The Human Fetus and Metabolic Adaptations to Hypoxia

Abstract. Thyroid hormones play an important role in body homeostasis by facilitating metabolism of lipids and glucose, regulating metabolic adaptations, responding to changes in energy intake, and controlling thermogenesis. Proper metabolism and action of these hormones requires the participation of various nutrients. Among them is zinc, whose interaction with thyroid hormones is complex. It is known to regulate both the synthesis and mechanism of action of these hormones. In the present review, we aim to shed light on the regulatory effects of zinc on thyroid hormones. Scientific evidence shows that zinc plays a key role in the metabolism of thyroid hormones, specifically by regulating deiodinases enzymes activity, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH) synthesis, as well as by modulating the structures of essential transcription factors involved in the synthesis of thyroid hormones. Serum concentrations of zinc also appear to influence the levels of serum T3, T4 and TSH. In addition, studies have shown that Zinc transporters (ZnTs) are present in the hypothalamus, pituitary and thyroid, but their functions remain unknown. Therefore, it is important to further investigate the roles of zinc in regulation of thyroid hormones metabolism, and their importance in the treatment of several diseases associated with thyroid gland dysfunction.

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Single-trocar alleviation of congenital high airway obstruction syndrome (CHAOS) in a human fetus with laryngeal atresia

Ultraschall in der Medizin - European Journal of Ultrasound ◽

10.1055/s-2008-1080880 ◽

2008 ◽

Vol 29 (S 2) ◽

Author(s):

R Stressig ◽

A Heep ◽

A Müller ◽

S Fröhlich ◽

U Jäger ◽

...

Keyword(s):

Airway Obstruction ◽

Human Fetus ◽

Laryngeal Atresia

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Faculty Opinions recommendation of Regulation of T cell responses in the developing human fetus.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1138012.595125 ◽

2009 ◽

Author(s):

Noel Rose ◽

Daniela Cihakova

Keyword(s):

T Cell ◽

Human Fetus ◽

T Cell Responses ◽

Cell Responses

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Faculty Opinions recommendation of The Human Fetus Preferentially Engages with Face-like Visual Stimuli.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.727709408.793560152 ◽

2019 ◽

Author(s):

Scott Johnson

Keyword(s):

Human Fetus ◽

Visual Stimuli

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Heart failure—emerging roles for the mitochondrial pyruvate carrier

Cell Death and Differentiation ◽

10.1038/s41418-020-00729-0 ◽

2021 ◽

Author(s):

Mariana Fernandez-Caggiano ◽

Philip Eaton

Keyword(s):

Heart Failure ◽

Warburg Effect ◽

Translational Regulation ◽

Hypertrophic Growth ◽

Metabolic Adaptations ◽

Mitochondrial Pyruvate Carrier ◽

Heart Failure Progression ◽

Mitochondrial Oxidation ◽

Human And Mouse ◽

The Warburg Effect

AbstractThe mitochondrial pyruvate carrier (MPC) is the entry point for the glycolytic end-product pyruvate to the mitochondria. MPC activity, which is controlled by its abundance and post-translational regulation, determines whether pyruvate is oxidised in the mitochondria or metabolised in the cytosol. MPC serves as a crucial metabolic branch point that determines the fate of pyruvate in the cell, enabling metabolic adaptations during health, such as exercise, or as a result of disease. Decreased MPC expression in several cancers limits the mitochondrial oxidation of pyruvate and contributes to lactate accumulation in the cytosol, highlighting its role as a contributing, causal mediator of the Warburg effect. Pyruvate is handled similarly in the failing heart where a large proportion of it is reduced to lactate in the cytosol instead of being fully oxidised in the mitochondria. Several recent studies have found that the MPC abundance was also reduced in failing human and mouse hearts that were characterised by maladaptive hypertrophic growth, emulating the anabolic scenario observed in some cancer cells. In this review we discuss the evidence implicating the MPC as an important, perhaps causal, mediator of heart failure progression.

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How N-Acetylcysteine Supplementation Affects Redox Regulation, Especially at Mitohormesis and Sarcohormesis Level: Current Perspective

Antioxidants ◽

10.3390/antiox10020153 ◽

2021 ◽

Vol 10 (2) ◽

pp. 153

Author(s):

Aslı Devrim-Lanpir ◽

Lee Hill ◽

Beat Knechtle

Keyword(s):

Oxidative Stress ◽

Oxidative Metabolism ◽

Adaptive Response ◽

Redox Regulation ◽

Therapeutic Agent ◽

Metabolic Effects ◽

Metabolic Adaptations ◽

Current Perspective ◽

Exercise Induced ◽

Response To Exercise

Exercise frequently alters the metabolic processes of oxidative metabolism in athletes, including exposure to extreme reactive oxygen species impairing exercise performance. Therefore, both researchers and athletes have been consistently investigating the possible strategies to improve metabolic adaptations to exercise-induced oxidative stress. N-acetylcysteine (NAC) has been applied as a therapeutic agent in treating many diseases in humans due to its precursory role in the production of hepatic glutathione, a natural antioxidant. Several studies have investigated NAC’s possible therapeutic role in oxidative metabolism and adaptive response to exercise in the athletic population. However, still conflicting questions regarding NAC supplementation need to be clarified. This narrative review aims to re-evaluate the metabolic effects of NAC on exercise-induced oxidative stress and adaptive response developed by athletes against the exercise, especially mitohormetic and sarcohormetic response.

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