TPOAb | eGDMD

By admin , 18 September 2025

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Literature evidence

Literature link	GPT Summary	Evidence category	Disease type


17334650	Leptin, an adipocyte-derived hormone, plays a crucial role in regulating immune responses, particularly T-lymphocyte activity, and its function is tightly linked to nutritional status. In this study, we demonstrate that leptin specifically modulates T-cell responses by enhancing the proliferation of naive T cells while suppressing memory T cell function. Additionally, leptin promotes Th1 cytokine production and inhibits Th2 cytokines, suggesting its role in shaping the immune response. Under conditions of acute starvation, leptin administration effectively counteracts the immunosuppressive effects, indicating its potential as a key mediator in linking nutritional status to immune function. These findings provide new insights into the molecular mechanisms underlying immune dysfunction during nutritional deprivation and highlight leptin’s pivotal role in maintaining immune homeostasis.	Mechanism	T1DM
39641893	This study investigates the role of fatty acid oxidation in the pathogenesis of Hashimoto's thyroiditis (HT) and its impact on CD4+ T cell differentiation. The imbalance between Treg and Th17 cells is a hallmark of HT, with Th17 cells being abnormally activated. The results show that fatty acid oxidation, particularly through the mTOR/ACC1/CPT1A pathway, plays a significant role in this process. In both in vitro and in vivo experiments, increased expression of key fatty acid oxidation proteins was observed in CD4+ T cells from HT patients and in EAT mice models. Treatment with Etomoxir, an inhibitor of fatty acid oxidation, reversed the abnormal differentiation of CD4+ T cells and ameliorated the severity of HT by reducing inflammation and lymphocyte infiltration in the thyroid. These findings suggest that targeting the fatty acid oxidation pathway could offer a potential therapeutic strategy for modulating immune responses and treating autoimmune thyroid diseases such as Hashimoto's thyroiditis.	Mechanism	Inflammatory
34956091	This prospective cohort study aimed to develop a predictive model for gestational diabetes mellitus (GDM) in early pregnancy using blood biomarkers. Among 413 pregnant women, 116 were diagnosed with GDM. Key differences between GDM and normal controls included age, pre-pregnancy BMI, fasting plasma glucose (FPG), HbA1c, triglycerides, progesterone, IgA levels, percentage of B lymphocytes, and thyroid peroxidase antibodies (TPOAb). A predictive nomogram incorporating these risk factors was developed and evaluated. The model achieved an AUC of 0.772, demonstrating good predictive accuracy. Calibration curves indicated strong agreement between predicted and observed outcomes, and decision curve analysis (DCA) confirmed the model's clinical utility. This nomogram provides a practical tool for early GDM risk assessment, potentially improving patient counseling and management during early pregnancy.	Risk factor	GDM
33486811	This study examined the relationship between thyroid markers during pregnancy and the risk of gestational diabetes mellitus (GDM) as well as post-partum glucose metabolism. Among 1467 pregnant women, the GDM group exhibited higher levels of free triiodothyronine (FT3), thyroid peroxidase antibody (TPOAb), and thyroglobulin antibody (TgAb) in the first trimester, and higher TPOAb and TgAb but lower free thyroxine (FT4) levels in the second trimester compared to the normal glucose tolerance (NGT) group. FT3, TPOAb, and TgAb in the first trimester, as well as FT4, TPOAb, and TgAb in the second trimester, were identified as risk factors for GDM. Post-partum, higher TPOAb and TgAb levels were associated with abnormal glucose tolerance (AGT). The findings indicate that altered thyroid markers during pregnancy, particularly thyroid antibodies, are associated with increased GDM risk and can predict post-partum glucose abnormalities in GDM patients.	Risk factor	GDM