Session: SAT 109-133-GHRH, GH & IGF Biology & Signaling
Bench to Bedside
Poster Board SAT-133
Aims: To investigate metabolic factors over specified period on HD mutation carriers who were either pre manifest or had moderate stage II/III HD and comparing with controls
Methods: Control (n=15), pre-manifest (n=14) and stage II/III (n=13) participants were studied with blood and plasma sampling over a standardized 24-h period at various points and a battery of clinical tests including neurological rating and function scales were performed.Blood samples were taken from an intravenous cannula, immediately centrifuged and plasma/serum extracted and stored at −80°C. IGF,GHRF and IGFBP3 were measured at three time points (fasting 3 pm and 11 pm). Insulin and Glucose were measured for and extended glucose tolerance test. Leptin and ghrelin were measured pre and post standardized meal. Plasma samples for amino acids were drawn fasting.
Results: There was no correlation between IGFBP3 and GHRF with CAG (disease burden).Contrary to other studies that show 10-25% (Farrer 1985) of patients with HD develop altered glucose metabolism, our study did not demonstrate an increased incidence of impaired glucose tolerance when compared to controls, pre manifest or moderates. Fasting ghrelin levels show a significant negative association with disease burden (p=0.009) and there is a significant positive association between fasting leptin levels, body mass index and scapular fat pad thickness.
Conclusions: Fasting ghrelin levels negatively correlated with progression of HD and this may be the cause of weight loss and other peripheral manifestations of HD. Further work is required to understand the underlying mechanism and its potential as an HD biomarker.
Nothing to Disclose: RN, ES, EK, NH, PCH, MB, TTW
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