Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2019) 61 P004 | DOI: 10.1530/endoabs.61.P004

OU2019 Poster Presentations (1) (9 abstracts)

Evidence of aberrant inflammation in patients with Lipodystrophy

Sehar Sajid 1 , Bernard Burke 1 , Christopher Mee 1 , David Savage 2 & Derek Renshaw 1

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1Coventry University, Coventry, UK; 2University of Cambridge, Cambridge, UK.


Introduction: Lipodystrophy is a rare medical condition with a varied etiology that is characterised by a complete or partial loss of adipose tissue, which can be generalised, partial or localised. Patients have altered secretion of adipokines, such as, Leptin and Adiponectin. Ectopic lipid accumulation is common and leads to metabolic complications associated with insulin resistance (IR) such as, diabetes mellitus (DM) and hypertriglyceridemia. Levels of circulating inflammatory markers are also altered; increase in proinflammatory cytokines, such as, TNF-α and IL-6 and decrease in anti-inflammatory proteins, such as, IL-10 are observed. Annexin A1 (AnxA1) is an anti-inflammatory/pro-resolution protein secreted by the adipose tissue and is decreased in obese individuals. Although obesity is opposite to lipodystrophy, they share similar metabolic alterations and cytokine profiles. Therefore, it was hypothesised that plasma AnxA1 levels are also decreased in lipodystrophy patients.

Aim: To investigate the plasma AnxA1 levels and C-Reactive protein (CRP) concentrations in lipodystrophy patients.

Methods: The plasma concentration of AnxA1 and CRP were measured using a specific Enzyme-linked immunosorbent Assay. Data obtained was analysed using GraphPad Prism version 5 and a four-parameter logistic curve. Statistical significance was determined using T test at 95% level.

Results: Plasma AnxA1 levels were significantly decreased in lipodystrophy patients in comparison to healthy controls (0.24 ng/ml ±0.243 S.D., n=9 and 1.24 ng/ml ±0.878 S.D., n=19 respectively, P=0.003). Conversely, Plasma CRP levels are significantly increased in lipodystrophy patients in comparison to healthy controls (3.26 μg/ml ±3.10 S.D., n=9 and 1.35 μg/ml ±1.46 S.D., n=19 respectively, P=0.03).

Conclusion: Lipodystrophy patients display an aberrant inflammatory balance, which may contribute to their dysfunctional glycaemic control.

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