Database : MEDLINE
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[PMID]: 29514047
[Au] Autor:Kors L; Rampanelli E; Stokman G; Butter L; Held NM; Claessen N; Larsen PWB; Verheij J; Zuurbier CJ; Liebisch G; Schmitz G; Girardin SE; Florquin S; Houtkooper RH; Leemans JC
[Ad] Address:Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands. Electronic address: l.kors@amc.uva.nl.
[Ti] Title:Deletion of NLRX1 increases fatty acid metabolism and prevents diet-induced hepatic steatosis and metabolic syndrome.
[So] Source:Biochim Biophys Acta;, 2018 Mar 04.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:NOD-like receptor (NLR)X1 (NLRX1) is an ubiquitously expressed inflammasome-independent NLR that is uniquely localized in mitochondria with as yet unknown effects on metabolic diseases. Here, we report that NLRX1 is essential in regulating cellular metabolism in non-immune parenchymal hepatocytes by decreasing mitochondrial fatty acid-dependent oxidative phosphorylation (OXPHOS) and promoting glycolysis. NLRX1 loss in mice has a profound impact on the prevention of diet-induced metabolic syndrome parameters, non-alcoholic fatty liver disease (NAFLD) progression, and renal dysfunction. Despite enhanced caloric intake, NLRX1 deletion in mice fed a western diet (WD) results in protection from liver steatosis, hepatic fibrosis, obesity, insulin resistance, glycosuria and kidney dysfunction parameters independent from inflammation. While mitochondrial content was equal, NLRX1 loss in hepatocytes leads to increased fatty acid oxidation and decreased steatosis. In contrast, glycolysis was decreased in NLRX1-deficient cells versus controls. Thus, although first implicated in immune regulation, we show that NLRX1 function extends to the control of hepatocyte energy metabolism via the restriction of mitochondrial fatty acid-dependent OXPHOS and enhancement of glycolysis. As such NLRX1 may be an attractive novel therapeutic target for NAFLD and metabolic syndrome.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher

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[PMID]: 29484379
[Au] Autor:Li Y; Liu J; Liao G; Zhang J; Chen Y; Li L; Li L; Liu F; Chen B; Guo G; Wang C; Yang L; Cheng J; Lu Y
[Ad] Address:Key Laboratory of Transplant Engineering and Immunology, National Health and Family Planning Commission (NHFPC), West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
[Ti] Title:Early intervention with mesenchymal stem cells prevents nephropathy in diabetic rats by ameliorating the inflammatory microenvironment.
[So] Source:Int J Mol Med;41(5):2629-2639, 2018 May.
[Is] ISSN:1791-244X
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Diabetic nephropathy (DN) is a major complication of diabetes and represents the leading cause of end-stage renal disease. Mesenchymal stem cell (MSC) treatment has been demonstrated to be effective in DN models by reducing albuminuria and attenuating glomerular injury; however, limited in-depth understanding of the underlying mechanism and a lack of clinical trials hinders its clinical use. Additionally, most of these experimental studies were conducted on the advanced stage of nephropathy, which is difficult to reverse and consequently showed limited therapeutic efficacy. We sought to evaluate whether early intervention by MSCs has the potential to prevent DN onset and progression as well as protect kidney function when intravenously administered to rats with diabetes. Diabetes was induced in adult male SD rats by streptozotocin (STZ) injection (55 mg/kg, i.p.). The diabetic rats were injected with or without bone marrow-derived MSCs (5x106 per rat), via tail vein at 2, 4, 5 and 7 weeks after diabetes onset. Fasting blood glucose (FBG), blood urea nitrogen (BUN) and serum creatinine (Scr) levels in serum samples and glycosuria (GLU), microalbumin (MAU), and albumin to creatinine ratio (ACR) in urine samples were determined. Renal pathology and immunohistochemistry (IHC) for CD68, MCP-1, fibronectin (FN), transforming growth factor-ß (TGF-ß) and pro-inflammatory cytokines were also performed. Expression levels of the above factors as well as interleukin-10 (IL-10), and epidermal growth factor (EGF) were assessed by qPCR and multiplex bead-based suspension array system, respectively. Additionally, MSC tracing in vivo was performed. Ex vivo, peritoneal macrophages were co-cultured with MSCs, and expression of inflammatory cytokines was detected as well. MSC treatment profoundly suppressed renal macrophage infiltration and inflammatory cytokine secretion in diabetic rats, resulting in prominently improved kidney histology, systemic homeostasis, and animal survival, although no significant effect on hyperglycemia was observed. Engrafted MSCs were primarily localized in deteriorated areas of the kidney and immune organs 48 h after infusion. MSC treatment upregulated serum anti-inflammatory cytokines IL-10 and EGF. Ex vivo, MSCs inhibited lipopolysaccharide (LPS)-stimulated rat peritoneal macrophage activation via the downregulation of inflammatory-related cytokines such as IL-6, MCP-1, tumor necrosis factor-α (TNF-α) and IL-1ß. Our results demonstrated that early intervention with MSCs prevented renal injury via immune regulation in diabetic rats, which restored the homeostasis of the immune microenvironment, contributing to the prevention of kidney dysfunction and glomerulosclerosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process
[do] DOI:10.3892/ijmm.2018.3501

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[PMID]: 29507272
[Au] Autor:Naji Ebrahimi Yazd Z; Hosseinian S; Shafei MN; Ebrahimzadeh Bideskan A; Entezari Heravi N; Parhizgar S; Shahraki S; Samadi Noshahr Z; Mahzari S; Khajavi Rad A
[Ti] Title:Protection Against Doxorubicin-induced Nephropathy by Plantago major in Rat.
[So] Source:Iran J Kidney Dis;12(2):99-106, 2018 Mar.
[Is] ISSN:1735-8604
[Cp] Country of publication:Iran
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Nephropathy is an important side effect of doxorubicin. The aim of the current study was to investigate the protective effect of Plantago major extract against doxorubicin-induced functional and histological damage in rat's kidney. MATERIALS AND METHODS: Sixty Albino rats were randomly divided into 6 groups. Doxorubicin, 5 mg/kg, was injected intravenously on the 7th day of the study. Animals were treated with dexamethasone, 0.9 mg/kg, vitamin E, 100 mg/kg, and P major extract, 600 mg/kg and 1200 mg/kg, for 7 days before and 4 weeks after doxorubicin administration. Glomerular filtration rate, urea clearance, and urine glucose concentration were determined on the 1st day and 1, 2, 3 and 4 weeks after doxorubicin injection. Histological changes were also examined and the end of the study. RESULTS: Doxorubicin caused significant decreases in glomerular filtration rate and urea clearance and significant glycosuria and kidney damage. Urea clearance in the rats treated with P major showed no significant change between different days of the experiment. Administration of dexamethasone, vitamin E, and low- and high-dose P major significantly improved the glycosuria and kidney tissue damage. CONCLUSIONS: These findings suggested that hydroalcoholic extract of P major protected renal tissue against doxorubicin-induced nephropathy. The protective effects of P major on renal lesions associated with doxorubicin may be due to its antioxidant and anti-inflammatory actions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Data-Review

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[PMID]: 29494520
[Au] Autor:Torlinska B; Bath SC; Janjua A; Boelaert K; Chan SY
[Ad] Address:Institute of Applied Health Research, University of Birmingham, Birmingham B15 2TT, UK. b.torlinska@bham.ac.uk.
[Ti] Title:Iodine Status during Pregnancy in a Region of Mild-to-Moderate Iodine Deficiency is not Associated with Adverse Obstetric Outcomes; Results from the Avon Longitudinal Study of Parents and Children (ALSPAC).
[So] Source:Nutrients;10(3), 2018 Mar 01.
[Is] ISSN:2072-6643
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Severe iodine deficiency during pregnancy has been associated with pregnancy/neonatal loss, and adverse pregnancy outcomes; however, the impact of mild-to-moderate iodine insufficiency, though prevalent in pregnancy, is not well-documented. We assessed whether mild iodine deficiency during pregnancy was associated with pregnancy/infant loss, or with other adverse pregnancy outcomes. We used samples and data from the Avon Longitudinal Study of Parents and Children (ALSPAC), from 3140 singleton pregnancies and from a further 42 women with pregnancy/infant loss. The group was classified as mildly-to-moderately iodine deficient with a median urinary iodine concentration of 95.3 µg/L (IQR 57.0-153.0; median urinary iodine-to-creatinine ratio (UI/Creat) 124 µg/g, IQR 82-198). The likelihood of pregnancy/infant loss was not different across four UI/Creat groups (<50, 50-149, 150-250, >250 µg/g). The incidence of pre-eclampsia, non-proteinuric gestational hypertension, gestational diabetes, glycosuria, anaemia, post-partum haemorrhage, preterm delivery, mode of delivery, being small for gestational age, and large for gestational age did not differ significantly among UI/Creat groups, nor were there any significant differences in the median UI/Creat. We conclude that maternal iodine status was not associated with adverse pregnancy outcomes in a mildly-to-moderately iodine-deficient pregnant population. However, in view of the low number of women with pregnancy/infant loss in our study, further research is required.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Process

  5 / 4928 MEDLINE  
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[PMID]: 29440005
[Au] Autor:Wilcox CS; Shen W; Boulton DW; Leslie BR; Griffen SC
[Ad] Address:Division of Nephrology and Hypertension, and Hypertension Research Center, Georgetown University, Washington, DC wilcoxch@georgetown.edu.
[Ti] Title:Interaction Between the Sodium-Glucose-Linked Transporter 2 Inhibitor Dapagliflozin and the Loop Diuretic Bumetanide in Normal Human Subjects.
[So] Source:J Am Heart Assoc;7(4), 2018 Feb 10.
[Is] ISSN:2047-9980
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Dapagliflozin inhibits the sodium-glucose-linked transporter 2 in the renal proximal tubule, thereby promoting glycosuria to reduce hyperglycemia in type 2 diabetes mellitus. Because these patients may require loop diuretics, and sodium-glucose-linked transporter 2 inhibition causes an osmotic diuresis, we evaluated the diuretic interaction between dapagliflozin and bumetanide. METHODS AND RESULTS: Healthy subjects (n=42) receiving a fixed diet with ≈110 mmol·d of Na were randomized to bumetanide (1 mg·d ), dapagliflozin (10 mg·d ), or both for 7 days, followed by 7 days of both. There were no meaningful pharmacokinetic interactions. Na excretion increased modestly with the first dose of dapagliflozin (22±6 mmol·d ; <0.005) but by more ( <0.005) with the first dose of bumetanide (74±7 mmol·d ; <0.005), which was not significantly different from both diuretics together (80±5 mmol·d ; <0.005). However, Na excretion with dapagliflozin was 190% greater ( <0.005) when added after 1 week of bumetanide (64±6 mmol·d ), and Na excretion with bumetanide was 36% greater ( <0.005) when added after 1 week of dapagliflozin (101±8 mmol·d ). Serum urate was increased 4% by bumetanide but reduced 40% by dapagliflozin or 20% by combined therapy ( <0.05). CONCLUSIONS: First-dose Na excretion with bumetanide and dapagliflozin is not additive, but the weekly administration of one diuretic enhances the initial Na excretion with the other, thereby demonstrating mutual adaptive natriuretic synergy. Combined therapy reverses bumetanide-induced hyperuricemia. This requires further study in diabetic patients with hyperglycemia who have enhanced glycosuria and natriuresis with dapagliflozin. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00930865.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Data-Review

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[PMID]: 29306791
[Au] Autor:Zhou H; Wang S; Zhu P; Hu S; Chen Y; Ren J
[Ad] Address:Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing 100853, China. Electronic address: zhouhao301@outlook.com.
[Ti] Title:Empagliflozin rescues diabetic myocardial microvascular injury via AMPK-mediated inhibition of mitochondrial fission.
[So] Source:Redox Biol;15:335-346, 2018 May.
[Is] ISSN:2213-2317
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Impaired cardiac microvascular function contributes to diabetic cardiovascular complications although effective therapy remains elusive. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor recently approved for treatment of type 2 diabetes, promotes glycosuria excretion and offers cardioprotective actions beyond its glucose-lowering effects. This study was designed to evaluate the effect of empagliflozin on cardiac microvascular injury in diabetes and the underlying mechanism involved with a focus on mitochondria. Our data revealed that empagliflozin improved diabetic myocardial structure and function, preserved cardiac microvascular barrier function and integrity, sustained eNOS phosphorylation and endothelium-dependent relaxation, as well as improved microvessel density and perfusion. Further study suggested that empagliflozin exerted its effects through inhibition of mitochondrial fission in an adenosine monophosphate (AMP)-activated protein kinase (AMPK)-dependent manner. Empagliflozin restored AMP-to-ATP ratio to trigger AMPK activation, suppressed Drp1 phosphorylation, and increased Drp1 phosphorylation, ultimately leading to inhibition of mitochondrial fission. The empagliflozin-induced inhibition of mitochondrial fission preserved cardiac microvascular endothelial cell (CMEC) barrier function through suppressed mitochondrial reactive oxygen species (mtROS) production and subsequently oxidative stress to impede CMEC senescence. Empagliflozin-induced fission loss also favored angiogenesis by promoting CMEC migration through amelioration of F-actin depolymerization. Taken together, these results indicated the therapeutic promises of empagliflozin in the treatment of pathological microvascular changes in diabetes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:In-Data-Review

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[PMID]: 29444358
[Au] Autor:Capulli M; Ponzetti M; Maurizi A; Gemini-Piperni S; Berger T; Mak TW; Teti A; Rucci N
[Ad] Address:Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, Italy.
[Ti] Title:A COMPLEX ROLE FOR LIPOCALIN 2 IN BONE METABOLISM: GLOBAL ABLATION IN MICE INDUCES OSTEOPENIA CAUSED BY AN ALTERED ENERGY METABOLISM.
[So] Source:J Bone Miner Res;, 2018 Feb 14.
[Is] ISSN:1523-4681
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Lipocalin 2 (Lcn2) is an adipokine that carries out a variety of functions in diverse organs. We investigated the bone phenotype and the energy metabolism of Lcn2 globally deleted mice (Lcn2 ) at different ages. Lcn2 mice were largely osteopenic, exhibiting lower trabecular bone volume, lesser trabecular number and higher trabecular separation when compared to wild type (WT) mice. Lcn2 mice showed a lower osteoblast number and surface over bone surface, and subsequently a significantly lower bone formation rate, while osteoclast variables were unremarkable. Surprisingly, we found no difference in Alkaline Phosphatase (ALP) activity or in nodule mineralization in Lcn2 calvaria osteoblast cultures, while less ALP-positive colonies were obtained from freshly isolated Lcn2 bone marrow stromal cells, suggesting a non-autonomous osteoblast response to Lcn2 ablation. Given that Lcn2 mice showed higher body weight and hyperphagia, we investigated whether their osteoblast impairment could be due to altered energy metabolism. Lcn2 mice showed lower fasted glycemia and hyperinsulinemia. Consistently, glucose tolerance was significantly higher in Lcn2 compared to WT mice, while insulin tolerance was similar. Lcn2 mice also exhibited polyuria, glycosuria, proteinuria and renal cortex vacuolization, suggesting a kidney contribution to their phenotype. Interestingly, the expression of the glucose transporter protein type 1, that conveys glucose into the osteoblasts and is essential for osteogenesis, was significantly lower in the Lcn2 bone, possibly explaining the in vivo osteoblast impairment induced by the global Lcn2 ablation. Taken together, these results unveil an important role of Lcn2 in bone metabolism, highlighting a link with glucose metabolism that is more complex than expected from the current knowledge. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180214
[Lr] Last revision date:180214
[St] Status:Publisher
[do] DOI:10.1002/jbmr.3406

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[PMID]: 28458353
[Au] Autor:Takasu T; Hayashizaki Y; Hirosumi J; Minoura H; Amino N; Kurosaki E; Takakura S
[Ad] Address:Tsukuba Research Center, Drug Discovery Research, Astellas Pharma Inc.
[Ti] Title:The Sodium Glucose Cotransporter 2 Inhibitor Ipragliflozin Promotes Preferential Loss of Fat Mass in Non-obese Diabetic Goto-Kakizaki Rats.
[So] Source:Biol Pharm Bull;40(5):675-680, 2017.
[Is] ISSN:1347-5215
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:Sodium glucose cotransporter 2 (SGLT2) inhibitors improve hyperglycemia in patients with type 2 diabetes mellitus (T2DM) by increasing urinary glucose excretion. In addition to their antihyperglycemic effect, SGLT2 inhibitors also reduce body weight and fat mass in obese and overweight patients with T2DM. However, whether or not SGLT2 inhibitors similarly affect body composition of non-obese patients with T2DM remains unclear. In this study, we investigated the effect of the SGLT2 inhibitor ipragliflozin on body composition in a Goto-Kakizaki (GK) rat model of non-obese T2DM. GK rats were treated with ipragliflozin once daily for 9 weeks, starting at 23 weeks of age. Body composition was then analyzed using dual-energy X-ray absorptiometry. Treatment with ipragliflozin increased urinary glucose excretion, reduced hemoglobin A1c (HbA1c) levels and suppressed body weight gain as the dose increased. Body composition analysis revealed that body fat mass was lower in the ipragliflozin-treated groups than in the control group, while lean body mass and bone mineral contents were comparable between groups. Thus, an SGLT2 inhibitor ipragliflozin was found to promote preferential loss of fat mass in a rat model of non-obese T2DM. Ipragliflozin might also promote preferential loss of fat in non-obese patients with T2DM.
[Mh] MeSH terms primary: Adipose Tissue/drug effects
Diabetes Mellitus, Type 2/drug therapy
Glucosides/pharmacology
Hypoglycemic Agents/pharmacology
Sodium-Glucose Transporter 2/antagonists & inhibitors
Thiophenes/pharmacology
[Mh] MeSH terms secundary: Absorptiometry, Photon
Adipose Tissue/pathology
Animals
Body Composition/drug effects
Diabetes Mellitus, Type 2/pathology
Diet, High-Fat
Eating/drug effects
Glycosuria/metabolism
Male
Rats
Rats, Wistar
Weight Loss/drug effects
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Glucosides); 0 (Hypoglycemic Agents); 0 (Sglt2 protein, rat); 0 (Sodium-Glucose Transporter 2); 0 (Thiophenes); 3N2N8OOR7X (ipragliflozin)
[Em] Entry month:1802
[Cu] Class update date: 180212
[Lr] Last revision date:180212
[Js] Journal subset:IM
[Da] Date of entry for processing:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00964

  9 / 4928 MEDLINE  
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[PMID]: 29301516
[Au] Autor:Sato T; Aizawa Y; Yuasa S; Kishi S; Fuse K; Fujita S; Ikeda Y; Kitazawa H; Takahashi M; Sato M; Okabe M
[Ad] Address:Cardiology, Tachikawa General Hospital, 561-1 Jyojyomachi Aza Yauchi, Nagaoka, Japan. kirotaro19731013@yahoo.co.jp.
[Ti] Title:The effect of dapagliflozin treatment on epicardial adipose tissue volume.
[So] Source:Cardiovasc Diabetol;17(1):6, 2018 Jan 04.
[Is] ISSN:1475-2840
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Glycosuria produced by sodium-glucose co-transporter-2 (SGLT-2) inhibitors is associated with weight loss. SGLT-2 inhibitors reportedly might reduce the occurrence of cardiovascular events. Epicardial adipose tissue (EAT) is a pathogenic fat depot that may be associated with coronary atherosclerosis. The present study evaluated the relationship between an SGLT-2 inhibitor (dapagliflozin) and EAT volume. METHODS: In 40 diabetes mellitus patients with coronary artery disease (10 women and 30 men; mean age of all 40 patients was 67.2 ± 5.4 years), EAT volume was compared prospectively between the dapagliflozin treatment group (DG; n = 20) and conventional treatment group (CTG; n = 20) during a 6-month period. EAT was defined as any pixel that had computed tomography attenuation of - 150 to - 30 Hounsfield units within the pericardial sac. Metabolic parameters, including HbA1c, tumor necrotic factor-α (TNF-α), and plasminogen activator inhibitor-1 (PAI-1) levels, were measured at both baseline and 6-months thereafter. RESULTS: There were no significant differences at baseline of EAT volume and HbA1c, PAI-1, and TNF-α levels between the two treatment groups. After a 6-month follow-up, the change in HbA1c levels in the DG decreased significantly from 7.2 to 6.8%, while body weight decreased significantly in the DG compared with the CTG (- 2.9 ± 3.4 vs. 0.2 ± 2.4 kg, p = 0.01). At the 6-month follow-up, serum PAI-1 levels tended to decline in the DG. In addition, the change in the TNF-α level in the DG was significantly greater than that in the CTG (- 0.5 ± 0.7 vs. 0.03 ± 0.3 pg/ml, p = 0.03). Furthermore, EAT volume significantly decreased in the DG at the 6-month follow-up compared with the CTG (- 16.4 ± 8.3 vs. 4.7 ± 8.8 cm , p = 0.01). Not only the changes in the EAT volume and body weight, but also those in the EAT volume and TNF-α level, showed significantly positive correlation. CONCLUSION: Treatment with dapagliflozin might improve systemic metabolic parameters and decrease the EAT volume in diabetes mellitus patients, possibly contributing to risk reduction in cardiovascular events.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180210
[Lr] Last revision date:180210
[St] Status:In-Data-Review
[do] DOI:10.1186/s12933-017-0658-8

  10 / 4928 MEDLINE  
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[PMID]: 29412123
[Au] Autor:Pantelidis P; Kalliakmanis A; Mitas C; Sideris M; Grassos C; Pittaras A; Manolis A
[Ad] Address:2nd Propedeutic Department of Internal Medicine, Aristotle University of Thessaloniki . Greece.
[Ti] Title:Sodium-glucose cotransporter 2 inhibitors: The pleiotropic mechanisms of actions.
[So] Source:Cardiovasc Hematol Disord Drug Targets;, 2018 Feb 06.
[Is] ISSN:2212-4063
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Sodium-glucose cotransporter 2 (SGLT-2) inhibitors are a new class of oral antidiabetic drugs. So far, there are three agents approved for use in Europe and in the USA, two in Japan and another four agents under testing. OBJECTIVE: The purpose of this study is to describe the mechanism of action and the favorable and adverse effects of SGLT-2 inhibitors. METHOD: A thorough review of literature indexed in PubMed, Scopus and Cochrane databases was conducted. Original papers, review papers and their relevant references in English, from 2005 to February 2017, were included. RESULTS: The main mechanism of action is the glycosuria induced by the inhibition of SGLT-2, located in the early segment of the proximal convoluted tubule. Along with large amounts of glucose, sodium, water and uric acid are also excessively excreted in urine. These actions have various, both desired and adverse, consequent implications in kidneys, blood pressure, cardiovascular system and other systems. Moreover, SGLT-2 inhibitors act directly to organs other than the kidneys, as SGLT-2 can be expressed there. CONCLUSION: The underlying mechanisms responsible for the SGLT-2 inhibitor actions, are pleiotropic and occur in the kidneys, as well as in other target organs. The comprehension of these mechanisms, not only permits us to understand their actions better, but it could also help us to predict more of their undisclosed favorable actions, as well as their rare adverse effects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180207
[Lr] Last revision date:180207
[St] Status:Publisher
[do] DOI:10.2174/1871529X18666180206130218


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