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Updated: May 10, 2025

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
Published on: April 28, 2016
Metabolic Signalling Peptides and Their Relation to Clinical and Demographic Characteristics in Acute and Recovered
Hiba Mutwalli1,2, Johanna L Keeler1, Raymond Chung3,4,5
1Centre for Research in Eating and Weight Disorders (CREW), Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London SE5 8AF, UK.
Abstract:
Background/Objectives: Recent research has established that metabolic factors may increase the vulnerability to develop anorexia nervosa (AN). The aim of this study was to explore the serum concentrations of leptin, insulin-like growth factor-1 (IGF-1), insulin and insulin receptor substrate (IRS-1) as possible state or trait biomarkers for AN in the acute and recovery (recAN) phases. Our secondary aim was to test associations between the tested markers and demographic and clinical characteristics. Methods: This cross-sectional study included data from 56 participants with AN, 24 recAN participants and 51 healthy controls (HCs). Enzyme-linked immunosorbent assays (ELISAs) were used to quantify serum concentrations of leptin, IGF-1, insulin and IRS-1. An analysis of covariance (ANCOVA) and linear regression models were utilised to test our results. Results: There were significant differences with a large effect size between the groups for serum leptin (p < 0.001; d = 0.80), whereby people with AN had lower leptin than those with recAN (p = 0.023; d = 0.35) and HCs (p < 0.001; d = 0.74). The between-group comparison of IGF-1 did not reach significance, although the effect size was moderate (d = 0.6) and was driven by lower levels of IGF-1 in people with acute AN compared to HCs (p = 0.036; d = 0.53). Serum insulin and IRS-1 did not differ between groups. Conclusions: Low leptin levels seen in individuals with AN may be due to starvation leading to fatty tissue depletion. Understanding the regulation of IGF-1 and insulin signalling over the course of the disorder requires further investigation.
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