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A delicate balance on thyroid hormones controls metabolic health and longevity in mice

ABSTRACT: A delicate balance on thyroid hormones controls metabolic health and longevity in mice

PROVIDER: PRJNA508103 | ENA |

REPOSITORIES: ENA

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Inadequate control of thyroid hormones sensitizes to hepatocarcinogenesis and unhealthy aging.

Project description:An inverse correlation between circulating thyroid hormone levels and longevity has been reported in several species and reduced thyroid hormone levels have been proposed as a biomarker for healthy aging and metabolic fitness in humans. However, hypothyroidism is a serious medical condition associated with reduced health and life expectancy. In this report, we show that severe and even subtle modulations on thyroid hormone levels leading to different forms of hyperthyroidism and hypothyroidism produce an overall unhealthy status and reduced lifespan in mice. A mild reduction in circulating T4 levels (~10%) resulted in hepatic mitochondrial dysfunction, increased ROS production and oxidative damage accumulation. These actions may contribute to the development of metabolic disorders, increased prevalence of hepatocellular carcinomas and early mortality in mice. Our findings raise concerns regarding the development of interventions aiming to modulate thyroid hormones to promote healthy aging or lifespan extension in mammals.

2020-04-13 | GSE123288 | GEO

Inadequate control of thyroid hormones sensitizes to hepatocarcinogenesis and unhealthy aging.

Project description:An inverse correlation between thyroid hormone levels and longevity has been reported in several species and reduced thyroid hormone levels have been proposed as a biomarker for healthy aging and metabolic fitness. However, hypothyroidism is a medical condition associated with compromised health and reduced life expectancy. Herein, we show, using wild-type and the Pax8 ablated model of hypothyroidism in mice, that hyperthyroidism and severe hypothyroidism are associated with an overall unhealthy status and shorter lifespan. Mild hypothyroid Pax8 +/- mice were heavier and displayed insulin resistance, hepatic steatosis and increased prevalence of liver cancer yet had normal lifespan. These pathophysiological conditions were precipitated by hepatic mitochondrial dysfunction and oxidative damage accumulation. These findings indicate that individuals carrying mutations on PAX8 may be susceptible to develop liver cancer and/or diabetes and raise concerns regarding the development of interventions aiming to modulate thyroid hormones to promote healthy aging or lifespan in mammals.

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Project description:Thyroid Hormones Promotes Terminal Differentiation of Medulloblastoma Tumor Cells

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miRNA profile of serum samples from metabolically healthy and unhealthy obese subjects

Project description:Obese individuals without metabolic comorbidities are categorized as metabolically healthy obese (MHO). MicroRNAs (miRNAs) may be implicated in MHO. This cross-sectional study explores the link between circulating miRNAs and the main components of metabolic syndrome (MetS) in the context of obesity. We also examine oxidative stress biomarkers in MHO vs. metabolically unhealthy obesity (MUO).

2021-03-23 | GSE169290 | GEO

Integrin αvβ3 acting as membrane receptor for thyroid hormones mediates angiogenesis in malignant T cells

Project description:We have found that thyroid hormones (THs), acting as soluble integrin αvβ3 ligands, activate growth-related signaling pathways in T-cell lymphomas (TCL). Specifically, TH-activated αvβ3 integrin signaling promotes TCL proliferation and angiogenesis, in part, via the up-regulation of VEGF. CUTLL1 cells were treated with T3- and T4-bound agarose or agarose alone for 24hrs. Total RNA was harvested from cells and used for expression profiling via RNA-seq.

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Project description:Normal thyroid hormone level is essential to maintain the normal physiologic function of the human body. Disturbances of these hormone levels have variable clinical manifestations ranging from asymptomatic to severe illness. Resistance to thyroid hormone (RTH) is a syndrome characterized by reduced intracellular action of T3, the active thyroid hormone. It is a rare autosomal dominant condition and occurs mostly due to heterogeneous mutations in the thyroid hormone receptor. Other causes of RTH include thyroid hormone cell membrane transport defect and thyroid hormone metabolism defect. Affected individuals present with symptoms of both increased and decreased thyroid hormone action, depending on the tissue's predominant receptor isoform expression, the magnitude of hormonal resistance, and the effectiveness of compensatory mechanisms. Here, we share our experience in diagnosing a case of RTH confirmed with a genetic test and found to have sequence variant mutation that is not well described in the literature previously due to the absence of genetic conclusive evidence.

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