Journal article 1008 views 343 downloads
Acyl-ghrelin mediated lipid retention and inflammation in obesity-related Type 2 diabetes
,
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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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...
| Published in: | Molecular and Cellular Endocrinology |
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| ISSN: | 0303-7207 |
| Published: |
2019
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| Online Access: |
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| 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. |
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| Start Page: |
8 |
| End Page: |
13 |