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  1. AU="Brian G. Drew"
  2. AU="Fabio Sallustio"
  3. AU=Fahde Youssef
  4. AU=Jones M Lloyd
  5. AU="Sorn, San"
  6. AU="Gamoudi Amel"
  7. AU=Weidner Lisa AU=Weidner Lisa
  8. AU="Park, Donghee"
  9. AU="Daniel Paull"
  10. AU="H Divecha"
  11. AU="Chetata, Nabil"
  12. AU="Zuo, Nan"
  13. AU="Lin, Raymond Tzer-Pin"
  14. AU="Whittington, Karen B"
  15. AU="Beutel, Gernot"
  16. AU="Koh, Siang Boon"
  17. AU="Rajki, Anikó"
  18. AU="Polina B. Drozdova"
  19. AU=Zhang Xiuhong AU=Zhang Xiuhong
  20. AU=Hauer Julia
  21. AU="Widiasih, Natalia"
  22. AU="Besnik Bajrami"
  23. AU=Mazza Mario Gennaro
  24. AU="Kwong, A S K"
  25. AU="Hadian, Marziye"
  26. AU="Chen, Yaying"
  27. AU="Ortega, Francisco B"
  28. AU=Cobb Samuel N
  29. AU="Abdelmohssin El Mokaddem"
  30. AU="Iwao Ojima"
  31. AU="Abazi, Sokol"
  32. AU="Cook, Rebecca"
  33. AU=Martin Flavius
  34. AU="Cipriani, Raffaela"
  35. AU="Levin, Michael E."
  36. AU="Yang, Dayu"

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Treffer 1 - 9 von insgesamt 9

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  1. Artikel ; Online: The potential of integrating human and mouse discovery platforms to advance our understanding of cardiometabolic diseases

    Aaron W Jurrjens / Marcus M Seldin / Corey Giles / Peter J Meikle / Brian G Drew / Anna C Calkin

    eLife, Vol

    2023  Band 12

    Abstract: Cardiometabolic diseases encompass a range of interrelated conditions that arise from underlying metabolic perturbations precipitated by genetic, environmental, and lifestyle factors. While obesity, dyslipidaemia, smoking, and insulin resistance are ... ...

    Abstract Cardiometabolic diseases encompass a range of interrelated conditions that arise from underlying metabolic perturbations precipitated by genetic, environmental, and lifestyle factors. While obesity, dyslipidaemia, smoking, and insulin resistance are major risk factors for cardiometabolic diseases, individuals still present in the absence of such traditional risk factors, making it difficult to determine those at greatest risk of disease. Thus, it is crucial to elucidate the genetic, environmental, and molecular underpinnings to better understand, diagnose, and treat cardiometabolic diseases. Much of this information can be garnered using systems genetics, which takes population-based approaches to investigate how genetic variance contributes to complex traits. Despite the important advances made by human genome-wide association studies (GWAS) in this space, corroboration of these findings has been hampered by limitations including the inability to control environmental influence, limited access to pertinent metabolic tissues, and often, poor classification of diseases or phenotypes. A complementary approach to human GWAS is the utilisation of model systems such as genetically diverse mouse panels to study natural genetic and phenotypic variation in a controlled environment. Here, we review mouse genetic reference panels and the opportunities they provide for the study of cardiometabolic diseases and related traits. We discuss how the post-GWAS era has prompted a shift in focus from discovery of novel genetic variants to understanding gene function. Finally, we highlight key advantages and challenges of integrating complementary genetic and multi-omics data from human and mouse populations to advance biological discovery.
    Schlagwörter systems genetics ; multi-omics ; genetic reference panels ; genome-wide association studies ; genetic mapping ; Hybrid Mouse Diversity Panel ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2023-03-01T00:00:00Z
    Verlag eLife Sciences Publications Ltd
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: The impact of ERα action on muscle metabolism and insulin sensitivity – Strong enough for a man, made for a woman

    Andrea L. Hevener / Zhenqi Zhou / Timothy M. Moore / Brian G. Drew / Vicent Ribas

    Molecular Metabolism, Vol 15, Iss , Pp 20-

    2018  Band 34

    Abstract: Background: The incidence of chronic disease is elevated in women after menopause. Natural variation in muscle expression of the estrogen receptor (ER)α is inversely associated with plasma insulin and adiposity. Moreover, reduced muscle ERα expression ... ...

    Abstract Background: The incidence of chronic disease is elevated in women after menopause. Natural variation in muscle expression of the estrogen receptor (ER)α is inversely associated with plasma insulin and adiposity. Moreover, reduced muscle ERα expression levels are observed in women and animals presenting clinical features of the metabolic syndrome (MetSyn). Considering that metabolic dysfunction impacts nearly a quarter of the U.S. adult population and elevates chronic disease risk including type 2 diabetes, heart disease, and certain cancers, treatment strategies to combat metabolic dysfunction and associated pathologies are desperately needed. Scope of the review: This review will provide evidence supporting a critical and protective role for skeletal muscle ERα in the regulation of metabolic homeostasis and insulin sensitivity, and propose novel ERα targets involved in the maintenance of metabolic health. Major conclusions: Studies identifying ERα-regulated pathways essential for disease prevention will lay the important foundation for the rational design of novel therapeutics to improve the metabolic health of women while limiting secondary complications that have plagued traditional hormone replacement interventions. Keywords: Estrogen action, Estrogen receptors, Insulin sensitivity, Metabolic homeostasis
    Schlagwörter Internal medicine ; RC31-1245
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2018-09-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: SOD2 in skeletal muscle

    Aowen Zhuang / Christine Yang / Yingying Liu / Yanie Tan / Simon T. Bond / Shannen Walker / Tim Sikora / Adrienne Laskowski / Arpeeta Sharma / Judy B. de Haan / Peter J. Meikle / Takahiko Shimizu / Melinda T. Coughlan / Anna C. Calkin / Brian G. Drew

    Redox Biology, Vol 47, Iss , Pp 102135- (2021)

    New insights from an inducible deletion model

    2021  

    Abstract: Metabolic conditions such as obesity, insulin resistance and glucose intolerance are frequently associated with impairments in skeletal muscle function and metabolism. This is often linked to dysregulation of homeostatic pathways including an increase in ...

    Abstract Metabolic conditions such as obesity, insulin resistance and glucose intolerance are frequently associated with impairments in skeletal muscle function and metabolism. This is often linked to dysregulation of homeostatic pathways including an increase in reactive oxygen species (ROS) and oxidative stress. One of the main sites of ROS production is the mitochondria, where the flux of substrates through the electron transport chain (ETC) can result in the generation of oxygen free radicals. Fortunately, several mechanisms exist to buffer bursts of intracellular ROS and peroxide production, including the enzymes Catalase, Glutathione Peroxidase and Superoxide Dismutase (SOD). Of the latter, there are two intracellular isoforms; SOD1 which is mostly cytoplasmic, and SOD2 which is found exclusively in the mitochondria. Developmental and chronic loss of these enzymes has been linked to disease in several studies, however the temporal effects of these disturbances remain largely unexplored. Here, we induced a post-developmental (8-week old mice) deletion of SOD2 in skeletal muscle (SOD2-iMKO) and demonstrate that 16 weeks of SOD2 deletion leads to no major impairment in whole body metabolism, despite these mice displaying alterations in aspects of mitochondrial abundance and voluntary ambulatory movement. This is likely partly explained by the suggestive data that a compensatory response may exist from other redox enzymes, including catalase and glutathione peroxidases. Nevertheless, we demonstrated that inducible SOD2 deletion impacts on specific aspects of muscle lipid metabolism, including the abundance of phospholipids and phosphatidic acid (PA), the latter being a key intermediate in several cellular signaling pathways. Thus, our findings suggest that post-developmental deletion of SOD2 induces a more subtle phenotype than previous embryonic models have shown, allowing us to highlight a previously unrecognized link between SOD2, mitochondrial function and bioactive lipid species including PA.
    Schlagwörter Skeletal muscle ; Superoxide ; ROS ; Lipid metabolism ; Mitochondria ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2021-11-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Deletion of Trim28 in committed adipocytes promotes obesity but preserves glucose tolerance

    Simon T. Bond / Emily J. King / Darren C. Henstridge / Adrian Tran / Sarah C. Moody / Christine Yang / Yingying Liu / Natalie A. Mellett / Artika P. Nath / Michael Inouye / Elizabeth J. Tarling / Thomas Q. de Aguiar Vallim / Peter J. Meikle / Anna C. Calkin / Brian G. Drew

    Nature Communications, Vol 12, Iss 1, Pp 1-

    2021  Band 13

    Abstract: The genetic determinants of sex-specific differences in obesity are still incompletely understood. Here, the authors demonstrate that adipocyte specific loss of Trim28 in committed adipocytes leads to sex specific differences in the development of ... ...

    Abstract The genetic determinants of sex-specific differences in obesity are still incompletely understood. Here, the authors demonstrate that adipocyte specific loss of Trim28 in committed adipocytes leads to sex specific differences in the development of obesity, and that this phenotype is associated with altered metabolic flexibility and lipid metabolism.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2021-01-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Tissue-specific expression of Cas9 has no impact on whole-body metabolism in four transgenic mouse lines

    Simon T. Bond / Aowen Zhuang / Christine Yang / Eleanor A.M. Gould / Tim Sikora / Yingying Liu / Ying Fu / Kevin I. Watt / Yanie Tan / Helen Kiriazis / Graeme I. Lancaster / Paul Gregorevic / Darren C. Henstridge / Julie R. McMullen / Peter J. Meikle / Anna C. Calkin / Brian G. Drew

    Molecular Metabolism, Vol 53, Iss , Pp 101292- (2021)

    2021  

    Abstract: Objective: CRISPR/Cas9 technology has revolutionized gene editing and fast tracked our capacity to manipulate genes of interest for the benefit of both research and therapeutic applications. Whilst many advances have, and continue to be made in this area, ...

    Abstract Objective: CRISPR/Cas9 technology has revolutionized gene editing and fast tracked our capacity to manipulate genes of interest for the benefit of both research and therapeutic applications. Whilst many advances have, and continue to be made in this area, perhaps the most utilized technology to date has been the generation of knockout cells, tissues and animals. The advantages of this technology are many fold, however some questions still remain regarding the effects that long term expression of foreign proteins such as Cas9, have on mammalian cell function. Several studies have proposed that chronic overexpression of Cas9, with or without its accompanying guide RNAs, may have deleterious effects on cell function and health. This is of particular concern when applying this technology in vivo, where chronic expression of Cas9 in tissues of interest may promote disease-like phenotypes and thus confound the investigation of the effects of the gene of interest. Although these concerns remain valid, no study to our knowledge has yet to demonstrate this directly. Methods: In this study we used the lox-stop-lox (LSL) spCas9 ROSA26 transgenic (Tg) mouse line to generate four tissue-specific Cas9-Tg models that express Cas9 in the heart, liver, skeletal muscle or adipose tissue. We performed comprehensive phenotyping of these mice up to 20-weeks of age and subsequently performed molecular analysis of their organs. Results: We demonstrate that Cas9 expression in these tissues had no detrimental effect on whole body health of the animals, nor did it induce any tissue-specific effects on whole body energy metabolism, liver health, inflammation, fibrosis, heart function or muscle mass. Conclusions: Our data suggests that these models are suitable for studying the tissue specific effects of gene deletion using the LSL-Cas9-Tg model, and that phenotypes observed utilizing these models can be confidently interpreted as being gene specific, and not confounded by the chronic overexpression of Cas9.
    Schlagwörter CRISPR ; Cas9 ; Transgenic mice ; Metabolism ; Tissue specific ; Phenotype ; Internal medicine ; RC31-1245
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2021-11-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Loss of the long non-coding RNA OIP5-AS1 exacerbates heart failure in a sex-specific manner

    Aowen Zhuang / Anna C. Calkin / Shannen Lau / Helen Kiriazis / Daniel G. Donner / Yingying Liu / Simon T. Bond / Sarah C. Moody / Eleanor A.M. Gould / Timothy D. Colgan / Sergio Ruiz Carmona / Michael Inouye / Thomas Q. de Aguiar Vallim / Elizabeth J. Tarling / Gregory A. Quaife-Ryan / James E. Hudson / Enzo R. Porrello / Paul Gregorevic / Xiao-Ming Gao /
    Xiao-Jun Du / Julie R. McMullen / Brian G. Drew

    iScience, Vol 24, Iss 6, Pp 102537- (2021)

    2021  

    Abstract: Summary: Long non-coding RNAs (lncRNAs) have been demonstrated to influence numerous biological processes, being strongly implicated in the maintenance and physiological function of various tissues including the heart. The lncRNA OIP5-AS1 (1700020I14Rik/ ... ...

    Abstract Summary: Long non-coding RNAs (lncRNAs) have been demonstrated to influence numerous biological processes, being strongly implicated in the maintenance and physiological function of various tissues including the heart. The lncRNA OIP5-AS1 (1700020I14Rik/Cyrano) has been studied in several settings; however its role in cardiac pathologies remains mostly uncharacterized. Using a series of in vitro and ex vivo methods, we demonstrate that OIP5-AS1 is regulated during cardiac development in rodent and human models and in disease settings in mice. Using CRISPR, we engineered a global OIP5-AS1 knockout (KO) mouse and demonstrated that female KO mice develop exacerbated heart failure following cardiac pressure overload (transverse aortic constriction [TAC]) but male mice do not. RNA-sequencing of wild-type and KO hearts suggest that OIP5-AS1 regulates pathways that impact mitochondrial function. Thus, these findings highlight OIP5-AS1 as a gene of interest in sex-specific differences in mitochondrial function and development of heart failure.
    Schlagwörter Cardiovascular medicine ; Molecular physiology ; Transcriptomics ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2021-06-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: Concordant peripheral lipidome signatures in two large clinical studies of Alzheimer’s disease

    Kevin Huynh / Wei Ling Florence Lim / Corey Giles / Kaushala S. Jayawardana / Agus Salim / Natalie A. Mellett / Adam Alexander T. Smith / Gavriel Olshansky / Brian G. Drew / Pratishtha Chatterjee / Ian Martins / Simon M. Laws / Ashley I. Bush / Christopher C. Rowe / Victor L. Villemagne / David Ames / Colin L. Masters / Matthias Arnold / Kwangsik Nho /
    Andrew J. Saykin / Rebecca Baillie / Xianlin Han / Rima Kaddurah-Daouk / Ralph N. Martins / Peter J. Meikle

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Band 11

    Abstract: The onset and pathology of Alzheimer’s disease (AD) is associated with changes to lipid metabolism. Here, the authors analysed 569 lipids from 32 classes and subclasses in two independent patient cohorts to identify key lipid pathways to link the plasma ... ...

    Abstract The onset and pathology of Alzheimer’s disease (AD) is associated with changes to lipid metabolism. Here, the authors analysed 569 lipids from 32 classes and subclasses in two independent patient cohorts to identify key lipid pathways to link the plasma lipidome with AD and the future onset of AD.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2020-11-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: Concordant peripheral lipidome signatures in two large clinical studies of Alzheimer’s disease

    Kevin Huynh / Wei Ling Florence Lim / Corey Giles / Kaushala S. Jayawardana / Agus Salim / Natalie A. Mellett / Adam Alexander T. Smith / Gavriel Olshansky / Brian G. Drew / Pratishtha Chatterjee / Ian Martins / Simon M. Laws / Ashley I. Bush / Christopher C. Rowe / Victor L. Villemagne / David Ames / Colin L. Masters / Matthias Arnold / Kwangsik Nho /
    Andrew J. Saykin / Rebecca Baillie / Xianlin Han / Rima Kaddurah-Daouk / Ralph N. Martins / Peter J. Meikle

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Band 11

    Abstract: The onset and pathology of Alzheimer’s disease (AD) is associated with changes to lipid metabolism. Here, the authors analysed 569 lipids from 32 classes and subclasses in two independent patient cohorts to identify key lipid pathways to link the plasma ... ...

    Abstract The onset and pathology of Alzheimer’s disease (AD) is associated with changes to lipid metabolism. Here, the authors analysed 569 lipids from 32 classes and subclasses in two independent patient cohorts to identify key lipid pathways to link the plasma lipidome with AD and the future onset of AD.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2020-11-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: Skeletal muscle insulin resistance associated with cholesterol-induced activation of macrophages is prevented by high density lipoprotein.

    Andrew L Carey / Andrew L Siebel / Medini Reddy-Luthmoodoo / Alaina K Natoli / Wilissa D'Souza / Peter J Meikle / Dmitri Sviridov / Brian G Drew / Bronwyn A Kingwell

    PLoS ONE, Vol 8, Iss 2, p e

    2013  Band 56601

    Abstract: Background Emerging evidence suggests that high density lipoprotein (HDL) may modulate glucose metabolism through multiple mechanisms including pancreatic insulin secretion as well as insulin-independent glucose uptake into muscle. We hypothesized that ... ...

    Abstract Background Emerging evidence suggests that high density lipoprotein (HDL) may modulate glucose metabolism through multiple mechanisms including pancreatic insulin secretion as well as insulin-independent glucose uptake into muscle. We hypothesized that HDL may also increase skeletal muscle insulin sensitivity via cholesterol removal and anti-inflammatory actions in macrophages associated with excess adiposity and ectopic lipid deposition. Methods Human primary and THP-1 macrophages were treated with vehicle (PBS) or acetylated low density lipoprotein (acLDL) with or without HDL for 18 hours. Treatments were then removed, and macrophages were incubated with fresh media for 4 hours. This conditioned media was then applied to primary human skeletal myotubes derived from vastus lateralis biopsies taken from patients with type 2 diabetes to examine insulin-stimulated glucose uptake. Results Conditioned media from acLDL-treated primary and THP-1 macrophages reduced insulin-stimulated glucose uptake in primary human skeletal myotubes compared with vehicle (primary macrophages, 168±21% of basal uptake to 104±19%; THP-1 macrophages, 142±8% of basal uptake to 108±6%; P<0.05). This was restored by co-treatment of macrophages with HDL. While acLDL increased total intracellular cholesterol content, phosphorylation of c-jun N-terminal kinase and secretion of pro- and anti-inflammatory cytokines from macrophages, none were altered by co-incubation with HDL. Insulin-stimulated Akt phosphorylation in human skeletal myotubes exposed to conditioned media was unaltered by either treatment condition. Conclusion Inhibition of insulin-stimulated glucose uptake in primary human skeletal myotubes by conditioned media from macrophages pre-incubated with acLDL was restored by co-treatment with HDL. However, these actions were not linked to modulation of common pro- or anti-inflammatory mediators or insulin signaling via Akt.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2013-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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