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Liver Volume and Hepatic Adiposity in Childhood: Relations to Body Growth and Visceral Fat

Overview
Specialty Endocrinology
Date 2017 Sep 20
PMID 28925408
Citations 2
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Abstract

Background And Objective: The sequence of prenatal growth restraint and postnatal catch-up growth may lead to hepato-visceral adiposity, insulin resistance and low-grade inflammation before the onset of puberty. In prepubertal children born appropriate for gestational age (AGA) or small for gestational age (SGA), we assessed potential relationships between the aforementioned sequence and liver volume.

Subjects/methods: The study population consisted of 86 children (41 AGA and 45 SGA with catch-up growth; age (mean±s.e.m.), 8.5±0.1 years), recruited into two prospective longitudinal studies. Anthropometry, endocrine-metabolic variables and inflammatory and hepatic markers were assessed, along with liver volume, hepatic adiposity and abdominal fat partitioning (by magnetic resonance imaging).

Results: AGA and SGA children differed in hepato-visceral adiposity, but had similar liver volumes. Boys had larger livers than girls, and higher sex hormone binding globulin and inflammation markers. Liver volume correlated with height Z-score, body mass index Z-score, HOMA-IR (homeostasis model assessment-insulin resistance) and with subcutaneous and visceral fat, but not with birth weight Z-score or with hepatic adiposity. Height, visceral fat, gender and HOMA-IR were major determinants of liver volume, together explaining 61% of its variance.

Conclusions: The trajectory from prenatal restraint, via postnatal catch-up, to hepato-visceral adiposity and insulin resistance does not appear to be detectably influenced by prepubertal alterations of liver volume. Further follow-up will disclose the potential role of liver volume in the pubertal segment of this trajectory, and whether the augmented fat content and visceral adiposity in SGA subjects is followed by the development of metabolic syndrome and hepatic dysfunction in adulthood.

Citing Articles

Determinants of non-alcoholic fatty liver disease in young people: Maternal, neonatal, and adolescent factors.

Nairz J, Messner A, Kiechl S, Winder B, Hochmayr C, Egger A PLoS One. 2024; 19(2):e0298800.

PMID: 38386674 PMC: 10883560. DOI: 10.1371/journal.pone.0298800.


Are body surface area based estimates of liver volume applicable to children with overweight or obesity? An in vivo validation study.

Hosey-Cojocari C, Chan S, Friesen C, Robinson A, Williams V, Swanson E Clin Transl Sci. 2021; 14(5):2008-2016.

PMID: 33982422 PMC: 8504846. DOI: 10.1111/cts.13059.

References
1.
Faienza M, Brunetti G, Ventura A, DAniello M, Pepe T, Giordano P . Nonalcoholic fatty liver disease in prepubertal children born small for gestational age: influence of rapid weight catch-up growth. Horm Res Paediatr. 2013; 79(2):103-9. DOI: 10.1159/000347217. View

2.
Santini F, Giannetti M, Mazzeo S, Fierabracci P, Scartabelli G, Marsili A . Ultrasonographic evaluation of liver volume and the metabolic syndrome in obese women. J Endocrinol Invest. 2007; 30(2):104-10. DOI: 10.1007/BF03347407. View

3.
Westerbacka J, Kolak M, Kiviluoto T, Arkkila P, Siren J, Hamsten A . Genes involved in fatty acid partitioning and binding, lipolysis, monocyte/macrophage recruitment, and inflammation are overexpressed in the human fatty liver of insulin-resistant subjects. Diabetes. 2007; 56(11):2759-65. DOI: 10.2337/db07-0156. View

4.
Giannetti M, Piaggi P, Ceccarini G, Mazzeo S, Querci G, Fierabracci P . Hepatic left lobe volume is a sensitive index of metabolic improvement in obese women after gastric banding. Int J Obes (Lond). 2011; 36(3):336-41. DOI: 10.1038/ijo.2011.243. View

5.
Lin S, Heba E, Bettencourt R, Lin G, Valasek M, Lunde O . Assessment of treatment response in non-alcoholic steatohepatitis using advanced magnetic resonance imaging. Aliment Pharmacol Ther. 2017; 45(6):844-854. PMC: 5346270. DOI: 10.1111/apt.13951. View