Role of serum fasting glucagon in hypothyroidism-related nonalcoholic fatty liver disease.

IF 3.9 2区 医学 Q2 NUTRITION & DIETETICS Nutrition & Metabolism Pub Date : 2025-03-11 DOI:10.1186/s12986-025-00899-z
Mervat M El-Eshmawy, Amira A Barakat, Azza A El-Baiomy, Mohamed M Abo El-Naga, Mohamed Elbasiony
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Abstract

Background: A bidirectional relationship between hypothyroidism and nonalcoholic fatty liver disease (NAFLD) has been proposed. Fasting hyperglucagonemia in patients with hypothyroidism induced NAFLD needs to be further clarified. The aim of the present study was to determine fasting serum glucagon levels in hypothyroid adults with and without NAFLD. The possible association between fasting glucagon and NAFLD in patients with hypothyroidism was also evaluated.

Methods: This study was comprised 60 patients with uncontrolled hypothyroidism and 30 healthy controls matched for age and sex. Patients with hypothyroidism were divided into 2 groups: 30 patients with NAFLD and 30 patients without NAFLD. Diagnosis of NAFLD was based on the combination of hepatic steatosis index (HSI) at a cutoff value of 36 and measurements of steatosis using fibroScan. Anthropometric measurements, lipids profile, homeostasis model assessment of insulin resistance (HOMA-IR), free thyroxine (FT4), triiodothyronine (FT3), thyroid stimulating hormone (TSH) and serum fasting glucagon were assessed.

Results: Serum fasting glucagon concentration was significantly higher in hypothyroid patients with and without NAFLD than in healthy controls; glucagon was also significantly higher in the hypothyroid patients with NAFLD than in those without NAFLD. Fasting glucagon was significantly correlated with waist circumference (WC), body mass index (BMI), TSH, HSI and fibroScan parameters in hypothyroid patients with NAFLD. Fasting glucagon predicts NAFLD in patients with hypothyroidism at a cutoff value 85 ng/L with 90% sensitivity, 100% specificity and p < 0.001. With multivariable analysis, age, BMI and TSH were significant positive predictors of NAFLD in patients with hypothyroidism.

Conclusion: Fasting glucagon concentration may play a role in the development of NAFLD in patients with hypothyroidism. However, the exact underlying mechanism needs further studies.

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背景:有人提出甲状腺功能减退症与非酒精性脂肪肝(NAFLD)之间存在双向关系。甲状腺功能减退症诱发非酒精性脂肪肝患者的空腹高胰高血糖素血症需要进一步明确。本研究旨在确定患有和未患有非酒精性脂肪肝的甲状腺功能减退症成人的空腹血清胰高血糖素水平。本研究还评估了甲状腺功能减退症患者空腹胰高血糖素与非酒精性脂肪肝之间可能存在的关联:本研究由 60 名未受控制的甲状腺功能减退症患者和 30 名年龄和性别匹配的健康对照组组成。甲减患者分为两组:30 名非酒精性脂肪肝患者和 30 名非酒精性脂肪肝患者。非酒精性脂肪肝的诊断依据是肝脏脂肪变性指数(HSI)(临界值为 36)和使用纤维扫描仪对脂肪变性的测量结果。对人体测量、血脂概况、胰岛素抵抗稳态模型评估(HOMA-IR)、游离甲状腺素(FT4)、三碘甲状腺原氨酸(FT3)、促甲状腺激素(TSH)和血清空腹胰高血糖素进行了评估:结果:患有和未患有非酒精性脂肪肝的甲状腺功能减退症患者的血清空腹胰高血糖素浓度明显高于健康对照组;患有非酒精性脂肪肝的甲状腺功能减退症患者的胰高血糖素浓度也明显高于未患有非酒精性脂肪肝的甲状腺功能减退症患者。在患有非酒精性脂肪肝的甲减患者中,空腹胰高血糖素与腰围(WC)、体重指数(BMI)、促甲状腺激素(TSH)、人血指数(HSI)和纤维扫描参数有明显相关性。空腹胰高血糖素可预测甲减患者的非酒精性脂肪肝,其临界值为85纳克/升,灵敏度为90%,特异性为100%,P为0 结论:空腹胰高血糖素浓度可能在甲减患者非酒精性脂肪肝的发病中起一定作用。然而,确切的内在机制还需要进一步研究。
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来源期刊
Nutrition & Metabolism
Nutrition & Metabolism 医学-营养学
CiteScore
8.40
自引率
0.00%
发文量
78
审稿时长
4-8 weeks
期刊介绍: Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.
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