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Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes

Rachel Churm Orcid Logo, S. Caplin, J. Barry, Jeffrey Davies Orcid Logo, J.W. Stephens, Sarah Prior Orcid Logo

Molecular and Cellular Endocrinology, Volume: 481, Pages: 8 - 13

Swansea University Authors: Rachel Churm Orcid Logo, Jeffrey Davies Orcid Logo, Sarah Prior Orcid Logo

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DOI (Published version): 10.1016/j.mce.2018.11.004

Abstract

Acyl-ghrelin has various peripheral effects including the potential role in mediating cellular lipid removal and macrophage polarization. Previous reports are contradictory as to how glycaemia and acyl-ghrelin mediates lipid retention and inflammation within individuals with Type 2 diabetes (T2D). O...

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Published in: Molecular and Cellular Endocrinology
ISSN: 0303-7207
Published: 2019
Online Access: Check full text

URI: https://cronfa.swan.ac.uk/Record/cronfa45975
first_indexed 2018-11-19T14:28:29Z
last_indexed 2020-07-20T13:07:24Z
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spelling 2020-07-20T12:44:49.5037878 v2 45975 2018-11-19 Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes c6cd8267ff0b13f2ea333bbfefdae144 0000-0001-9855-6282 Rachel Churm Rachel Churm true false 2cb3d1d96a7870a84d2f758e865172e6 0000-0002-4234-0033 Jeffrey Davies Jeffrey Davies true false cdda101035997acfaa6fdf17097f52b2 0000-0001-8703-8092 Sarah Prior Sarah Prior true false 2018-11-19 EAAS Acyl-ghrelin has various peripheral effects including the potential role in mediating cellular lipid removal and macrophage polarization. Previous reports are contradictory as to how glycaemia and acyl-ghrelin mediates lipid retention and inflammation within individuals with Type 2 diabetes (T2D). Our aim was to explore acyl-ghrelin levels and ghrelin expression in relation to lipid and inflammatory markers within an ex vivo human model, biopsied visceral adipose tissue.Results indicated that acyl-ghrelin was associated with a decline in key lipid homeostasis genes ABCG1 and LXRβ expression. Within T2D there was also a down regulation of these genes which was independent of acyl-ghrelin levels. Circulatory pro-inflammatory markers (IL-6 and TNFα) had no association with ghrelin expression nor circulating acyl-ghrelin levels. Anti-inflammatory marker (IL-10) and total antioxidant status (TAOS%) were positively associated with ghrelin expression across samples from all groups combined (total sample cohort) and specifically within the obesity sample cohorts.Data supported the hypothesis that hyperglycaemia and acyl-ghrelin have a regulatory role in lipid retention. Furthermore, that both acyl- and desacyl-ghrelin is responsible for a protective inflammatory response; however this response is diminished in T2D. Journal Article Molecular and Cellular Endocrinology 481 8 13 0303-7207 5 2 2019 2019-02-05 10.1016/j.mce.2018.11.004 COLLEGE NANME Engineering and Applied Sciences School COLLEGE CODE EAAS Swansea University 2020-07-20T12:44:49.5037878 2018-11-19T12:03:48.8766833 Rachel Churm 0000-0001-9855-6282 1 S. Caplin 2 J. Barry 3 Jeffrey Davies 0000-0002-4234-0033 4 J.W. Stephens 5 Sarah Prior 0000-0001-8703-8092 6 0045975-19112018120648.pdf Churm2018.pdf 2018-11-19T12:06:48.8270000 Output 922216 application/pdf Accepted Manuscript true 2019-11-13T00:00:00.0000000 Released under the terms of a Creative Commons Attribution Non-Commercial No Derivatives License (CC-BY-NC-ND). true eng
title Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes
spellingShingle Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes
Rachel Churm
Jeffrey Davies
Sarah Prior
title_short Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes
title_full Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes
title_fullStr Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes
title_full_unstemmed Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes
title_sort Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes
author_id_str_mv c6cd8267ff0b13f2ea333bbfefdae144
2cb3d1d96a7870a84d2f758e865172e6
cdda101035997acfaa6fdf17097f52b2
author_id_fullname_str_mv c6cd8267ff0b13f2ea333bbfefdae144_***_Rachel Churm
2cb3d1d96a7870a84d2f758e865172e6_***_Jeffrey Davies
cdda101035997acfaa6fdf17097f52b2_***_Sarah Prior
author Rachel Churm
Jeffrey Davies
Sarah Prior
author2 Rachel Churm
S. Caplin
J. Barry
Jeffrey Davies
J.W. Stephens
Sarah Prior
format Journal article
container_title Molecular and Cellular Endocrinology
container_volume 481
container_start_page 8
publishDate 2019
institution Swansea University
issn 0303-7207
doi_str_mv 10.1016/j.mce.2018.11.004
document_store_str 1
active_str 0
description Acyl-ghrelin has various peripheral effects including the potential role in mediating cellular lipid removal and macrophage polarization. Previous reports are contradictory as to how glycaemia and acyl-ghrelin mediates lipid retention and inflammation within individuals with Type 2 diabetes (T2D). Our aim was to explore acyl-ghrelin levels and ghrelin expression in relation to lipid and inflammatory markers within an ex vivo human model, biopsied visceral adipose tissue.Results indicated that acyl-ghrelin was associated with a decline in key lipid homeostasis genes ABCG1 and LXRβ expression. Within T2D there was also a down regulation of these genes which was independent of acyl-ghrelin levels. Circulatory pro-inflammatory markers (IL-6 and TNFα) had no association with ghrelin expression nor circulating acyl-ghrelin levels. Anti-inflammatory marker (IL-10) and total antioxidant status (TAOS%) were positively associated with ghrelin expression across samples from all groups combined (total sample cohort) and specifically within the obesity sample cohorts.Data supported the hypothesis that hyperglycaemia and acyl-ghrelin have a regulatory role in lipid retention. Furthermore, that both acyl- and desacyl-ghrelin is responsible for a protective inflammatory response; however this response is diminished in T2D.
published_date 2019-02-05T13:34:44Z
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