Journalartikel

Jahr der Veröffentlichung: 2019

Seiten: 764-771

Zeitschrift: Endocrine Connections

Bandnummer: 8

Heftnummer: 6

ISSN: 2049-3614

Open Access Status: Gold

DOI Link: https://doi.org/10.1530/EC-18-0536

Verlag: BioScientifica

Abstract: 

Objective: Analysis of steroids by gas chromatography-mass spectrometry (GC-MS) defines a subject's steroidal fingerprint. Here, we compare the steroidal fingerprints of obese children with or without liver disease to identify the 'steroid metabolomic signature' of childhood nonalcoholic fatty liver disease.

Methods: Urinary samples of 85 children aged 8.5-18.0 years with BMI >97% were quantified for 31 steroid metabolites by GC-MS. The fingerprints of 21 children with liver disease (L1) as assessed by sonographic steatosis (L1(L)), elevated alanine aminotransferases (L1(A)) or both (L1(AL)), were compared to 64 children without markers of liver disease (L0). The steroidal signature of the liver disease was generated as the difference in profiles of L1 against L0 groups.

Results: L1 comparing to L0 presented higher fasting triglycerides (P = 0.004), insulin (P = 0.002), INS/GLU (P = 0.003), HOMA-IR (P = 0.002), GGTP (P = 0.006), AST/SGOT (P = 0.002), postprandial glucose (P = 0.001) and insulin (P = 0.011). L1(AL) showed highest level of T-cholesterol and triglycerides (P = 0.029; P = 0.044). Fasting insulin, postprandial glucose, INS/GLU and HOMA-IR were highest in L1(L) and L1(AL) (P = 0.001; P = 0.017; P = 0.001; P = 0.001). The liver disease steroidal signature was marked by lower DHEA and its metabolites, higher glucocorticoids (mostly tetrahydrocortisone) and lower mineralocorticoid metabolites than L0. L1 patients showed higher 5 alpha-reductase and 21-hydroxylase activity (the highest in L1(A) and L1(AL)) and lower activity of 11 beta HSD1 than L0 (P = 0.041, P = 0.009, P = 0.019).

Conclusions: The 'steroid metabolomic signature' of liver disease in childhood obesity provides a new approach to the diagnosis and further understanding of its metabolic consequences. It reflects the derangements of steroid metabolism in NAFLD that includes enhanced glucocorticoids and deranged androgens and mineralocorticoids.

Harvard-Zitierstil: Gawlik, A., Shmoish, M., Hartmann, M., Wudy, S., Olczak, Z., Gruszczynska, K., et al. (2019) Steroid metabolomic signature of liver disease in nonsyndromic childhood obesity, Endocrine Connections, 8(6), pp. 764-771. https://doi.org/10.1530/EC-18-0536

APA-Zitierstil: Gawlik, A., Shmoish, M., Hartmann, M., Wudy, S., Olczak, Z., Gruszczynska, K., & Hochberg, Z. (2019). Steroid metabolomic signature of liver disease in nonsyndromic childhood obesity. Endocrine Connections. 8(6), 764-771. https://doi.org/10.1530/EC-18-0536