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THU074 Plasma Spexin In Metabolic Syndrome Related To Adult Growth Hormone Deficiency: A Cross-sectional Study
Disclosure: E. Vergani: None. A. Oliva: None. C. Bruno: None. D. Currò: None. A. Mancini: None. Adult growth hormone deficiency (aGHD) shares with metabolic syndrome some clinical features such as higher fat mass percentage, increased total cholesterol, LDL, triglycerides, reduced HDL, and higher ri...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10555926/ http://dx.doi.org/10.1210/jendso/bvad114.1154 |
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author | Vergani, Edoardo Oliva, Alessandro Bruno, Carmine Currò, Diego Mancini, Antonio |
author_facet | Vergani, Edoardo Oliva, Alessandro Bruno, Carmine Currò, Diego Mancini, Antonio |
author_sort | Vergani, Edoardo |
collection | PubMed |
description | Disclosure: E. Vergani: None. A. Oliva: None. C. Bruno: None. D. Currò: None. A. Mancini: None. Adult growth hormone deficiency (aGHD) shares with metabolic syndrome some clinical features such as higher fat mass percentage, increased total cholesterol, LDL, triglycerides, reduced HDL, and higher risk of developing type 2 diabetes mellitus and cardiovascular complications. Spexin, also known as neuropeptide Q, is a 14-aminoacid polypeptide, related to the galanin-kisspeptin family, produced in several human tissues. It is also secreted along with insulin by pancreatic beta cells; via paracrine effects they blunted reciprocal secretion. In type 2 diabetes mellitus spexin is closely correlated to fasting and post prandial glucose, glycosylated hemoglobin and HOMA index. Moreover, spexin infusion seems to ameliorate ALT and AST levels in non-alcoholic fatty liver disease. Given its controversial role in condition of metabolic impairment, we aimed to evaluate spexin plasmatic levels in aGHD. Thirty-eight subjects were included in the study, 18 aGHD patients (7 females and 11 males) and 20 healthy controls (12 females and 8 males). aGHD was diagnosed by a GHRH plus arginine test. Etiologies of GHD were as follows: 7 empty sellas, 5 post-surgical hypopituitarism, and 6 idiopathic with negative MRI scans. GHRH plus arginine stimulation tests were repeated twice in idiopathic aGHD to confirm the diagnosis. They were evaluated for glucose and insulin, HOMA and QUICKI index, total/LDL/HDL cholesterol, triglycerides, uric acid and IGF-1. Spexin was measured by ELISA, according to manufacturers’ protocols. Fat mass percentage was evaluated by DXA. Mean±SEM age of aGHD group was 59.7±2.7 years, while BMI was 30.2±2.2 kg/m(2); control group aged 47.1±2.5 years, while BMI was 24.5±0.9 kg/m(2). As expected, aGHD patients showed higher HOMA index, triglycerides and lower HDL than controls. Furthermore mean±SEM fat mass percentage was significantly higher in aGHD than controls (44.41±3.15 vs 32.2±3.64). Spexin levels were similar in the two groups (aGHD 1.17±0.21 vs controls 1.25±0.10 ng/ml). significant correlations were found in both populations. These results, although preliminary, seem to exclude a possible role of spexin in aGHD; however, spexin could represent another possible element of differentiation between aGHD and metabolic syndrome. Such controversial topic requires further evaluations. Presentation: Thursday, June 15, 2023 |
format | Online Article Text |
id | pubmed-10555926 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-105559262023-10-07 THU074 Plasma Spexin In Metabolic Syndrome Related To Adult Growth Hormone Deficiency: A Cross-sectional Study Vergani, Edoardo Oliva, Alessandro Bruno, Carmine Currò, Diego Mancini, Antonio J Endocr Soc Neuroendocrinology And Pituitary Disclosure: E. Vergani: None. A. Oliva: None. C. Bruno: None. D. Currò: None. A. Mancini: None. Adult growth hormone deficiency (aGHD) shares with metabolic syndrome some clinical features such as higher fat mass percentage, increased total cholesterol, LDL, triglycerides, reduced HDL, and higher risk of developing type 2 diabetes mellitus and cardiovascular complications. Spexin, also known as neuropeptide Q, is a 14-aminoacid polypeptide, related to the galanin-kisspeptin family, produced in several human tissues. It is also secreted along with insulin by pancreatic beta cells; via paracrine effects they blunted reciprocal secretion. In type 2 diabetes mellitus spexin is closely correlated to fasting and post prandial glucose, glycosylated hemoglobin and HOMA index. Moreover, spexin infusion seems to ameliorate ALT and AST levels in non-alcoholic fatty liver disease. Given its controversial role in condition of metabolic impairment, we aimed to evaluate spexin plasmatic levels in aGHD. Thirty-eight subjects were included in the study, 18 aGHD patients (7 females and 11 males) and 20 healthy controls (12 females and 8 males). aGHD was diagnosed by a GHRH plus arginine test. Etiologies of GHD were as follows: 7 empty sellas, 5 post-surgical hypopituitarism, and 6 idiopathic with negative MRI scans. GHRH plus arginine stimulation tests were repeated twice in idiopathic aGHD to confirm the diagnosis. They were evaluated for glucose and insulin, HOMA and QUICKI index, total/LDL/HDL cholesterol, triglycerides, uric acid and IGF-1. Spexin was measured by ELISA, according to manufacturers’ protocols. Fat mass percentage was evaluated by DXA. Mean±SEM age of aGHD group was 59.7±2.7 years, while BMI was 30.2±2.2 kg/m(2); control group aged 47.1±2.5 years, while BMI was 24.5±0.9 kg/m(2). As expected, aGHD patients showed higher HOMA index, triglycerides and lower HDL than controls. Furthermore mean±SEM fat mass percentage was significantly higher in aGHD than controls (44.41±3.15 vs 32.2±3.64). Spexin levels were similar in the two groups (aGHD 1.17±0.21 vs controls 1.25±0.10 ng/ml). significant correlations were found in both populations. These results, although preliminary, seem to exclude a possible role of spexin in aGHD; however, spexin could represent another possible element of differentiation between aGHD and metabolic syndrome. Such controversial topic requires further evaluations. Presentation: Thursday, June 15, 2023 Oxford University Press 2023-10-05 /pmc/articles/PMC10555926/ http://dx.doi.org/10.1210/jendso/bvad114.1154 Text en © The Author(s) 2023. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Neuroendocrinology And Pituitary Vergani, Edoardo Oliva, Alessandro Bruno, Carmine Currò, Diego Mancini, Antonio THU074 Plasma Spexin In Metabolic Syndrome Related To Adult Growth Hormone Deficiency: A Cross-sectional Study |
title | THU074 Plasma Spexin In Metabolic Syndrome Related To Adult Growth Hormone Deficiency: A Cross-sectional Study |
title_full | THU074 Plasma Spexin In Metabolic Syndrome Related To Adult Growth Hormone Deficiency: A Cross-sectional Study |
title_fullStr | THU074 Plasma Spexin In Metabolic Syndrome Related To Adult Growth Hormone Deficiency: A Cross-sectional Study |
title_full_unstemmed | THU074 Plasma Spexin In Metabolic Syndrome Related To Adult Growth Hormone Deficiency: A Cross-sectional Study |
title_short | THU074 Plasma Spexin In Metabolic Syndrome Related To Adult Growth Hormone Deficiency: A Cross-sectional Study |
title_sort | thu074 plasma spexin in metabolic syndrome related to adult growth hormone deficiency: a cross-sectional study |
topic | Neuroendocrinology And Pituitary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10555926/ http://dx.doi.org/10.1210/jendso/bvad114.1154 |
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