Key result
Adolescent obesity linked to ~46% lower serum omentin-1 levels regardless of NAFLD.
Why the study?
Decreased omentin-1 levels have been reported in obese patients, but the relationship between NAFLD and omentin-1 remains contradictory.
Cross-Sectional (n=88)
No
Omentin-1 levels are decreased in obese adolescents regardless of NAFLD presence, suggesting it is a marker of obesity rather than hepatic steatosis specifically.
Answers are grounded in this paper and cite their sources.
Should not guide NAFLD assessment in obese adolescents; leaves open omentin-1 as obesity marker pending prospective studies.
Background: Omentin-1 is an adipocytokine secreted from visceral adipose tissue that is thought to increase insulin sensitivity. Non-alcoholic fatty liver disease (NAFLD) is a comparatively extensive problem in obese adolescents. Decreased omentin-1 levels have been reported in obese patients, but the relationship between NAFLD and omentin-1 is contradictory. Objectives: We aimed to evaluate the omentin-1 levels in the sera of obese adolescents with and without NAFLD and compare them with each other. Methods: In this study, a total of 88 adolescents (56 obese and 32 normal-weight) were enrolled. Abdominal ultrasonography (US) identified 28 obese adolescents with grade 2 - 3 hepatosteatosis constituting the NAFLD group and 28 without hepatosteatosis on US constituting the non-NAFLD group. The control group included 32 age- and gender-matched cases without hepatosteatosis and with normal percentile body mass index (BMI). Serum omentin-1 levels were evaluated and compared. Results: The mean age of the research group was 12.72 ± 1.91 years. Unsurprisingly, BMI, glycated hemoglobin (HbA1c), liver transaminases (AST, ALT), total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL), homeostatic model assessment for insulin resistance (HOMA-IR), and insulin rates were noticeably elevated in obese adolescents compared to controls (P < 0.05). However, omentin-1 and high-density lipoprotein cholesterol (HDL) levels were remarkably lower in the obese group (P < 0.05). No significant difference was found between the NAFLD and non-NAFLD groups regarding omentin-1, HbA1c, glucose, urea, creatinine, AST, C-reactive protein (CRP), total cholesterol, triglyceride, HDL, LDL, thyroid stimulating hormone, 25-hydroxyvitamin D3, HOMA-IR, and insulin. The BMI and ALT grades of the non-NAFLD group were notably lower than the NAFLD group (P < 0.05). While there was no significant difference between omentin-1 and other parameters in obese adolescents without NAFLD (P > 0.05), we found a significant difference between omentin-1 and BMI, AST, ALT, HOMA-IR, and insulin values in obese adolescents with NAFLD (P < 0.05). Conclusions: Omentin-1 levels were decreased in obese adolescents regardless of the presence of NAFLD. However, in obese patients with NAFLD, there was a significant difference between omentin-1 and several markers of obesity and insulin resistance.
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Türkkan et al. (2021) conducted a cross-sectional in Obesity and Non-alcoholic Fatty Liver Disease (NAFLD) (n=88). Obesity (with or without NAFLD) vs. Normal-weight was evaluated on Serum omentin-1 levels (ng/mL) (p=<0.0001). Obesity in adolescents was associated with significantly lower serum omentin-1 levels (5.06 ng/mL) compared to normal-weight controls (9.3 ng/mL), regardless of the presence of NAFLD.
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