Pubertal Status and Gonadal Functions in Obese Boys with Fatty Liver.


Journal

Metabolic syndrome and related disorders
ISSN: 1557-8518
Titre abrégé: Metab Syndr Relat Disord
Pays: United States
ID NLM: 101150318

Informations de publication

Date de publication:
03 2019
Historique:
pubmed: 8 1 2019
medline: 26 11 2019
entrez: 8 1 2019
Statut: ppublish

Résumé

In adult studies, obese subjects with nonalcoholic fatty liver disease (NAFLD) have been shown to have poor sperm quality, and lower testosterone and luteinizing hormone levels. The aim of this study was to investigate the pubertal status and gonadal functions in obese boys with NAFLD. The study included 119 obese and 78 nonobese age-matched adolescents. The obese boys were separated into two groups based on the presence (NAFLD group) or absence of liver steatosis with high transaminases (non-NAFLD group). The levels of serum AMH (anti-Mullerian hormone), inhibin B, gonadotropins, total testosterone, lipids, high-sensitivity C-reactive protein, fasting glucose, insulin levels, and aortic intima media thickness were measured in all subjects. Of the total 197 children, 174 had reached puberty. There were no significant differences between the groups in respect of testicular sizes and the prevalence of pubertal status among the groups (84.3% of NAFLD vs. 70.6% of non-NAFLD vs. 98.7% of control subjects). No significant differences were found in respect of gonadotropins and AMH levels. Total testosterone levels in the NAFLD group were significantly lower than those of the non-NAFLD obese group (P < 0.001) and the control group (P < 0.001). Inhibin B levels were also significantly lower in all (NAFLD and non-NAFLD) obese groups compared to the control group (P = 0.008). The results of the study demonstrated that diminished testosterone and inhibin B levels occur in pubertal obese boys with NAFLD. No significant differences were detected according to pubertal status, AMH levels, and testicular volumes in the age-matched groups.

Sections du résumé

BACKGROUND
In adult studies, obese subjects with nonalcoholic fatty liver disease (NAFLD) have been shown to have poor sperm quality, and lower testosterone and luteinizing hormone levels. The aim of this study was to investigate the pubertal status and gonadal functions in obese boys with NAFLD.
MATERIALS AND METHODS
The study included 119 obese and 78 nonobese age-matched adolescents. The obese boys were separated into two groups based on the presence (NAFLD group) or absence of liver steatosis with high transaminases (non-NAFLD group). The levels of serum AMH (anti-Mullerian hormone), inhibin B, gonadotropins, total testosterone, lipids, high-sensitivity C-reactive protein, fasting glucose, insulin levels, and aortic intima media thickness were measured in all subjects.
RESULTS
Of the total 197 children, 174 had reached puberty. There were no significant differences between the groups in respect of testicular sizes and the prevalence of pubertal status among the groups (84.3% of NAFLD vs. 70.6% of non-NAFLD vs. 98.7% of control subjects). No significant differences were found in respect of gonadotropins and AMH levels. Total testosterone levels in the NAFLD group were significantly lower than those of the non-NAFLD obese group (P < 0.001) and the control group (P < 0.001). Inhibin B levels were also significantly lower in all (NAFLD and non-NAFLD) obese groups compared to the control group (P = 0.008).
CONCLUSIONS
The results of the study demonstrated that diminished testosterone and inhibin B levels occur in pubertal obese boys with NAFLD. No significant differences were detected according to pubertal status, AMH levels, and testicular volumes in the age-matched groups.

Identifiants

pubmed: 30614770
doi: 10.1089/met.2018.0050
doi:

Substances chimiques

Hormones 0
inhibin B 0
Testosterone 3XMK78S47O
Inhibins 57285-09-3

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

102-107

Auteurs

Hüseyin Kurku (H)

1 Department of Biochemistry, University of Health Sciences, Konya Training and Research Hospital, Konya, Turkey.

Müge Atar (M)

2 Department of Pediatric Endocrinology and Diabetes, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.

Özgür Pirgon (Ö)

2 Department of Pediatric Endocrinology and Diabetes, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.

Muammer Büyükinan (M)

3 Department of Pediatric Endocrinology and Diabetes and University of Health Sciences, Konya Training and Research Hospital, Konya, Turkey.

Said Sami Erdem (SS)

1 Department of Biochemistry, University of Health Sciences, Konya Training and Research Hospital, Konya, Turkey.

İsa Deniz (İ)

4 Department of Radiology, University of Health Sciences, Konya Training and Research Hospital, Konya, Turkey.

Yavuz Turgut Gederet (YT)

1 Department of Biochemistry, University of Health Sciences, Konya Training and Research Hospital, Konya, Turkey.

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Classifications MeSH