001374

  8 / 39168 MEDLINE  
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[PMID]: 29270996
[Au] Autor:Maldonado MR; Bracht L; de Sá-Nakanishi AB; Corrêa RCG; Comar JF; Peralta RM; Bracht A
[Ad] Address:Department of Biochemistry, University of Maringá, Maringá, Brazil.
[Ti] Title:Actions of p-synephrine on hepatic enzyme activities linked to carbohydrate metabolism and ATP levels in vivo and in the perfused rat liver.
[So] Source:Cell Biochem Funct;36(1):4-12, 2018 Jan.
[Is] ISSN:1099-0844
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:p-Synephrine is one of the main active components of the fruit of Citrus aurantium (bitter orange). Extracts of the bitter orange and other preparations containing p-synephrine have been used worldwide to promote weight loss and for sports performance. The purpose of the study was to measure the action of p-synephrine on hepatic enzyme activities linked to carbohydrate and energy metabolism and the levels of adenine mononucleotides. Enzymes and adenine mononucleotides were measured in the isolated perfused rat liver and in vivo after oral administration of the drug (50 and 300 mg/kg) by using standard techniques. p-Synephrine increased the activity of glycogen phosphorylase in vivo and in the perfused liver. It decreased, however, the activities of pyruvate kinase and pyruvate dehydrogenase also in vivo and in the perfused liver. p-Synephrine increased the hepatic pools of adenosine diphosphate and adenosine triphosphate. Stimulation of glycogen phosphorylase is consistent with the reported increased glycogenolysis in the perfused liver and increased glycemia in rats. The decrease in the pyruvate dehydrogenase activity indicates that p-synephrine is potentially capable of inhibiting the transformation of carbohydrates into lipids. The capability of increasing the adenosine triphosphate-adenosine diphosphate pool indicates a beneficial effect of p-synephrine on the cellular energetics.
[Mh] MeSH terms primary: Adenosine Triphosphate/metabolism
Carbohydrate Metabolism/drug effects
Liver/drug effects
Liver/enzymology
Synephrine/pharmacology
[Mh] MeSH terms secundary: Administration, Oral
Animals
Citrus/chemistry
Glycogen Phosphorylase/metabolism
Liver/blood supply
Liver/surgery
Male
Pyruvate Dehydrogenase Complex/antagonists & inhibitors
Pyruvate Dehydrogenase Complex/metabolism
Pyruvate Kinase/antagonists & inhibitors
Pyruvate Kinase/metabolism
Rats
Rats, Wistar
Synephrine/administration & dosage
Synephrine/chemistry
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Pyruvate Dehydrogenase Complex); 8L70Q75FXE (Adenosine Triphosphate); EC 2.4.1.- (Glycogen Phosphorylase); EC 2.7.1.40 (Pyruvate Kinase); PEG5DP7434 (Synephrine)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171223
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3311

  9 / 39168 MEDLINE  
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[PMID]: 29513564
[Au] Autor:Miotto PM; McGlory C; Holloway TM; Phillips SM; Holloway GP
[Ad] Address:Department of Human Health and Nutritional Sciences, University of Guelph, Canada.
[Ti] Title:Sex-differences in mitochondrial respiratory function in human skeletal muscle.
[So] Source:Am J Physiol Regul Integr Comp Physiol;, 2018 Mar 07.
[Is] ISSN:1522-1490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mitochondrial bioenergetic contributions to sex-differences in human skeletal muscle metabolism remain poorly defined. The primary aim of this study was to determine if mitochondrial respiratory kinetics differed between healthy young men and women in permeabilized skeletal muscle fibres. While men and women displayed similar (P>0.05) maximal respiration rates and abundance of mitochondrial/adenosine diphosphate (ADP) transport proteins, women had lower (P<0.05) mitochondrial ADP sensitivity (+30% apparent Km) and absolute respiration rates at a physiologically relevant ADP concentration (100M). Moreover, although men and women exhibited similar carnitine palmitoyl transferase-I protein content and palmitoyl-CoA supported respiration, women displayed greater sensitivity to malonyl-CoA mediated respiratory inhibition. These data establish baseline sex-differences in mitochondrial bioenergetics, and provide the foundation for studying mitochondrial function within the context of metabolic perturbations/diseases that affect men and women differently.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1152/ajpregu.00025.2018

  10 / 39168 MEDLINE  
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[PMID]: 29416045
[Au] Autor:Basco D; Zhang Q; Salehi A; Tarasov A; Dolci W; Herrera P; Spiliotis I; Berney X; Tarussio D; Rorsman P; Thorens B
[Ad] Address:Center for Integrative Genomics, University of Lausanne, 1015, Lausanne, Switzerland.
[Ti] Title:α-cell glucokinase suppresses glucose-regulated glucagon secretion.
[So] Source:Nat Commun;9(1):546, 2018 02 07.
[Is] ISSN:2041-1723
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Glucagon secretion by pancreatic α-cells is triggered by hypoglycemia and suppressed by high glucose levels; impaired suppression of glucagon secretion is a hallmark of both type 1 and type 2 diabetes. Here, we show that α-cell glucokinase (Gck) plays a role in the control of glucagon secretion. Using mice with α-cell-specific inactivation of Gck (αGckKO mice), we find that glucokinase is required for the glucose-dependent increase in intracellular ATP/ADP ratio and the closure of K channels in α-cells and the suppression of glucagon secretion at euglycemic and hyperglycemic levels. αGckKO mice display hyperglucagonemia in the fed state, which is associated with increased hepatic gluconeogenic gene expression and hepatic glucose output capacity. In adult mice, fed hyperglucagonemia is further increased and glucose intolerance develops. Thus, glucokinase governs an α-cell metabolic pathway that suppresses secretion at or above normoglycemic levels; abnormal suppression of glucagon secretion deregulates hepatic glucose metabolism and, over time, induces a pre-diabetic phenotype.
[Mh] MeSH terms primary: Glucagon-Secreting Cells/metabolism
Glucagon/secretion
Glucokinase/genetics
Glucose Intolerance/metabolism
Glucose/metabolism
Hypoglycemia/metabolism
[Mh] MeSH terms secundary: Adenosine Diphosphate/metabolism
Adenosine Triphosphate/metabolism
Animals
Biological Transport
Female
Gene Expression
Glucagon-Secreting Cells/pathology
Glucokinase/deficiency
Glucose Intolerance/genetics
Glucose Intolerance/pathology
Hypoglycemia/genetics
Hypoglycemia/pathology
Insulin/metabolism
KATP Channels/genetics
KATP Channels/metabolism
Liver/metabolism
Male
Mice
Mice, Knockout
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Insulin); 0 (KATP Channels); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate); 9007-92-5 (Glucagon); EC 2.7.1.2 (Glucokinase); IY9XDZ35W2 (Glucose)
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:IM
[Da] Date of entry for processing:180209
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-03034-0


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