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Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes / Rachel Churm; S. Caplin; J. Barry; Jeffrey Davies; J.W. Stephens; Sarah Prior

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

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

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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
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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). 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.
Start Page: 8
End Page: 13