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  • S. Karger AG  (26)
  • Englisch  (26)
  • 2015-2019  (26)
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  • S. Karger AG  (26)
Person/Organisation
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  • Englisch  (26)
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  • 2015-2019  (26)
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Fachgebiete(RVK)
  • 1
    Online-Ressource
    Online-Ressource
    Guidelines for Diagnosis and Treatment of Primary Liver Cancer in China (2017 Edition)
    S. Karger AG ; 2018
    In:  Liver Cancer Vol. 7, No. 3 ( 2018), p. 235-260
    Details
    In: Liver Cancer, S. Karger AG, Vol. 7, No. 3 ( 2018), p. 235-260
    Kurzfassung: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Hepatocellular carcinoma (HCC) (about 85–90% of primary liver cancer) is particularly prevalent in China because of the high prevalence of chronic hepatitis B infection. HCC is the fourth most common malignancy and the third leading cause of tumor-related deaths in China. It poses a significant threat to the life and health of Chinese people. 〈 b 〉 〈 i 〉 Summary: 〈 /i 〉 〈 /b 〉 This guideline presents official recommendations of the National Health and Family Planning Commission of the People’s Republic of China on the surveillance, diagnosis, staging, and treatment of HCC occurring in China. The guideline was written by more than 50 experts in the field of HCC in China (including liver surgeons, medical oncologists, hepatologists, interventional radiologists, and diagnostic radiologists) on the basis of recent evidence and expert opinions, balance of benefits and harms, cost-benefit strategies, and other clinical considerations. 〈 b 〉 〈 i 〉 Key Messages: 〈 /i 〉 〈 /b 〉 The guideline presents the Chinese staging system, and recommendations regarding patients with HCC in China to ensure optimum patient outcomes.
    Materialart: Online-Ressource
    ISSN: 2235-1795 , 1664-5553
    URL: Article
    DOI: 10.1159/000488035
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2018
    ZDB Id: 2666925-0
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 2
    Online-Ressource
    Online-Ressource
    Comparison of Clinical Efficacy of Cytarabine with Different Regimens in Postremission Consolidation Therapy for Adult t(8;21) AML Patients: A Multicenter Retrospective Study in China
    S. Karger AG ; 2016
    In:  Acta Haematologica Vol. 136, No. 4 ( 2016), p. 201-209
    Details
    In: Acta Haematologica, S. Karger AG, Vol. 136, No. 4 ( 2016), p. 201-209
    Kurzfassung: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 The survival of patients with acute myeloid leukemia (AML) with t(8;21) was reported to be shorter in China than in other countries. 〈 b 〉 〈 i 〉 Patients: 〈 /i 〉 〈 /b 〉 We analyzed the correlation between different cytarabine (Ara-c) regimens and outcome in 255 t(8;21) AML patients in China who received postremission consolidation chemotherapy only. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 The 5-year overall survival (OS) of the high-dose Ara-c group (HDAC; 2≤ Ara-c ≤3 g/m 〈 sup 〉 2 〈 /sup 〉 ), intermediate-dose Ara-c group (MDAC; 1.0≤ Ara-c 〈 2.0 g/m 〈 sup 〉 2 〈 /sup 〉 ), low-dose Ara-c group (LDAC; 0.2 〈 Ara-c 〈 1.0 g/m 〈 sup 〉 2 〈 /sup 〉 ) and standard-dose Ara-c group (SDAC; 0.1≤ Ara-c ≤0.2 g/m 〈 sup 〉 2 〈 /sup 〉 ) were 65.3, 39.4, 25.2 and 27.9%, respectively (p = 0.003). In the HDAC group, but not in the MDAC group, the 5-year OS of patients who achieved 3-4 cycles of chemotherapy was superior to those who underwent 1-2 cycles (84.4 vs. 43.6%, p 〈 0.05), and the 3-year OS of patients who achieved an accumulated 36 g/m 〈 sup 〉 2 〈 /sup 〉 of Ara-c was significantly higher compared to those who did not (85.3 vs. 39.2%, p 〈 0.05). Multivariate analysis indicated that factors such as WBC 〉 3.5 × 10 〈 sup 〉 9 〈 /sup 〉 /l, PLT ≤30 × 10 〈 sup 〉 9 〈 /sup 〉 /l, and extramedullary infiltration were associated with a poor prognosis. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 The survival of t(8;21) AML patients treated with high-dose Ara-c (≥2 g/m 〈 sup 〉 2 〈 /sup 〉 ) was superior to other dose levels in postremission consolidation chemotherapy. Patient survival was improved by 3-4 cycles of chemotherapy with an accumulated concentration of 36 g/m 〈 sup 〉 2 〈 /sup 〉 of Ara-c. WBC 〉 3.5 × 10 〈 sup 〉 9 〈 /sup 〉 /l, PLT ≤30 × 10 〈 sup 〉 9 〈 /sup 〉 /l and extramedullary infiltration could be indicative of a poor clinical prognosis.
    Materialart: Online-Ressource
    ISSN: 0001-5792 , 1421-9662
    URL: Article
    DOI: 10.1159/000448209
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2016
    ZDB Id: 1481888-7
    ZDB Id: 80008-9
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 3
    Online-Ressource
    Online-Ressource
    Activation of TGF-β1/α-SMA/Col I Profibrotic Pathway in Fibroblasts by Galectin-3 Contributes to Atrial Fibrosis in Experimental Models and Patients
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 47, No. 2 ( 2018), p. 851-863
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 47, No. 2 ( 2018), p. 851-863
    Kurzfassung: Background/Aims: This study aimed to evaluate whether galectin-3 (Gal-3) contributes actively to atrial fibrosis both in patients and experimental atrial fibrillation (AF) models. Methods: Mouse HL-1 cardiomyocytes were subjected to rapid electrical stimulation (RES) to explore Gal-3 expression and secretion levels by western blotting (WB) and enzyme linked immunosorbent assay (ELISA). Neonatal rat cardiac fibroblasts were treated with conditioned culture medium and recombinant human Gal-3 to evaluate the activation of the transforming growth factor (TGF)-β1/α-smooth muscle actin (SMA)/collagen I (Col I) profibrotic pathway (WB) and fibroblast proliferation with a Cell Counting Kit-8 (CCK-8). Furthermore, in the rapid atrial pacing (RAP) rabbit AF model, atrial Gal-3 expression and its effects on the profibrotic pathway were evaluated (WB and Masson’s trichrome staining). Moreover, 44 consecutive patients who underwent single mitral valve repair/replacement were included, consisting of 28 patients with persistent AF (PeAF) and 16 with sinus rhythm (SR). Coronary sinus blood was also sampled to test circulating Gal-3 levels (ELISA), and atrial myocardium Gal-3 and its downstream TGF-β1/α-SMA pathway were also measured by WB and immunohistochemical staining. Results: Gal-3 expression in HL-1 cells and its secretion level in culture medium were greatly increased after 24 h RES. Treatment of neonatal rat cardiac fibroblasts with conditioned media collected from the RES group or recombinant human Gal-3 protein (10 and 30 µg/mL) for 72 h induced the activation of the TGF-β1/α-SMA/Col I profibrotic pathway. RAP increased Gal-3 levels and activated the TGF-β1/α-SMA/Col I pathway in rabbit left atria, while the Gal-3 inhibitor N-acetyllactosamine, injected at 4.5 mg/kg every 3 days, mitigated these adverse changes. Furthermore, Gal-3 levels in coronary sinus blood samples and myocardial Gal-3 expression levels were higher in the PeAF patients than in the SR patients, and higher level profibrotic pathway activation was also confirmed. Conclusions: Activation of Gal-3 expression in the atria can subsequently activate the TGF-β1/α-SMA/Col I pathway in cardiac fibroblasts, which may enhance atrial fibrosis.
    Materialart: Online-Ressource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000490077
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2018
    ZDB Id: 1482056-0
    SSG: 12
    SSG: 15,3
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 4
    Online-Ressource
    Online-Ressource
    Effect of Exercise on Physical Recovery of People with Locked-In Syndrome after Stroke: What Do We Know from the Current Evidence? A Systematic Review
    S. Karger AG ; 2018
    In:  Cerebrovascular Diseases Extra Vol. 8, No. 2 ( 2018-7-13), p. 90-95
    Details
    In: Cerebrovascular Diseases Extra, S. Karger AG, Vol. 8, No. 2 ( 2018-7-13), p. 90-95
    Kurzfassung: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 Locked-in syndrome (LIS) results from a brainstem lesion in the pons. Ischemic stroke is the most common etiology of LIS. People with LIS have poor mobility with serious complications due to immobilization. Benefits of exercise after stroke have been widely reported. However, little is known about what and how much exercise should be prescribed for these patients. 〈 b 〉 〈 i 〉 Objectives: 〈 /i 〉 〈 /b 〉 To explore and evaluate the effect of exercise on the physical recovery of people with LIS after stroke. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We searched the following databases (last searched August 2017): EMBASE, MEDLINE, PubMed, CINAHL, AMED, PEDro, Cochrane Central Register of Controlled Trials, REHABDATA, Google Scholar, WANFANG, CNKI, and CQVIP. Handsearching of relevant journals and reference lists was also performed. The Oxford Centre for Evidence-Based Medicine was used to assess the evidence level of the included studies. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 We identified 5 papers from 207 papers involving 35 cases; 26 cases had various degrees of improvement in physical performance after exercise; 9 cases had no change. Five types of exercises and prescriptions were adopted. Study designs and interventions were heterogeneous. All studies contained mixed rehabilitation interventions. A total of 8 different outcome measurement tools have been reported in the studies. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Studies indicate a positive trend of effect of exercise for physical recovery of people with LIS after stroke including the improvement of muscle strength, tone, walking ability, and activity in daily living. Mixed physical exercises were used. The effects were not significant. No adverse event has been reported. The quality of the existing evidence is relatively low since the papers were either case series or case studies. Further studies are needed on exercise types and dosages for better prescriptions for people with LIS after stroke. This may help to extend their lives with better control of the complications and to improve their quality of life.
    Materialart: Online-Ressource
    ISSN: 1664-5456
    URL: Article
    DOI: 10.1159/000490312
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2018
    ZDB Id: 2651613-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    Online-Ressource
    Online-Ressource
    Synergistic Anticancer Activity of Combined Use of Caffeic Acid with Paclitaxel Enhances Apoptosis of Non-Small-Cell Lung Cancer H1299 Cells in Vivo and in Vitro
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 48, No. 4 ( 2018), p. 1433-1442
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 48, No. 4 ( 2018), p. 1433-1442
    Kurzfassung: Background/Aims: Caffeic acid (CA) is known to possess multiple biological activities including anti-cancer activities. However, the molecular mechanisms underlying these activities in non-small-cell lung cancer (NSCLC) cells are not fully understood. We attempted to clarify whether CA could enhance paclitaxel (PTX)-induced cytotoxicity in H1299 cells. Methods: First, we tested the cytotoxic effects in both H1299 cells and normal human Bease-2b cells by cell proliferation experiments. Next, we use Annexin V/propidium iodide apoptosis analysis and flow cytometric analysis to investigate apoptosis and cell cycle arrest under the treatments mentioned above. To further pinpoint changes in apoptosis, we tested the caspase-associated apoptotic pathway, which involves the activities of caspase-3 and caspase-9. Moreover, apoptosis-related proteins and MAPK pathway proteins were examined by western blot. An H1299 xenograft nude mice model was used to further evaluate the tumor-suppressing effects of CA and PTX in vivo. Results: Combination treatment with low-dose CA and PTX decreased the proliferation of NSCLC H1299 cells but not normal Beas-2b cells. Flow cytometry showed that H1299 cells were arrested in the sub-G1 phase and apoptosis was significantly increased in H1299 cells after CA treatment. Caspase-3 and caspase-9 activities were both increased after CA treatment. Furthermore, CA increased the PTX-induced activation of Bax, Bid, and downstream cleaved PARP, and phosphorylation of extracellular signal regulated kinase1/2 and c-Jun NH2-terminal protein kinase1/2. An in vivo tumor-suppression assay demonstrated that CA and PTX combined treatment exerted a more effective suppressive effect on tumor growth in H1299 xenografts without causing significant adverse effects. Conclusions: Our results indicated that CA inhibited NSCLC H1299 cell growth by inducing apoptosis and CA and PTX combined produced a synergistic anti-cancer effect in H1299 cells.
    Materialart: Online-Ressource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000492253
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2018
    ZDB Id: 1482056-0
    SSG: 12
    SSG: 15,3
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 6
    Online-Ressource
    Online-Ressource
    Exosomes Derived from Mesenchymal Stem Cells Rescue Myocardial Ischaemia/Reperfusion Injury by Inducing Cardiomyocyte Autophagy Via AMPK and Akt Pathways
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 43, No. 1 ( 2017), p. 52-68
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 43, No. 1 ( 2017), p. 52-68
    Kurzfassung: Background/Aims: Reperfusion after an ischaemic insult might cause infarct extension. Mesenchymal stem cell (MSC)-derived exosomes could attenuate myocardial remodelling in animal models of myocardial ischaemia reperfusion injury (MIRI), and the present study aimed to explore the related mechanisms. Methods: In vitro, rat H9C2 cardiomyocytes (H9C2s) were exposed to H2O2. Cell viability was detected by the CCK-8 assay, apoptosis was detected by Annexin V-PE/7-AAD staining, ROS production was detected by fluorescence microscopy and flow cytometry, and apoptosis-related proteins and signalling pathway-related proteins were detected by western blot analysis. Autophagic flux was measured using the tandem fluorescent mRFG-GFP-LC3 assay. MSC-derived exosomes were extracted using the total exosome isolation reagent. Apoptosis, myocardial infarction size, heart function and myocardial LC3B expression were examined in an in vivo I/R model by the TUNEL assay, TTC/Evan blue staining, echocardiography and immunohistochemicalstaining, respectively. Results: In vitro, H2O2 dose-dependently increased ROS production and cell apoptosis in H9C2s and blocked autophagic flux after 3 h of exposure; autophagy gradually decreased thereafter, and the lowest level was detected at 12 h after exposure. MSC-derived exosomes reduced H2O2-induced ROS production and cell apoptosis and enhanced autophagy at 12 h after exposure. In H9C2 cells exposed to H2O2 for 12 h, treatment with exosomes enhanced autophagy via the AMPK/mTOR and Akt/mTOR pathways. Likewise, in vivo exosome injections in rats that underwent I/R injury significantly reduced apoptosis and the myocardial infarct size and upregulated myocardial LC3B expression as well as improved heart function. Conclusions: Our results indicate that MSC-derived exosomes could reduce MIRI by inducing cardiomyocyte autophagy via AMPK/mTOR and Akt/mTOR pathways.
    Materialart: Online-Ressource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000480317
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2017
    ZDB Id: 1482056-0
    SSG: 12
    SSG: 15,3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
    Online-Ressource
    Online-Ressource
    MicroRNA-125a Regulates Cell Proliferation Via Directly Targeting E2F2 in Osteosarcoma
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 43, No. 2 ( 2017), p. 768-774
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 43, No. 2 ( 2017), p. 768-774
    Kurzfassung: Background/Aims: Increasing evidence has shown that miR-125a plays important role in human cancer progression. However, little is known about the function of miR-125a in osteosarcoma. Methods: The expression of miR-125a in osteosarcoma tissues and cell lines were examined by qRT-PCR. The biological role of miR-125a in osteosarcoma cell proliferation was examined in vitro. The targets of miR-125a were identified by a dual-luciferase reporter assay. Results: The results showed that the expression of miR-125a expression is significantly lower in osteosarcoma tissues and cell lines. Survival curves showed that the survival of patients in high miR-125a expression was significantly longer than that of patients with low miR-125a expression, and multivariate analysis suggested that miR-125a is an independent prognostic factor for osteosarcoma patients. In addition, it was found in this study that miR-125a can inhibit the growth of osteosarcoma cells. The dual-luciferase reporter assay demonstrated that E2F2 is a novel target gene for miR-125a. In addition, in a recovery experiment, it was shown that miR-125a inhibits the biological function of osteosarcoma cells by inhibiting the expression of E2F2. Conclusion: Our results suggest that miR-125a acts as a tumor suppressor via regulation of E2F2 expression in osteosarcoma progression, and miR-125a may represent a novel therapeutic target for the treatment of osteosarcoma.
    Materialart: Online-Ressource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000481560
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2017
    ZDB Id: 1482056-0
    SSG: 12
    SSG: 15,3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
    Online-Ressource
    Online-Ressource
    Regulation of Insulin Resistance by Multiple MiRNAs via Targeting the GLUT4 Signalling Pathway
    S. Karger AG ; 2016
    In:  Cellular Physiology and Biochemistry Vol. 38, No. 5 ( 2016), p. 2063-2078
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 38, No. 5 ( 2016), p. 2063-2078
    Kurzfassung: Background/Aims: Type 2 Diabetes Mellitus (T2DM) is characterized by insulin resistance (IR), but the underlying molecular mechanisms are incompletely understood. MicroRNAs (miRNAs) have been demonstrated to participate in the signalling pathways relevant to glucose metabolism in IR. The purpose of this study was to test whether the multiple-target anti-miRNA antisense oligonucleotides (MTg-AMO) technology, an innovative miRNA knockdown strategy, can be used to interfere with multiple miRNAs that play critical roles in regulating IR. Methods: An MTg-AMO carrying the antisense sequences targeting miR-106b, miR-27a and miR-30d was constructed (MTg-AMO106b/27a/30d). Protein levels were determined by Western blot analysis, and transcript levels were detected by real-time RT-PCR (qRT-PCR). Insulin resistance was analysed with glucose consumption and glucose uptake assays. Results: We found that the protein level of glucose transporter 4 (GLUT4), Mitogen-activated protein kinase 14 (MAPK 14), Phosphatidylinositol 3-kinase regulatory subunit beta (PI3K regulatory subunit beta) and mRNA level of Slc2a4 (encode GLUT4), Mapk14 (encode MAPK 14) and Pik3r2 (encode PI3K regulatory subunit beta) were all significantly down-regulated in the skeletal muscle of diabetic rats and in insulin-resistant L6 cells. Overexpression of miR-106b, miR-27a and miR-30d in L6 cells decreased glucose consumption and glucose uptake, and reduced the expression of GLUT4, MAPK 14 and PI3K regulatory subunit beta. Conversely, silencing of endogenous miR-106b, miR-27a and miR-30d in insulin-resistant L6 cells enhanced glucose consumption and glucose uptake, and increased the expression of GLUT4, MAPK 14 and PI3K regulatory subunit beta. MTg-AMO106b/27a/30d up-regulated the protein levels of GLUT4, MAPK 14 and PI3K regulatory subunit beta, enhanced glucose consumption and glucose uptake. Conclusion: Our data suggested that miR-106b, miR-27a and miR-30d play crucial roles in the regulation of glucose metabolism by targeting the GLUT4 signalling pathway in L6 cells. Moreover, MTg-AMO106b/27a/30d offers more potent effects than regular singular AMOs.
    Materialart: Online-Ressource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000445565
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2016
    ZDB Id: 1482056-0
    SSG: 12
    SSG: 15,3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
    Online-Ressource
    Online-Ressource
    Factors Influencing Repair Outcomes of Vesicovaginal Fistula: A Retrospective Review of 139 Procedures
    S. Karger AG ; 2017
    In:  Urologia Internationalis Vol. 99, No. 1 ( 2017), p. 22-28
    Details
    In: Urologia Internationalis, S. Karger AG, Vol. 99, No. 1 ( 2017), p. 22-28
    Kurzfassung: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 We aimed to report the outcomes of patients undergoing vesicovaginal fistula (VVF) repair to identify prognostic factors. 〈 b 〉 〈 i 〉 Materials and Methods: 〈 /i 〉 〈 /b 〉 Patients who underwent VVF repair between January 2009 and October 2015 were reviewed. Primary outcome was fistula closure at 3 months. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 A total of 123 patients and 139 procedures of VVF repair were reviewed. The overall success rate was 85.6%. There were no significant differences in age (p = 0.476), etiology (p = 0.900), fistula duration (p = 0.491) and number of repairs (p = 0.509) between success and fail group. Moderate or severe perifistula fibrosis and multiple fistula were associated with failure in repair of fistula (70.8 vs. 93.4%, p 〈 0.001; 62.5 vs. 88.6%, p = 0.005). No difference was seen in success rate of vaginal and abdominal approaches (86.0 vs. 85.0%, p = 0.800). Logistic regression analysis identified fistula number (p = 0.003) and perifistula fibrosis (p = 0.002) as 2 independent prognostic factors. Medium/large fistulas were 3.2 times more likely to fail in repair than small fistulas (OR 3.2, 95% CI 0.95-10.6, p = 0.061). 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Fistula number and perifistula fibrosis were 2 independent prognostic factors for fistula repair. Unsuccessful closure was more likely in medium/large VVF.
    Materialart: Online-Ressource
    ISSN: 0042-1138 , 1423-0399
    URL: Article
    DOI: 10.1159/000452166
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2017
    ZDB Id: 1464417-4
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
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    Pharmacological Effects of EGLP-1, a Novel Analog of Glucagon-Like Peptide-1, on Carbohydrate and Lipid Metabolism
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 48, No. 3 ( 2018), p. 1112-1122
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 48, No. 3 ( 2018), p. 1112-1122
    Kurzfassung: Background/Aims: Abnormal glucose metabolism and lipid metabolism are two key issues in Type 1 diabetes mellitus (T1DM). Insulin can control carbohydrate metabolism adequately, but cannot regulate lipid metabolism well in patients with T1DM. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have cured type 2 diabetes mellitus in clinical trials and have improved T1DM glycemic control in preclinical studies. However, previous studies have not reported whether GLP-1 can lower the serum concentration of non-esterified fatty acids (NEFAs). In this study, we examine whether GLP-1 can affect serum NEFA levels. Methods: The bioactivity of EGLP-1 (a novel GLP-1 analog) in vitro was analyzed in CG-HEK293 cells and with high-performance liquid chromatography. An intraperitoneal glucose tolerance test (IPGTT) was used to analyze the acute and sustained hypoglycemic effects of EGLP-1 in normal C57BL/6J mice. Streptozotocin-induced hyperglycemic mice were used to study the effects of EGLP-1 on blood glucose and NEFAs as well as its mechanism. Results: EGLP-1 activated GLP-1R and resisted dipeptidyl peptidase-IV digestion in vitro. Additionally, EGLP-1 had an insulinotropic action in vivo that lasted for approximately 6 h. In Streptozotocin-induced hyperglycemic mice, EGLP-1 improved hyperglycemia, inhibited food intake, and increased β-cell area. Serum physiological indexes showed that insulin and C-peptide levels were increased, while NEFA and triacylglycerol concentrations were decreased. Western blot analysis revealed that EGLP-1 significantly reduced phosphorylated-hormone sensitive lipase (pHSL) levels in white adipose tissue. Conclusions: EGLP-1 can improve hyperglycemia by increasing islet β-cell area and improving β-cell function, possibly due to reduced NEFA content in serum by lowering pHSL levels.
    Materialart: Online-Ressource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000491978
    Sprache: Englisch
    Verlag: S. Karger AG
    Publikationsdatum: 2018
    ZDB Id: 1482056-0
    SSG: 12
    SSG: 15,3
    Standort Signatur Einschränkungen Verfügbarkeit
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