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  1. Article ; Online: The PI3K/Akt1-FoxO1 Translocation Pathway Mediates EXf Effects on NIT-1 Cell Survival.

    Hou, Guo-Jiang / Li, Cai-Na / Huan, Yi / Liu, Shuai-Nan / Liu, Quan / Liu, Min-Zhi / Shen, Zhu-Fang

    Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association

    2017  Volume 125, Issue 10, Page(s) 669–676

    Abstract: EXf, a glucagon-like peptide 1 (GLP-1) receptor agonist, stimulates β-cell proliferation and reduces apoptosis in diabetic animal models, but the underlying mechanisms are not fully understood. We constructed a FoxO1-GFP fusion protein expression plasmid ...

    Abstract EXf, a glucagon-like peptide 1 (GLP-1) receptor agonist, stimulates β-cell proliferation and reduces apoptosis in diabetic animal models, but the underlying mechanisms are not fully understood. We constructed a FoxO1-GFP fusion protein expression plasmid and transiently transfected it into NIT-1 cells to investigate whether FoxO1 mediates EXf effects on NIT-1 cell survival. Our results showed that EXf could increase cell viability by inhibiting apoptosis and stimulating proliferation, and it could also promote the translocation of the FoxO1-GFP fusion protein from the nucleus to the cytoplasm in NIT-1 cells. However, the above effects of EXf were suppressed by the inhibitor of PI3K. Comparative transcription analysis showed up-regulation of igf-1r, irs-2, pI3k, akt1 and pdx-1 in NIT-1 cells after EXf treatment. Moreover, the up-regulation of PI3K and phosphorylation of Akt1 upon EXf treatment was confirmed by Western blot, both phenomena were abrogated by wortmannin, an inhibitor of PI3K. In summary, FoxO1 may mediate the effects of EXf on NIT-1 cell survival by activating the PI3K/Akt1 pathway.
    MeSH term(s) Animals ; Cell Line ; Cell Survival ; Forkhead Box Protein O1/metabolism ; Glucagon-Like Peptide-1 Receptor/agonists ; Glucagon-Like Peptide-1 Receptor/metabolism ; Humans ; Hypoglycemic Agents/pharmacology ; Insulin-Secreting Cells/metabolism ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Translocation, Genetic ; Up-Regulation
    Chemical Substances FOXO1 protein, human ; Forkhead Box Protein O1 ; Glucagon-Like Peptide-1 Receptor ; Hypoglycemic Agents ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; AKT1 protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2017-11
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1225416-2
    ISSN 1439-3646 ; 0947-7349
    ISSN (online) 1439-3646
    ISSN 0947-7349
    DOI 10.1055/s-0043-117048
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article: The PI3K/Akt1-FoxO1 Translocation Pathway Mediates EXf Effects on NIT-1 Cell Survival

    Hou, Guo-jiang / Li, Cai-na / Huan, Yi / Liu, Shuai-nan / Liu, Quan / Liu, Min-zhi / Shen, Zhu-fang

    Experimental and Clinical Endocrinology & Diabetes

    2017  Volume 125, Issue 10, Page(s) 669–676

    Abstract: EXf, a glucagon-like peptide 1 (GLP-1) receptor agonist, stimulates β-cell proliferation and reduces apoptosis in diabetic animal models, but the underlying mechanisms are not fully understood. We constructed a FoxO1-GFP fusion protein expression plasmid ...

    Abstract EXf, a glucagon-like peptide 1 (GLP-1) receptor agonist, stimulates β-cell proliferation and reduces apoptosis in diabetic animal models, but the underlying mechanisms are not fully understood. We constructed a FoxO1-GFP fusion protein expression plasmid and transiently transfected it into NIT-1 cells to investigate whether FoxO1 mediates EXf effects on NIT-1 cell survival. Our results showed that EXf could increase cell viability by inhibiting apoptosis and stimulating proliferation, and it could also promote the translocation of the FoxO1-GFP fusion protein from the nucleus to the cytoplasm in NIT-1 cells. However, the above effects of EXf were suppressed by the inhibitor of PI3K. Comparative transcription analysis showed up-regulation of igf-1r, irs-2, pI3k, akt1 and pdx-1 in NIT-1 cells after EXf treatment. Moreover, the up-regulation of PI3K and phosphorylation of Akt1 upon EXf treatment was confirmed by Western blot, both phenomena were abrogated by wortmannin, an inhibitor of PI3K. In summary, FoxO1 may mediate the effects of EXf on NIT-1 cell survival by activating the PI3K/Akt1 pathway.
    Keywords EXf ; GLP-1 ; FoxO1 ; NIT-1 cells ; translocation
    Language English
    Publishing date 2017-09-11
    Publisher © Georg Thieme Verlag KG
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 1225416-2
    ISSN 1439-3646 ; 0947-7349
    ISSN (online) 1439-3646
    ISSN 0947-7349
    DOI 10.1055/s-0043-117048
    Database Thieme publisher's database

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.91: Show issues Location:
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  3. Article ; Online: Long-term treatment with EXf, a peptide analog of Exendin-4, improves β-cell function and survival in diabetic KKAy mice.

    Hou, Guo-jiang / Li, Cai-na / Liu, Shuai-nan / Huan, Yi / Liu, Quan / Sun, Su-juan / Li, Lin-yi / Hou, Shao-cong / Shen, Zhu-fang

    Peptides

    2013  Volume 40, Page(s) 123–132

    Abstract: EXf is a C-terminally truncated fragment of Exendin-4 with two amino acid substitutions. Previous studies showed that EXf controls plasma glucose level acting as a glucagon-like peptide 1 (GLP-1) receptor agonist. The purpose of this study was to ... ...

    Abstract EXf is a C-terminally truncated fragment of Exendin-4 with two amino acid substitutions. Previous studies showed that EXf controls plasma glucose level acting as a glucagon-like peptide 1 (GLP-1) receptor agonist. The purpose of this study was to evaluate the effects of EXf on β-cell function and survival in diabetic KKAy mice. EXf treatment significantly improved the glucose intolerance and reduced non-fasting and fasting plasma glucose levels, as well as plasma triglyceride levels in diabetic KKAy mice. In hyperglycemic clamp test, EXf-treated mice displayed an increased glucose infusion rate and first-phase insulin secretion. Treatment with EXf also led to a significant restoration of islet morphology, an increase in Ki67 expression in β-cells, and a reduction in the number of TUNEL positive β-cells. In the pancreas, comparative transcription analysis showed up-regulation of Akt1. The up-regulation of phosphorylated Akt1 was confirmed by Western blot, and changes in the protein levels of members of the Akt1 pathway, such as PI3K, Bim, Bcl-2, Bax, Caspase-3, and Caspase-9, PDX-1, were observed as well. Therefore, EXf treatment could improve β-cell function and survival in diabetic KKAy mice, likely as a result of islet morphology restoration, stimulation of β-cell proliferation, and inhibition of β-cell apoptosis.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Blood Glucose/drug effects ; Exenatide ; Glucagon-Like Peptide 1/antagonists & inhibitors ; Glucose Intolerance/drug therapy ; Glucose Intolerance/metabolism ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Ki-67 Antigen/metabolism ; Mice ; Mice, Inbred NOD ; Peptide Fragments/pharmacology ; Peptides/chemistry ; Peptides/pharmacology ; Proto-Oncogene Proteins c-akt/metabolism ; Triglycerides/blood ; Venoms/chemistry ; Venoms/pharmacology
    Chemical Substances Blood Glucose ; Insulin ; Ki-67 Antigen ; Peptide Fragments ; Peptides ; Triglycerides ; Venoms ; Glucagon-Like Peptide 1 (89750-14-1) ; Exenatide (9P1872D4OL) ; Akt1 protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2013-01-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 769028-9
    ISSN 1873-5169 ; 0196-9781
    ISSN (online) 1873-5169
    ISSN 0196-9781
    DOI 10.1016/j.peptides.2013.01.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1649: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  4. Article: Long-term treatment with EXf, a peptide analog of Exendin-4, improves β-cell function and survival in diabetic KKAy mice

    Hou, Guo-jiang / Li, Cai-na / Liu, Shuai-nan / Huan, Yi / Liu, Quan / Sun, Su-juan / Li, Lin-yi / Hou, Shao-cong / Shen, Zhu-fang

    Peptides

    Volume v. 40

    Abstract: EXf is a C-terminally truncated fragment of Exendin-4 with two amino acid substitutions. Previous studies showed that EXf controls plasma glucose level acting as a glucagon-like peptide 1 (GLP-1) receptor agonist. The purpose of this study was to ... ...

    Abstract EXf is a C-terminally truncated fragment of Exendin-4 with two amino acid substitutions. Previous studies showed that EXf controls plasma glucose level acting as a glucagon-like peptide 1 (GLP-1) receptor agonist. The purpose of this study was to evaluate the effects of EXf on β-cell function and survival in diabetic KKAy mice. EXf treatment significantly improved the glucose intolerance and reduced non-fasting and fasting plasma glucose levels, as well as plasma triglyceride levels in diabetic KKAy mice. In hyperglycemic clamp test, EXf-treated mice displayed an increased glucose infusion rate and first-phase insulin secretion. Treatment with EXf also led to a significant restoration of islet morphology, an increase in Ki67 expression in β-cells, and a reduction in the number of TUNEL positive β-cells. In the pancreas, comparative transcription analysis showed up-regulation of Akt1. The up-regulation of phosphorylated Akt1 was confirmed by Western blot, and changes in the protein levels of members of the Akt1 pathway, such as PI3K, Bim, Bcl-2, Bax, Caspase-3, and Caspase-9, PDX-1, were observed as well. Therefore, EXf treatment could improve β-cell function and survival in diabetic KKAy mice, likely as a result of islet morphology restoration, stimulation of β-cell proliferation, and inhibition of β-cell apoptosis.
    Keywords cells ; Western blotting ; phosphatidylinositol 3-kinase ; agonists ; apoptosis ; blood glucose ; islets of Langerhans ; amino acid substitution ; glucagon-like peptide 1 ; caspase-9 ; Mice ; fasting ; caspase-3 ; gene expression regulation ; mice ; insulin secretion ; glucose ; triacylglycerols
    Language English
    Document type Article
    ISSN 0196-9781
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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