scholarly journals Mechanisms of Energy Metabolism in Skeletal Muscle Mitochondria Following Radiation Exposure

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 950 ◽  
Author(s):  
Kim ◽  
Lee ◽  
Kim ◽  
Kim ◽  
Yi
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Ionizing Radiation ◽  
Radiation Exposure ◽  
Biological Effects ◽  
Mitochondrial Protein ◽  
Metabolic Effects ◽  
Acid Oxidation ◽  
Mitochondrial Energy Metabolism ◽  
Effects Of Radiation

An understanding of cellular processes that determine the response to ionizing radiation exposure is essential for improving radiotherapy and assessing risks to human health after accidental radiation exposure. Radiation exposure leads to many biological effects, but the mechanisms underlying the metabolic effects of radiation are not well known. Here, we investigated the effects of radiation exposure on the metabolic rate and mitochondrial bioenergetics in skeletal muscle. We show that ionizing radiation increased mitochondrial protein and mass and enhanced proton leak and mitochondrial maximal respiratory capacity, causing an increase in the fraction of mitochondrial respiration devoted to uncoupling reactions. Thus, mice and cells treated with radiation became energetically efficient and displayed increased fatty acid and amino acid oxidation metabolism through the citric acid cycle. Finally, we demonstrate that radiation-induced alterations in mitochondrial energy metabolism involved adenosine monophosphate-activated kinase signaling in skeletal muscle. Together, these results demonstrate that alterations in mitochondrial mass and function are important adaptive responses of skeletal muscle to radiation.

Responses of skeletal muscle lipid metabolism in rat gastrocnemius to hypothyroidism and iodothyronine administration: a putative role for FAT/CD36

2012 ◽  
Vol 303 (10) ◽  
pp. E1222-E1233 ◽  
Author(s):  
Assunta Lombardi ◽  
Rita De Matteis ◽  
Maria Moreno ◽  
Laura Napolitano ◽  
Rosa Anna Busiello ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipid Metabolism ◽  
Protein Level ◽  
Oxidation Rate ◽  
Mitochondrial Protein ◽  
Acid Oxidation ◽  
Mrna Levels ◽  
Muscle Lipid ◽  
Mitochondrial Fatty Acid ◽  
Skeletal Muscle Lipid

Iodothyronines such as triiodothyronine (T3) and 3,5-diiodothyronine (T2) influence energy expenditure and lipid metabolism. Skeletal muscle contributes significantly to energy homeostasis, and the above iodothyronines are known to act on this tissue. However, little is known about the cellular/molecular events underlying the effects of T3 and T2 on skeletal muscle lipid handling. Since FAT/CD36 is involved in the utilization of free fatty acids by skeletal muscle, specifically in their import into that tissue and presumably their oxidation at the mitochondrial level, we hypothesized that related changes in lipid handling and in FAT/CD36 expression and subcellular redistribution would occur due to hypothyroidism and to T3 or T2 administration to hypothyroid rats. In gastrocnemius muscles isolated from hypothyroid rats, FAT/CD36 was upregulated (mRNA levels and total tissue, sarcolemmal, and mitochondrial protein levels). Administration of either T3 or T2 to hypothyroid rats resulted in 1) little or no change in FAT/CD36 mRNA level, 2) a decreased total FAT/CD36 protein level, and 3) further increases in FAT/CD36 protein level in sarcolemma and mitochondria. Thus, the main effect of each iodothyronine seemed to be exerted at the level of FAT/CD36 cellular distribution. The effect of further increases in FAT/CD36 protein level in sarcolemma and mitochondria was already evident at 1 h after iodothyronine administration. Each iodothyronine increased the mitochondrial fatty acid oxidation rate. However, the mechanisms underlying their rapid effects seem to differ; T2 and T3 each induce FAT/CD36 translocation to mitochondria, but only T2 induces increases in carnitine palmitoyl transferase system activity and in the mitochondrial substrate oxidation rate.

scholarly journals Substrate oxidation in primary human skeletal muscle cells is influenced by donor age

2020 ◽  
Vol 382 (3) ◽  
pp. 599-608
Author(s):  
Vigdis Aas ◽  
G. Hege Thoresen ◽  
Arild C. Rustan ◽  
Jenny Lund
Keyword(s):  
Skeletal Muscle ◽  
Oleic Acid ◽  
Energy Metabolism ◽  
Substrate Oxidation ◽  
Pyruvate Dehydrogenase Kinase ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Donor Age ◽  
Human Myotubes ◽  
Human Skeletal Muscle Cells

AbstractPrimary human myotubes represent an alternative system to intact skeletal muscle for the study of human diseases related to changes in muscle energy metabolism. This work aimed to study if fatty acid and glucose metabolism in human myotubes in vitro were related to muscle of origin, donor gender, age, or body mass index (BMI). Myotubes from a total of 82 donors were established from three different skeletal muscles, i.e., musculus vastus lateralis, musculus obliquus internus abdominis, and musculi interspinales, and cellular energy metabolism was evaluated. Multiple linear regression analyses showed that donor age had a significant effect on glucose and oleic acid oxidation after correcting for gender, BMI, and muscle of origin. Donor BMI was the only significant contributor to cellular oleic acid uptake, whereas cellular glucose uptake did not rely on any of the variables examined. Despite the effect of age on substrate oxidation, cellular mRNA expression of pyruvate dehydrogenase kinase 4 (PDK4) and peroxisome proliferator–activated receptor gamma coactivator 1 alpha (PPARGC1A) did not correlate with donor age. In conclusion, donor age significantly impacts substrate oxidation in cultured human myotubes, whereas donor BMI affects cellular oleic acid uptake.

Abstract 13921: Targeting Receptor-Interacting Protein 140 to Modulate Energy Metabolism in the Failing Heart

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Tsunehisa Yamamoto ◽  
Elizabeth Pruzinsky ◽  
Kirill Batmanov ◽  
Daniel P Kelly
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Interacting Protein ◽  
Failing Heart ◽  
Metabolic Genes ◽  
Cardiac Energy

The nuclear receptors, peroxisome proliferator-activated receptors (PPARs), estrogen-related receptors (ERRs), and their co-regulator PPARγ coactivator-1α (PGC-1α), control postnatal cardiac mitochondrial biogenesis and energy metabolism. During the development of heart failure (HF), the activity of PGC-1/PPAR/ERR is reduced resulting in diminished capacity for fatty acid oxidation (FAO) and ATP production potentially contributing to an “energy-starved” state that contributes to progression of HF. Receptor-Interacting protein 140 (RIP140) serves as a co-repressor of PGC-1/PPAR/ERR in skeletal muscle and adipose tissue. We hypothesized that RIP140 represses cardiac energy metabolism in the normal and failing heart. Accordingly, we targeted Nrip1 (encoding RIP140) using a muscle creatinine kinase (MCK)-driven Cre recombinase to generate striated muscle-specific RIP140 knockout (msRIP140 KO) mice. msRIP140 KO mice appeared normal at baseline with no difference in survival or cardiac systolic function compared to littermate controls. RNA-sequence analysis demonstrated that the expression of genes involved in a wide array of mitochondrial energy metabolic pathways including FAO, tricarboxylic acid (TCA) cycle, oxidative phosphorylation (OXPHOS), and branched-chain amino acid (BCAA) degradation pathways were upregulated in msRIP140 KO ventricles, and in msRIP140 KO skeletal muscle. msRIP140 KO mice exhibited significantly less cardiac hypertrophy and diastolic dysfunction in response to chronic pressure overload. Next, cardiac-specific (cs) RIP140 KO mice were generated and subjected to transverse aortic constriction/apical myocardial infarction surgery (TAC/MI), an established HF model. csRIP140 KO mice exhibited less cardiac remodeling and systolic dysfunction compared to littermate controls, along with less downregulation of metabolic genes and induction of cardiac stress ( Nppa and Nppb ) and fibrosis response markers ( Tgfb2 and Col3a1 ). We conclude that RIP140 serves as a global co-repressor of cardiac energy metabolic genes in the adult heart and that modulation of RIP140 activity could prove to be a novel therapeutic approach for HF.

Studi Paparan Radiasi pada Pekerja Radiasi Cathlab dengan Menggunakan My Dose Mini sebagai Upaya Keselamatan Radiasi di RSUP Adam Malik Medan

2021 ◽  
Vol 1 (1) ◽  
pp. 41-46
Author(s):  
Martua Damanik ◽  
◽  
Josepa ND Simanjuntak ◽  
Elvita Rahmi Daulay
Keyword(s):  
Radiation Exposure ◽  
Biological Effects ◽  
Exposure Dose ◽  
Radiological Protection ◽  
Safe Level ◽  
Radiation Sources ◽  
Radiation Worker ◽  
Radiation Workers ◽  
Effects Of Radiation ◽  
Radiation Exposure Dose

Cathlab radiation workers, when performing interventional procedures, are at high risk of the effects of radiation exposure. The risk of radiation exposure is deterministic and stochastic biological effects. Therefore, radiation exposure studies of radiation workers at the cath lab were conducted to determine the value of radiation exposure received. This radiation exposure study was conducted by measuring and recording radiation exposure doses received by radiation workers. Measurements are made when the radiation officer performs the intervention procedure. The research was carried out for one month in the cath lab room of the Adam Malik General Hospital, Medan. The modalities used are GE Medical System Interventional Fluoroscopy and Phillips Allura Xper FD20. The dosimeter used is “my dose mini”, which is placed inside a shield or apron worn by radiation workers. The size of the apron shield used is 0.50 mm Pb at the front and 0.25 mm Pb at the rear. Radiation officers whose radiation exposure dose was measured consisted of 10 doctors, 11 nurses, and one radiographer. Each inspection procedure of each radiation worker has a different distance, time, and shield from the radiation source. The measurement of radiation exposure dose is (1-59 μSv) for doctors, (1-58 μSv) for nurses, and 1 μSv for radiographers. To protect against radiation must pay attention to the factors of time, distance, and shielding. Ways that can do are to avoid being close to radiation sources for too long, keep a space at a safe level from radiation, and use shields such as Pb-coated aprons, use Pb gloves, Pb goggles, and thyroid protectors. The amount of radiation exposure dose received by each radiation worker at the time of measurement is still within the tolerance limit. The Nuclear Energy Regulatory Agency (BAPETEN) regulation, which the International Commission recommends on Radiological Protection (ICRP), is 20 mSv/year. The results of this study are expected to be used as input for improving the quality of service for monitoring radiation exposure doses in the Cathlab and as reference material for further research.

scholarly journals Comparison of the Effects of Cyclosporin a on the Metabolism of Perfused Rat Brain Slices during Normoxia and Hypoxia

2002 ◽  
Vol 22 (3) ◽  
pp. 342-352 ◽  
Author(s):  
Natalie Serkova ◽  
Paul Donohoe ◽  
Sven Gottschalk ◽  
Carsten Hainz ◽  
Claus U. Niemann ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cyclosporin A ◽  
Rat Brain ◽  
Ex Vivo ◽  
Brain Slices ◽  
High Energy ◽  
Metabolic Effects ◽  
Resonance Spectroscopy ◽  
Buffer Solution ◽  
Mitochondrial Energy Metabolism

The authors evaluated and compared the metabolic effects of cyclosporin A in the rat brain during normoxia and hypoxia/reperfusion. Ex vivo31P magnetic resonance spectroscopy experiments based on perfused rat brain slices showed that under normoxic conditions, 500 μg/L cyclosporin A significantly reduced mitochondrial energy metabolism (nucleotide triphosphate, 83 ± 9% of controls; phosphocreatine, 69 ± 9%) by inhibition of the Krebs cycle (glutamate, 77 ± 5%) and oxidative phosphorylation (NAD+, 65 ± 14%) associated with an increased generation of reactive oxygen species (285 ± 78% of control). However, the same cyclosporin A concentration (500 μg/L) was found to be the most efficient concentration to inhibit the hypoxia-induced mitochondrial release of Ca2+ in primary rat hippocampal cells with cytosolic Ca2+ concentrations not significantly different from normoxic controls. Addition of 500 μg/L cyclosporin A to the perfusion medium protected high-energy phosphate metabolism (nucleotide triphosphate, 11 ± 15% of control vs. 35 ± 9% with 500 μg/L cyclosporin A) and the intracellular pH (6.2 ± 0.1 control vs. 6.6 ± 0.1 with cyclosporin A) in rat brain slices during 30 minutes of hypoxia. Results indicate that cyclosporin A simultaneously decreases and protects cell glucose and energy metabolism. Whether the overall effect was a reduction or protection of cell energy metabolism depended on the concentrations of both oxygen and cyclosporin A in the buffer solution.

3,5-Diiodo-l-thyronine rapidly enhances mitochondrial fatty acid oxidation rate and thermogenesis in rat skeletal muscle: AMP-activated protein kinase involvement

2009 ◽  
Vol 296 (3) ◽  
pp. E497-E502 ◽  
Author(s):  
A. Lombardi ◽  
P. de Lange ◽  
E. Silvestri ◽  
R. A. Busiello ◽  
A. Lanni ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Energy Metabolism ◽  
Fatty Acid Oxidation ◽  
Atp Synthesis ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Mitochondrial Fatty Acid ◽  
Amp Activated Protein Kinase

Triiodothyronine regulates energy metabolism and thermogenesis. Among triiodothyronine derivatives, 3,5-diiodo-l-thyronine (T2) has been shown to exert marked effects on energy metabolism by acting mainly at the mitochondrial level. Here we investigated the capacity of T2 to affect both skeletal muscle mitochondrial substrate oxidation and thermogenesis within 1 h after its injection into hypothyroid rats. Administration of T2 induced an increase in mitochondrial oxidation when palmitoyl-CoA (+104%), palmitoylcarnitine (+80%), or succinate (+30%) was used as substrate, but it had no effect when pyruvate was used. T2 was able to 1) activate the AMPK-ACC-malonyl-CoA metabolic signaling pathway known to direct lipid partitioning toward oxidation and 2) increase the importing of fatty acids into the mitochondrion. These results suggest that T2 stimulates mitochondrial fatty acid oxidation by activating several metabolic pathways, such as the fatty acid import/β-oxidation cycle/FADH2-linked respiratory pathways, where fatty acids are imported. T2 also enhanced skeletal muscle mitochondrial thermogenesis by activating pathways involved in the dissipation of the proton-motive force not associated with ATP synthesis (“proton leak”), the effect being dependent on the presence of free fatty acids inside mitochondria. We conclude that skeletal muscle is a target for T2, and we propose that, by activating processes able to enhance mitochondrial fatty acid oxidation and thermogenesis, T2 could play a role in protecting skeletal muscle against excessive intramyocellular lipid storage, possibly allowing it to avoid functional disorders.

Results of the 66-th Session of the United Nations Scientific Committee on the Effects of the Atomic Radiation (UNSCEAR) (Vienna, 10–14 June, 2019)

2019 ◽  
Vol 64 (5) ◽  
pp. 81-88
Author(s):  
В. Уйба ◽  
V. Uyba ◽  
А. Аклеев ◽  
A. Akleev ◽  
Т. Азизова ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Radiation Exposure ◽  
Nuclear Power ◽  
Occupational Exposures ◽  
Epidemiological Studies ◽  
Future Research ◽  
Second Primary ◽  
Cancer Risks ◽  
Low Dose Radiation ◽  
Effects Of Radiation

The current paper is devoted to the outcomes of the 66-th UNSCEAR Session which took place in Vienna during 10–14 June 2018. Within the framework of the meetings of the Working Group and subgroups the documents on the following projects were discussed: R.733. Evaluation of selected health effects and inference of risk due to radiation exposure. R.734. Evaluation of medical exposures to ionizing radiation. R.735. Evaluation of occupational exposures to ionizing radiation. R.736. Lung cancer from exposure to radon. R.737. Biological mechanisms relevant for the inference of cancer risks from low-dose radiation. R.738. Levels and effects of radiation exposure due to the accident at the Fukushima Daiichi nuclear power station: implications of information published since the 2013 UNSCEAR report. R.739. Second primary cancer after radiotherapy. R.740. Epidemiological studies of radiation and cancer. The Committee also discussed: the future research program; report to the UN General Assembly; implementation of a strategy plan to improve collection, analysis and dissemination of data on radiation exposure; public outreach activity including the strategy for the period 2020–2024.

Results of the 65th Session of the United Nations Scientific Committee on the Effects of the Atomic Radiation (UNSCEAR) (Vienna, 11–14 June, 2018)

2018 ◽  
pp. 77-88
Author(s):  
В. Уйба ◽  
V. Uyba ◽  
А. Аклеев ◽  
A. Akleev ◽  
Т. Азизова ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Radiation Exposure ◽  
Health Effects ◽  
Future Research ◽  
Low Dose Radiation ◽  
Cancer Data ◽  
Organizational Issues ◽  
Working Groups ◽  
Effects Of Radiation ◽  
Dose Radiation

Current paper is devoted to the main outcomes of the 64th UNSCEAR Session which took place in Vienna during 10 – 14 June 2018. Within the framework of the meetings of the working group and subgroups the documents on the following projects were discussed: - Biological mechanisms influencing health effects from low-dose radiation exposure. - Developments since the 2013 UNSCEAR report on the levels and effects of radiation exposure due to the nuclear accident following the great East-Japan earthquake and tsunami: review of 2016 scientific literature including an evaluation of thyroid cancer data in regions affected by the Chernobyl accident. - Exposure of patients to ionizing radiation. - Exposure of workers to ionizing radiation. - Selected evaluations of health effects and of risk inference due to radiation exposure. - Lung cancer from exposure to radon and to penetrating radiation. In the course of the discussion, some organizational issues such as preparation of UNSCEAR publications, feasibility of establishing standing working groups, public outreach activities, future research program, report to the General Assembly etc., were considered.

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