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      Angiopoietin-like 8 (ANGPTL8) as a potential predictor of NAFLD in paediatric patients with Prader-Willi Syndrome

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          Abstract

          Purpose

          Angiopoietin-like 8 (ANGPTL8) is a liver- and adipose tissue-produced protein that predicts non-alcoholic fatty liver disease (NAFLD) and altered metabolic homeostasis in the general population as well as in persons with common and genetic obesity, including the Prader–Willi syndrome (PWS). However, its metabolic correlate in paediatric patients with respect to PWS is unknown.

          Methods

          This cross-sectional study investigated circulating ANGPTL8 and adipocytokines levels in 28 PWS and 28 age-, sex- and BMI-matched children and adolescents (age, 7.0–17.8y) in relation to NAFLD and metabolic homeostasis assessed by OGTT, paediatric metabolic index (PMI) and fatty liver index (FLI), liver ultrasonography (US), as well as dual-energy X-ray absorptiometry (DEXA) for analysis of fat (FM) and fat-free mass (FFM).

          Results

          At the set level of significance, PWS children showed lower values of FFM ( p < 0.01) but healthier insulin profiles ( p < 0.01) and PMI values ( p < 0.05) than matched controls. By US, the prevalence of NAFLD was similar between groups but less severe in PWS than controls. Analysis of ANGPTL8 levels showed no difference between groups, yet only in PWS ANGPTL8 levels were associated with ALT levels, FLI values and NAFLD. In stepwise multivariable regression analysis on merged data, ANGPTL8 levels were independently predicted by BMI SDS, leptin levels and NAFLD.

          Conclusion

          ANGPTL8 levels are similar in PWS and controls and, overall, they are directly associated with the presence and severity of NAFLD in patients with PWS.

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          Most cited references51

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          The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases.

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            Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

            The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
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              Establishing a standard definition for child overweight and obesity worldwide: international survey.

              To develop an internationally acceptable definition of child overweight and obesity, specifying the measurement, the reference population, and the age and sex specific cut off points. International survey of six large nationally representative cross sectional growth studies. Brazil, Great Britain, Hong Kong, the Netherlands, Singapore, and the United States. 97 876 males and 94 851 females from birth to 25 years of age. Body mass index (weight/height(2)). For each of the surveys, centile curves were drawn that at age 18 years passed through the widely used cut off points of 25 and 30 kg/m(2) for adult overweight and obesity. The resulting curves were averaged to provide age and sex specific cut off points from 2-18 years. The proposed cut off points, which are less arbitrary and more internationally based than current alternatives, should help to provide internationally comparable prevalence rates of overweight and obesity in children.
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                Author and article information

                Contributors
                paolo.marzullo@med.uniupo.it
                Journal
                J Endocrinol Invest
                J Endocrinol Invest
                Journal of Endocrinological Investigation
                Springer International Publishing (Cham )
                0391-4097
                1720-8386
                16 October 2020
                16 October 2020
                2021
                : 44
                : 7
                : 1447-1456
                Affiliations
                [1 ]GRID grid.16563.37, ISNI 0000000121663741, Division of Endocrinology, Department of Translational Medicine, , University of Piemonte Orientale, ; Novara, Italy
                [2 ]GRID grid.418224.9, ISNI 0000 0004 1757 9530, Division of General Medicine, , Istituto Auxologico Italiano, IRCCS, San Giuseppe Hospital, ; Piancavallo, Verbania, Italy
                [3 ]GRID grid.414125.7, ISNI 0000 0001 0727 6809, Reference Center for Prader-Willi Syndrome, , Bambino Gesù Children’s Hospital, Research Institute, ; Palidoro (Rome), Italy
                [4 ]GRID grid.418224.9, ISNI 0000 0004 1757 9530, Laboratory of Metabolic Research, , Istituto Auxologico Italiano, IRCCS, San Giuseppe Hospital, ; Piancavallo, Verbania, Italy
                [5 ]GRID grid.414125.7, ISNI 0000 0001 0727 6809, Radiology Unit, , Bambino Gesù Children’s Hospital, Research Institute, ; Palidoro (Rome), Italy
                [6 ]GRID grid.418224.9, ISNI 0000 0004 1757 9530, Division of Auxology and Metabolic Diseases, , Istituto Auxologico Italiano, IRCCS, San Giuseppe Hospital, ; Piancavallo, Verbania, Italy
                Author information
                http://orcid.org/0000-0003-3215-5747
                Article
                1444
                10.1007/s40618-020-01444-w
                8195791
                33067796
                3d14b604-5e7e-4a50-84b3-8875407f7cdb
                © The Author(s) 2020

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 27 May 2020
                : 6 October 2020
                Funding
                Funded by: Università degli Studi del Piemonte Orientale Amedeo Avogrado
                Categories
                Original Article
                Custom metadata
                © Italian Society of Endocrinology (SIE) 2021

                angptl8,prader–willi syndrome,nafld
                angptl8, prader–willi syndrome, nafld

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