ICEECE2012 Poster Presentations Pituitary Clinical (183 abstracts)
An insight into the mechanisms underlying the sympathoinhibition of acromegaly
C. Carzaniga 1, , G. Seravalle 2 , R. Attanasio 3 , G. Grassi 4 , L. Lonati 2 , C. Facchini 2 , R. Cozzi 5 , L. Fatti 3 , M. Montini 6 , G. Vitale 1, , G. Sciortino 1 , S. Damanti 1 , G. Brambilla 4 , F. Cavagnini 1 , G. Mancia 4 , M. Scacchi 1, & L. Persani 1,
1University of Milan, Milan, Italy; 2Istituto Auxologico Italiano, Milan, Italy; 3Istituto Galeazzi, Milan, Italy; 4University of Milano Bicocca, Milan, Italy; 5Ospedale Niguarda Cà Granda, Milan, Italy; 6Ospedali Riuniti, Bergamo, Italy.
By direct measurement of muscle sympathetic nerve activity (MSNA) we previously demonstrated a markedly decreased adrenergic tone in newly diagnosed acromegalic patients. The present study was aimed at confirming this finding in a larger group of patients and establishing the pathophysiological role of insulin resistance, GH and IGF1 levels, circulating leptin and extracellular water (ECW) in this abnormality.
Study design: Fifteen de novo patients with active acromegaly without obstructive sleep apnoea and cardiac hypertrophy, and 15 healthy subjects matched for age, sex and BMI were recruited. After evaluating ECW by BIA and glucose metabolism, and measuring circulating GH, IGF1 and leptin, direct recording of sympathetic outflow via the microneurographic technique was performed.
Results: A marked sympathetic inhibition was confirmed in patients compared to controls (MSNA 18.3±8.10 vs 37.3±6.48 bursts/min, P<0.0001) in spite of a significatly increased HOMA index (4.2±2.39 vs 1.6±0.19, P<0.001). ECW was comparable in patients and controls. A clear-cut reduction of plasma leptin (1.6±1.04 vs 6.5±2.01 μg/l, P<0.0001) was recorded in the patients. In these latter MSNA was not correlated with ECW, GH or IGF1, but was positively correlated with leptin (P<0.0001). Leptin was the only independent predictor of MSNA in a multiple regression analysis.
Conclusions: Acromegalic patients display a decreased sympathetic outflow in spite of insulin resistance. The lack of correlation between ECW and MSNA does not support the hypothesis of a sympathoinhibition due to baroreceptor activation by volume expansion. A putative role of the GH–IGF1 system as direct central inhibitor of sympathetic drive is not likely, given the lack of correlations between these two parameters and MSNA. On the contrary, the highly significant correlation with leptin points to hypoleptinemia as a major contributor to the sympathoinhibiton of acromegaly, consistent with previous studies in obese animal models.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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