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  1. Article ; Online: A role for SPARC in the moderation of human insulin secretion.

    Lorna W Harries / Laura J McCulloch / Janet E Holley / Thomas J Rawling / Hannah J Welters / Katarina Kos

    PLoS ONE, Vol 8, Iss 6, p e

    2013  Volume 68253

    Abstract: Aims/hypothesis We have previously shown the implication of the multifunctional protein SPARC (Secreted protein acidic and rich in cysteine)/osteonectin in insulin resistance but potential effects on beta-cell function have not been assessed. We ... ...

    Abstract Aims/hypothesis We have previously shown the implication of the multifunctional protein SPARC (Secreted protein acidic and rich in cysteine)/osteonectin in insulin resistance but potential effects on beta-cell function have not been assessed. We therefore aimed to characterise the effect of SPARC on beta-cell function and features of diabetes. Methods We measured SPARC expression by qRT-PCR in human primary pancreatic islets, adipose tissue, liver and muscle. We then examined the relation of SPARC with glucose stimulated insulin secretion (GSIS) in primary human islets and the effect of SPARC overexpression on GSIS in beta cell lines. Results SPARC was expressed at measurable levels in human islets, adipose tissue, liver and skeletal muscle, and demonstrated reduced expression in primary islets from subjects with diabetes compared with controls (p< = 0.05). SPARC levels were positively correlated with GSIS in islets from control donors (p< = 0.01). Overexpression of SPARC in cultured beta-cells resulted in a 2.4-fold increase in insulin secretion in high glucose conditions (p< = 0.01). Conclusions Our data suggest that levels of SPARC are reduced in islets from donors with diabetes and that it has a role in insulin secretion, an effect which appears independent of SPARC's modulation of obesity-induced insulin resistance in adipose tissue.
    Keywords Medicine ; R ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: PYY-Dependent Restoration of Impaired Insulin and Glucagon Secretion in Type 2 Diabetes following Roux-En-Y Gastric Bypass Surgery

    Reshma D. Ramracheya / Laura J. McCulloch / Anne Clark / David Wiggins / Helene Johannessen / Magnus Kringstad Olsen / Xing Cai / Chun-Mei Zhao / Duan Chen / Patrik Rorsman

    Cell Reports, Vol 15, Iss 5, Pp 944-

    2016  Volume 950

    Abstract: Roux-en-Y gastric bypass (RYGB) is a weight-reduction procedure resulting in rapid resolution of type 2 diabetes (T2D). The role of pancreatic islet function in this restoration of normoglycemia has not been fully elucidated. Using the diabetic Goto- ... ...

    Abstract Roux-en-Y gastric bypass (RYGB) is a weight-reduction procedure resulting in rapid resolution of type 2 diabetes (T2D). The role of pancreatic islet function in this restoration of normoglycemia has not been fully elucidated. Using the diabetic Goto-Kakizaki (GK) rat model, we demonstrate that RYGB restores normal glucose regulation of glucagon and insulin secretion and normalizes islet morphology. Culture of isolated islets with serum from RYGB animals mimicked these effects, implicating a humoral factor. These latter effects were reversed following neutralization of the gut hormone peptide tyrosine tyrosine (PYY) but persisted in the presence of a glucagon-like peptide-1 (GLP-1) receptor antagonist. The effects of RYGB on secretion were replicated by chronic exposure of diabetic rat islets to PYY in vitro. These findings indicate that the mechanism underlying T2D remission may be mediated by PYY and suggest that drugs promoting PYY release or action may restore pancreatic islet function in T2D.
    Keywords Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2016-05-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article: Functional characterisation of ADIPOQ variants using individuals recruited by genotype

    Lee, Benjamin P / Bridget Knight / Giles Cory / Hanieh Yaghootkar / Henry O. Lloyd-Laney / Jonathan M. Locke / Katarina Kos / Laura J. McCulloch / Lorna W. Harries / Timothy M. Frayling

    Molecular and Cellular Endocrinology. 2016 June 15, v. 428

    2016  

    Abstract: Four non-coding GWAS variants in or near the ADIPOQ gene (rs17300539, rs17366653, rs3821799 and rs56354395) together explain 4% of the variation in circulating adiponectin. The functional basis for this is unknown.We tested the effect of these variants ... ...

    Abstract Four non-coding GWAS variants in or near the ADIPOQ gene (rs17300539, rs17366653, rs3821799 and rs56354395) together explain 4% of the variation in circulating adiponectin. The functional basis for this is unknown.We tested the effect of these variants on ADIPOQ transcription, splicing and stability respectively in adipose tissue samples from participants recruited by rs17366653 genotype.Transcripts carrying rs17300539 demonstrated a 17% increase in expression (p = 0.001). Variant rs17366653 was associated with disruption of ADIPOQ splicing leading to a 7 fold increase in levels of a non-functional transcript (p = 0.002). Transcripts carrying rs56354395 demonstrated a 59% decrease in expression (p = <0.0001). No effects of rs3821799 genotype on expression was observed.Association between variation in the ADIPOQ gene and serum adiponectin may arise from effects on mRNA transcription, splicing or stability. These studies illustrate the utility of recruit-by-genotype studies in relevant human tissues in functional interpretation of GWAS signals.
    Keywords adiponectin ; adipose tissue ; blood serum ; genes ; genotype ; humans ; messenger RNA
    Language English
    Dates of publication 2016-0615
    Size p. 49-57.
    Publishing place Elsevier Ireland Ltd
    Document type Article
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2016.03.020
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: A genome-wide association search for type 2 diabetes genes in African Americans.

    Nicholette D Palmer / Caitrin W McDonough / Pamela J Hicks / Bong H Roh / Maria R Wing / S Sandy An / Jessica M Hester / Jessica N Cooke / Meredith A Bostrom / Megan E Rudock / Matthew E Talbert / Joshua P Lewis / DIAGRAM Consortium / MAGIC Investigators / Assiamira Ferrara / Lingyi Lu / Julie T Ziegler / Michele M Sale / Jasmin Divers /
    Daniel Shriner / Adebowale Adeyemo / Charles N Rotimi / Maggie C Y Ng / Carl D Langefeld / Barry I Freedman / Donald W Bowden / Benjamin F Voight / Laura J Scott / Valgerdur Steinthorsdottir / Andrew P Morris / Christian Dina / Ryan P Welch / Eleftheria Zeggini / Cornelia Huth / Yurii S Aulchenko / Gudmar Thorleifsson / Laura J McCulloch / Teresa Ferreira / Harald Grallert / Najaf Amin / Guanming Wu / Cristen J Willer / Soumya Raychaudhuri / Steve A McCarroll / Claudia Langenberg / Oliver M Hofmann / Josée Dupuis / Lu Qi / Ayellet V Segrè / Mandy van Hoek

    PLoS ONE, Vol 7, Iss 1, p e

    2012  Volume 29202

    Abstract: African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African ... ...

    Abstract African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African American population. We performed a Genome Wide Association Study (GWAS) using the Affymetrix 6.0 array in 965 African-American cases with T2DM and end-stage renal disease (T2DM-ESRD) and 1029 population-based controls. The most significant SNPs (n = 550 independent loci) were genotyped in a replication cohort and 122 SNPs (n = 98 independent loci) were further tested through genotyping three additional validation cohorts followed by meta-analysis in all five cohorts totaling 3,132 cases and 3,317 controls. Twelve SNPs had evidence of association in the GWAS (P<0.0071), were directionally consistent in the Replication cohort and were associated with T2DM in subjects without nephropathy (P<0.05). Meta-analysis in all cases and controls revealed a single SNP reaching genome-wide significance (P<2.5×10(-8)). SNP rs7560163 (P = 7.0×10(-9), OR (95% CI) = 0.75 (0.67-0.84)) is located intergenically between RND3 and RBM43. Four additional loci (rs7542900, rs4659485, rs2722769 and rs7107217) were associated with T2DM (P<0.05) and reached more nominal levels of significance (P<2.5×10(-5)) in the overall analysis and may represent novel loci that contribute to T2DM. We have identified novel T2DM-susceptibility variants in the African-American population. Notably, T2DM risk was associated with the major allele and implies an interesting genetic architecture in this population. These results suggest that multiple loci underlie T2DM susceptibility in the African-American population and that these loci are distinct from those identified in other ethnic populations.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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