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

MOLECULAR AND CELLULAR ENDOCRINOLOGY

卷:481

Article

Churm, R.¹  Caplin, S.²  Barry, J.²  Davies, J. S.³  Stephens, J. W.¹  Prior, S. L.¹ 

[1] Swansea Univ, Diabet Res Grp, Grove Bldg, Swansea, W Glam, Wales

[2] Morriston Hosp, Welsh Inst Metab & Obes Surg, Swansea, W Glam, Wales

[3] Swansea Univ, Inst Life Sci 1, Mol Neurobiol Res Grp, Swansea, W Glam, Wales

关键词: Acyl-ghrelin;    Type 2 diabetes;    Lipid retention;    Inflammation;   

DOI  :  10.1016/j.mce.2018.11.004

来源: Elsevier

【 摘 要 】

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 LXR beta i e expression. Within T2D there was also a down regulation of these genes which was independent of acylghrelin levels. Circulatory pro-inflammatory markers (IL-6 and TNF alpha) 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.

【 授权许可】

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