scholarly journals A comparison of chronic AICAR treatment-induced metabolic adaptations in red and white muscles of rats

2014 ◽  
Vol 65 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Masataka Suwa ◽  
Hiroshi Nakano ◽  
Zsolt Radak ◽  
Shuzo Kumagai
2019 ◽  
Vol 89 (1-2) ◽  
pp. 80-88 ◽  
Author(s):  
Juliana Soares Severo ◽  
Jennifer Beatriz Silva Morais ◽  
Taynáh Emannuelle Coelho de Freitas ◽  
Ana Letícia Pereira Andrade ◽  
Mayara Monte Feitosa ◽  
...  

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.


Author(s):  
Mariana Fernandez-Caggiano ◽  
Philip Eaton

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.


Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 153
Author(s):  
Aslı Devrim-Lanpir ◽  
Lee Hill ◽  
Beat Knechtle

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.


1959 ◽  
Vol 234 (6) ◽  
pp. 1350-1354
Author(s):  
R.A. Freedland ◽  
A.E. Harper

1964 ◽  
Vol 239 (4) ◽  
pp. 1156-1163 ◽  
Author(s):  
J.E. Wergedal ◽  
A.E. Harper

Science ◽  
1967 ◽  
Vol 157 (3785) ◽  
pp. 199-199 ◽  
Author(s):  
A. W. Sexton ◽  
J. W. Gersten

2008 ◽  
Vol 586 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Kirsten A. Burgomaster ◽  
Krista R. Howarth ◽  
Stuart M. Phillips ◽  
Mark Rakobowchuk ◽  
Maureen J. MacDonald ◽  
...  

1972 ◽  
Vol 57 (2) ◽  
pp. 551-567
Author(s):  
T. YAMAMOTO

1. Electrical and mechanical properties of the red muscle (M. levator pinnae pectoralis) and white muscle (M. levator pinnae lateralis abdominis) in the silver carp (Carassius auratus Linné) were investigated by using caffeine and thymol. 2. A complete tetanus could be produced in the red muscle. But in the white muscle no tetanus was produced and there was a gradual decrease in tension during continuous stimulation, even at a frequency of 1 c/s or less. 3. Caffeine (0.5-1 mM) and thymol (0.25-0.5 mM) potentiated the twitch tension in both muscles without an increase in the resting tension; they produced a contracture in both muscles when the concentration was increased further. 4. The falling phase of the active state of contraction was nearly the same in both muscles and was prolonged by caffeine (0.5 mmM) and by thymol (0.25 mM). 5. The resting membrane potential of the red muscle was scarcely affected by caffeine (0.5-5 mM), whereas in the white muscles a depolarization of 10 mV was observed with caffeine of more than 2 mM. The resting potential of both muscles was little changed by o.25 mm thymol. However, at a concentration of more than 0.5mM thymol depolarized the membrane in both muscles to the same extent. 6. In caffeine (2-3 mM) solution the mean specific membrane resistance was reduced from 8.8 kΩ cm2 to 6.0 kΩ cm2 in the red muscle, and from 5.0 kΩ cm2 to 2.7 kΩ cm2 in the white muscle. In thymol (0.5-1 mM) solution it was reduced from 11.2 kΩcm2 to 6.5 kΩ cm2 in the red muscle, and from 5.4kΩ cm2 to 3.1 kΩ) cm2 in the white muscle. The specific membrane capacitance, calculated from the time constant and the membrane resistance, remained more or less the same in both muscles after a treatment with these agents. 7. Electrical properties of the muscles and the effects of caffeine and thymol on mechanical responses suggest that there are no fundamental differences between red and white muscles except for the excitation-contraction coupling. A lack of summation of twitch, a successive decline of twitch, and inability to produce potassium contracture in the white muscle may be due to the fact that the Ca-releasing mechanism is easily inactivated by depolarization of the membrane.


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