ArticleNutrition & metabolism2025
Role of serum fasting glucagon in hypothyroidism-related nonalcoholic fatty liver disease.
Article in Nutrition & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA 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.
methodsThis 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.
resultsSerum 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.
conclusionFasting glucagon concentration may play a role in the development of NAFLD in patients with hypothyroidism. However, the exact underlying mechanism needs further studies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.