Database : MEDLINE
Search on : metabolic and diseases [Words]
References found : 121299 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 12130 go to page                         

  1 / 121299 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 29524414
[Au] Autor:Liu P; Feng T; Zuo X; Wang X; Luo J; Li N; Han X; Zhu N; Xu S; Xu Y; Jin ZG; Si S
[Ad] Address:Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.
[Ti] Title:A novel SIRT1 activator E6155 improves insulin sensitivity in type 2 diabetic KKA mice.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Sirtuin 1 (SIRT1) is an NAD -dependent protein deacetylase that plays a critical role in controlling energy metabolism, stress response and aging. Hence, enhancing SIRT1 activity could be a potential therapeutic strategy to treat metabolic diseases such as diabetes. However, pharmacological activators for SIRT1 are scarce to date. In this study, using the optimized high throughput screening, we identified E6155, a piperazine 1, 4- diamide compound, as a new small molecular activator of SIRT1. We further found that E6155 significantly upregulated glucose uptake in cultured mouse liver cells and skeletal muscle cells through increasing SIRT1 deacetylase activity. In type 2 diabetic KKA mice, E6155 treatment markedly decreased the level of fasting glucose. Moreover, E6155 improved oral glucose tolerance and insulin tolerance. Euglycemic clamp and the homeostasis model assessment of insulin resistance index showed that E6155 ameliorated the insulin resistance and increased insulin sensitivity in diabetic mice. Mechanistically, we observed that the antidiabetic effects of E6155 were involved in SIRT1 dependent activation of LKB1/AMPK and IRS1/AKT pathways. In conclusion, our findings identified E6155 as a novel SIRT1 activator and suggested that E6155 could be a promising drug candidate for treating insulin resistance and diabetes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 121299 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29524372
[Au] Autor:Gavurová B; Kubák M; Soltés M; Barták M; Vagasová T
[Ad] Address:Faculty of Economics, Technical University of Kosice, Kosice, Slovak Republic.
[Ti] Title:Time Trend, Age and Sex Distribution of Deceased from Diabetes Mellitus at the Regional Level in the Slovak Republic.
[So] Source:Cent Eur J Public Health;25 Suppl 2:S64-S71, 2017 Dec.
[Is] ISSN:1210-7778
[Cp] Country of publication:Czech Republic
[La] Language:eng
[Ab] Abstract:AIM: To describe the time trends, age and sex distribution of death from diabetes mellitus (E10-E14) as a significant part of endocrine, nutritional and metabolic diseases (E00-E90), during 1996-2014 in the Slovak regions, and to estimate the influence of social characteristics on mortality. METHODS: Secondary data on deaths during 1996-2014 were gathered from the National Health Information Center in the Slovak Republic. The total crude death rate per 100,000 of the standard Slovak population and age-standardized death rate per 100,000 of the standard European population were calculated by direct standardization. Multilevel logistic regression analysis was performed. RESULTS: Deaths from diabetes mellitus account for 91.6% of deaths registered in the endocrine, nutritional and metabolic diseases Chapter. The age-standardized death rate per 100,000 of inhabitants decreased from 19.2 in 1996 to 15.3 in 2014 in the Slovak Republic, although a massive increase of up to 32.5 was reported in 1999. The highest age-standardized death rates per 100,000 inhabitants were typical for the Kosice, Nitra and Trencín regions. On the other hand, the lowest counts were recorded in the Bratislava region. Mortality from diabetes mellitus starts to be evident in the 45-49 year age-group in both sexes. The median age of death for women is lower in the 75-79 year age-group in comparison to men although the total crude death rate for men in lower age groups is higher. After age 80 the situation is reversed. The odds of dying due to endocrine, nutritional and metabolic diseases decreases by 0.4% each year. The odds of dying are lower by 17% and 12.3%, respectively, in the Zilina and Presov regions compared to Bratislava region. Women have a higher probability of dying by 38% in contrast to men, and married couples by 16.7% than singles. Age is proved to be an insignificant factor. CONCLUSIONS: In spite of the declining trend of mortality from diabetes mellitus, it is necessary to reduce the risk of its incidence by healthier food consumption and physical activity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.21101/cejph.a5052

  3 / 121299 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29511163
[Au] Autor:Delprat B; Maurice T; Delettre C
[Ad] Address:INSERM UMR-S1198, 34095, Montpellier, France. benjamin.delprat@inserm.fr.
[Ti] Title:Wolfram syndrome: MAMs' connection?
[So] Source:Cell Death Dis;9(3):364, 2018 Mar 06.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Wolfram syndrome (WS) is a rare neurodegenerative disease, the main pathological hallmarks of which associate with diabetes, optic atrophy, and deafness. Other symptoms may be identified in some but not all patients. Prognosis is poor, with death occurring around 35 years of age. To date, no treatment is available. WS was first described as a mitochondriopathy. However, the localization of the protein on the endoplasmic reticulum (ER) membrane challenged this hypothesis. ER contacts mitochondria to ensure effective Ca transfer, lipids transfer, and apoptosis within stabilized and functionalized microdomains, termed "mitochondria-associated ER membranes" (MAMs). Two types of WS are characterized so far and Wolfram syndrome type 2 is due to mutation in CISD2, a protein mostly expressed in MAMs. The aim of the present review is to collect evidences showing that WS is indeed a mitochondriopathy, with established MAM dysfunction, and thus share commonalities with several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, as well as metabolic diseases, such as diabetes.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0406-3

  4 / 121299 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29476731
[Au] Autor:Sudrié-Arnaud B; Marguet F; Patrier S; Martinovic J; Louillet F; Broux F; Charbonnier F; Dranguet H; Coutant S; Vezain M; Lanos R; Tebani A; Fuller M; Lamari F; Chambon P; Brehin AC; Trestard L; Tournier I; Marret S; Verspyck E; Laquerrière A; Bekri S
[Ad] Address:Department of Metabolic Biochemistry, Rouen University Hospital, Rouen 76000, France.
[Ti] Title:Metabolic causes of nonimmune hydrops fetalis: A next-generation sequencing panel as a first-line investigation.
[So] Source:Clin Chim Acta;481:1-8, 2018 Feb 22.
[Is] ISSN:1873-3492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:PURPOSES: Hydrops fetalis is a life-threatening fetal condition, and 85% of all cases are classified as nonimmune hydrops fetalis (NIHF). Up to 15% of NIHF cases may be due to inborn errors of metabolism (IEM), but a large proportion of cases linked to metabolic disorders remains undiagnosed. This lack of diagnosis may be related to the limitations of conventional biological procedures, which involve sequential investigations and require multiple samples and steps. In addition, this approach is time consuming. We have developed a next-generation sequencing (NGS) panel to investigate metabolic causes of NIHF, ascites, and polyhydramnios associated to another fetal abnormality. METHODS: The hydrops fetalis (HydFet) panel was designed to cover the coding regions and flanking intronic sequences of 41 genes. A retrospective study of amniotic fluid samples from 40 subjects was conducted. A prospective study was subsequently initiated, and six samples were analyzed using the NGS panel. RESULTS: Five IEM diagnoses were made using the HydFet panel (Niemann-Pick type C (NPC), Barth syndrome, HNF1Β deficiency, GM1 gangliosidosis, and Gaucher disease). This analysis also allowed the identification of 8p sequence triplication in an additional case. CONCLUSION: NGS combined with robust bioinformatics analyses is a useful tool for identifying the causative variants of NIHF. Subsequent functional characterization of the protein encoded by the altered gene and morphological studies may confirm the diagnosis. This paradigm shift allows a significant improvement of IEM diagnosis in NIHF.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 121299 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29462705
[Au] Autor:Ghasemi M; Mayasi Y; Hannoun A; Eslami SM; Carandang R
[Ad] Address:Department of Neurology, University of Massachusetts Medical School, Worcester, MA 01655, USA. Electronic address: mehdi.ghasemi@umassmemorial.org.
[Ti] Title:Nitric Oxide and Mitochondrial Function in Neurological Diseases.
[So] Source:Neuroscience;376:48-71, 2018 Feb 17.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mitochondria are key cellular organelles that play crucial roles in the energy production and regulation of cellular metabolism. Accumulating evidence suggests that mitochondrial activity can be modulated by nitric oxide (NO). As a key neurotransmitter in biologic systems, NO mediates the majority of its function through activation of the cyclic guanylyl cyclase (cGC) signaling pathway and S-nitrosylation of a variety of proteins involved in cellular functioning including those involved in mitochondrial biology. Moreover, excess NO or the formation of reactive NO species (RNS), e.g., peroxynitrite (ONOO ), impairs mitochondrial functioning and this, in conjunction with nuclear events, eventually affects neuronal cell metabolism and survival, contributing to the pathogenesis of several neurodegenerative diseases. In this review we highlight the possible mechanisms underlying the noxious effects of excess NO and RNS on mitochondrial function including (i) negative effects on electron transport chain (ETC); (ii) ONOO -mediated alteration in mitochondrial permeability transition; (iii) enhanced mitochondrial fragmentation and autophagy through S-nitrosylation of key proteins involved in this process such as dynamin-related protein 1 (DRP-1) and Parkin/PINK1 (protein phosphatase and tensin homolog-induced kinase 1) complex; (iv) alterations in the mitochondrial metabolic pathways including Krebs cycle, glycolysis, fatty acid metabolism, and urea cycle; and finally (v) mitochondrial ONOO -induced nuclear toxicity and subsequent release of apoptosis-inducing factor (AIF) from mitochondria, causing neuronal cell death. These proposed mechanisms highlight the multidimensional nature of NO and its signaling in the mitochondrial function. Understanding the mechanisms by which NO mediates mitochondrial (dys)function can provide new insights into the treatment of neurodegenerative diseases.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 121299 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29454073
[Au] Autor:Geffroy G; Benyahia R; Frey S; Desquiret-Dumas V; Gueguen N; Bris C; Belal S; Inisan A; Renaud A; Chevrollier A; Henrion D; Bonneau D; Letournel F; Lenaers G; Reynier P; Procaccio V
[Ad] Address:UMR CNRS 6015-INSERM U1083, MitoVasc Institute, Angers University, Angers, France.
[Ti] Title:The accumulation of assembly intermediates of the mitochondrial complex I matrix arm is reduced by limiting glucose uptake in a neuronal-like model of MELAS syndrome.
[So] Source:Biochim Biophys Acta;1864(5 Pt A):1596-1608, 2018 Feb 14.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Ketogenic diet (KD) which combined carbohydrate restriction and the addition of ketone bodies has emerged as an alternative metabolic intervention used as an anticonvulsant therapy or to treat different types of neurological or mitochondrial disorders including MELAS syndrome. MELAS syndrome is a severe mitochondrial disease mainly due to the m.3243A > G mitochondrial DNA mutation. The broad success of KD is due to multiple beneficial mechanisms with distinct effects of very low carbohydrates and ketones. To evaluate the metabolic part of carbohydrate restriction, transmitochondrial neuronal-like cybrid cells carrying the m.3243A > G mutation, shown to be associated with a severe complex I deficiency was exposed during 3 weeks to glucose restriction. Mitochondrial enzyme defects were combined with an accumulation of complex I (CI) matrix intermediates in the untreated mutant cells, leading to a drastic reduction in CI driven respiration. The severe reduction of CI was also paralleled in post-mortem brain tissue of a MELAS patient carrying high mutant load. Importantly, lowering significantly glucose concentration in cell culture improved CI assembly with a significant reduction of matrix assembly intermediates and respiration capacities were restored in a sequential manner. In addition, OXPHOS protein expression and mitochondrial DNA copy number were significantly increased in mutant cells exposed to glucose restriction. The accumulation of CI matrix intermediates appeared as a hallmark of MELAS pathophysiology highlighting a critical pathophysiological mechanism involving CI disassembly, which can be alleviated by lowering glucose fuelling and the induction of mitochondrial biogenesis, emphasizing the usefulness of metabolic interventions in MELAS syndrome.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 121299 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Clinical Trials Registry
Full text

[PMID]: 29397305
[Au] Autor:Gordon BA; Blazey TM; Su Y; Hari-Raj A; Dincer A; Flores S; Christensen J; McDade E; Wang G; Xiong C; Cairns NJ; Hassenstab J; Marcus DS; Fagan AM; Jack CR; Hornbeck RC; Paumier KL; Ances BM; Berman SB; Brickman AM; Cash DM; Chhatwal JP; Correia S; Förster S; Fox NC; Graff-Radford NR; la Fougère C; Levin J; Masters CL; Rossor MN; Salloway S; Saykin AJ; Schofield PR; Thompson PM; Weiner MM; Holtzman DM; Raichle ME; Morris JC; Bateman RJ; Benzinger TLS
[Ad] Address:Mallinckrodt Institute of Radiology, Washington University, St Louis, MO, USA; Knight Alzheimer's Disease Research Center, Washington University, St Louis, MO, USA; Department of Psychological & Brain Sciences, Washington University, St Louis, MO, USA. Electronic address: bagordon@wustl.edu.
[Ti] Title:Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer's disease: a longitudinal study.
[So] Source:Lancet Neurol;17(3):241-250, 2018 Mar.
[Is] ISSN:1474-4465
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Models of Alzheimer's disease propose a sequence of amyloid ß (Aß) accumulation, hypometabolism, and structural decline that precedes the onset of clinical dementia. These pathological features evolve both temporally and spatially in the brain. In this study, we aimed to characterise where in the brain and when in the course of the disease neuroimaging biomarkers become abnormal. METHODS: Between Jan 1, 2009, and Dec 31, 2015, we analysed data from mutation non-carriers, asymptomatic carriers, and symptomatic carriers from families carrying gene mutations in presenilin 1 (PSEN1), presenilin 2 (PSEN2), or amyloid precursor protein (APP) enrolled in the Dominantly Inherited Alzheimer's Network. We analysed C-Pittsburgh Compound B ( C-PiB) PET, F-Fluorodeoxyglucose ( F-FDG) PET, and structural MRI data using regions of interest to assess change throughout the brain. We estimated rates of biomarker change as a function of estimated years to symptom onset at baseline using linear mixed-effects models and determined the earliest point at which biomarker trajectories differed between mutation carriers and non-carriers. This study is registered at ClinicalTrials.gov (number NCT00869817) FINDINGS: C-PiB PET was available for 346 individuals (162 with longitudinal imaging), F-FDG PET was available for 352 individuals (175 with longitudinal imaging), and MRI data were available for 377 individuals (201 with longitudinal imaging). We found a sequence to pathological changes, with rates of Aß deposition in mutation carriers being significantly different from those in non-carriers first (across regions that showed a significant difference, at a mean of 18·9 years [SD 3·3] before expected onset), followed by hypometabolism (14·1 years [5·1] before expected onset), and lastly structural decline (4·7 years [4·2] before expected onset). This biomarker ordering was preserved in most, but not all, regions. The temporal emergence within a biomarker varied across the brain, with the precuneus being the first cortical region for each method to show divergence between groups (22·2 years before expected onset for Aß accumulation, 18·8 years before expected onset for hypometabolism, and 13·0 years before expected onset for cortical thinning). INTERPRETATION: Mutation carriers had elevations in Aß deposition, reduced glucose metabolism, and cortical thinning compared with non-carriers which preceded the expected onset of dementia. Accrual of these pathologies varied throughout the brain, suggesting differential regional and temporal vulnerabilities to Aß, metabolic decline, and structural atrophy, which should be taken into account when using biomarkers in a clinical setting as well as designing and evaluating clinical trials. FUNDING: US National Institutes of Health, the German Center for Neurodegenerative Diseases, and the Medical Research Council Dementias Platform UK.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Data-Review

  8 / 121299 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29305304
[Au] Autor:Acevedo MB; Eagon JC; Bartholow BD; Klein S; Bucholz KK; Pepino MY
[Ad] Address:Department of Food Science and Human Nutrition, College of Agricultural, Consumer and Environmental Sciences, University of Illinois, Urbana-Champaign, Illinois.
[Ti] Title:Sleeve gastrectomy surgery: when 2 alcoholic drinks are converted to 4.
[So] Source:Surg Obes Relat Dis;14(3):277-283, 2018 Mar.
[Is] ISSN:1878-7533
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: While it is well established that Roux-en-Y gastric bypass (RYGB) causes a rapid and heightened peak blood alcohol concentration (BAC), results from previous studies on the effects of sleeve gastrectomy (SG) on alcohol pharmacokinetics are conflicting. Data from 2 studies found SG did not affect BAC, whereas another study found SG caused a heightened peak BAC after alcohol ingestion. Moreover, these 3 studies estimated BAC from breathalyzers, which might not reliably estimate peak BAC. OBJECTIVES: The aims of this study were to evaluate (1) the effect of SG, relative to RYGB and a presurgery group, on alcohol pharmacokinetics and subjective effects, and (2) whether breathalyzers are reliable in this population. SETTING: Single-center prospective nonrandomized trial. METHODS: We performed alcohol challenge tests in 11 women who had SG surgery 1.9 ± .1 years ago (body mass index = 35.1 ± 6.6 kg/m ), 8 women who had RYGB surgery 2.2 ± .4 years ago (body mass index = 30.0 ± 5.2 kg/m ), and 9 women who were scheduled for bariatric surgery (body mass index = 44.1 ± 4.0 kg/m ). BACs were estimated from breath samples and measured by gas chromatography at various times after consuming approximately 2 standard drinks. RESULTS: BAC increased faster, peak BAC was approximately 2-fold higher, and feelings of drunkenness were heightened in both SG and RYGB groups relative to the presurgery group (P values<.001). BAC estimated from breath samples underestimated BAC by 27% (standard deviation = 13%) and missed peak BACs postsurgery. CONCLUSIONS: SG, similar to RYGB, causes marked alterations in the response to alcohol ingestion manifested by a faster and higher peak BAC. The breathalyzer is invalid to assess effects of gastric surgeries on pharmacokinetics of ingested alcohol.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  9 / 121299 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29524236
[Au] Autor:Tougaard RS; Hansen ESS; Laustsen C; Lindhardt J; Schroeder M; Bøtker HE; Kim WY; Wiggers H; Stødkilde-Jørgensen H
[Ad] Address:Department of Cardiology, Aarhus University Hospital, Denmark.
[Ti] Title:Acute hypertensive stress imaged by cardiac hyperpolarized [1- C]pyruvate magnetic resonance.
[So] Source:Magn Reson Med;, 2018 Mar 09.
[Is] ISSN:1522-2594
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: Deranged metabolism is now recognized as a key causal factor in a variety of heart diseases, and is being studied extensively. However, invasive methods may alter metabolism, and conventional imaging techniques measure tracer uptake but not downstream metabolism. These challenges may be overcome by hyperpolarized MR, a noninvasive technique currently crossing the threshold into human trials. The aim of this study was to image metabolic changes in the heart in response to endogastric glucose bolus and to acute hypertension. METHODS: Five postprandial pigs were scanned with hyperpolarized [1- C]pyruvate cardiac MR at baseline, after oral glucose bolus, and after infusion of angiotensin-II. RESULTS: No effect of glucose bolus was seen using hyperpolarized [1- C]pyruvate MR despite changes in circulating substrates. During angiotensin-II infusion, blood pressure increased 179% (P = 0.008) and ejection fraction decreased from 54 ± 2% to 47 ± 6% (P = 0.03) The hemodynamic changes were accompanied by increases in the hyperpolarized [1- C]pyruvate MR derived ratios of lactate/alanine (from 0.58 ± 0.13 to 0.78 ± 0.06, P = 0.03) and bicarbonate/alanine (from 0.55 ± 0.12 to 0.91 ± 0.14, P = 0.007). CONCLUSION: Glucose loading did not alter cardiac metabolism, but during acute hypertensive stress, cardiac aerobic, carbohydrate metabolism, and pyruvate-lactate exchange was altered. Hyperpolarized MR allows noninvasive evaluation of acute changes in cardiac metabolism. However, hemodynamics must be taken into account when interpreting the results.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1002/mrm.27164

  10 / 121299 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 29524196
[Au] Autor:Tripathi D; Mani V; Pal RP
[Ad] Address:National Dairy Research Institute, Karnal, Haryana, India. deepika.trip03@gmail.com.
[Ti] Title:Vanadium in Biosphere and Its Role in Biological Processes.
[So] Source:Biol Trace Elem Res;, 2018 Mar 09.
[Is] ISSN:1559-0720
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Ultra-trace elements or occasionally beneficial elements (OBE) are the new categories of minerals including vanadium (V). The importance of V is attributed due to its multifaceted biological roles, i.e., glucose and lipid metabolism as an insulin-mimetic, antilipemic and a potent stress alleviating agent in diabetes when vanadium is administered at lower doses. It competes with iron for transferrin (binding site for transportation) and with lactoferrin as it is secreted in milk also. The intracellular enzyme protein tyrosine phosphatase, causing the dephosphorylation at beta subunit of the insulin receptor, is inhibited by vanadium, thus facilitating the uptake of glucose inside the cell but only in the presence of insulin. Vanadium could be useful as a potential immune-stimulating agent and also as an antiinflammatory therapeutic metallodrug targeting various diseases. Physiological state and dose of vanadium compounds hold importance in causing toxicity also. Research has been carried out mostly on laboratory animals but evidence for vanadium importance as a therapeutic agent are available in humans and large animals also. This review examines the potential biochemical and molecular role, possible kinetics and distribution, essentiality, immunity, and toxicity-related study of vanadium in a biological system.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s12011-018-1289-y


page 1 of 12130 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information