scholarly journals The Effect of Different Programs of Exercise on The Expression of Genes Associated with Endurance and Energy Metabolism

2021 ◽  
pp. 482-490
Author(s):  
Neşe AKPINAR KOCAKULAK ◽  
Serpil TAHERİ ◽  
Elif Funda ŞENER ◽  
Kenan AYCAN ◽  
Yusuf ÖZKUL
Author(s):  
Ramesh Gogulothu ◽  
Devika Nagar ◽  
Srividya Gopalakrishnan ◽  
Venkat R. Garlapati ◽  
Prathap R. Kallamadi ◽  
...  

2019 ◽  
Vol 41 ◽  
pp. e42709
Author(s):  
Gabriele Casarotto ◽  
Tiago Edu Kaspary ◽  
Luan Cutti ◽  
André Luis Thomas ◽  
Jose Fernandes Barbosa Neto

The flooded environment brings about injuries to soybeans that vary depending on the adaptation ability of the genotype. Oxygen deprivation promotes the induction of the expression of genes related to glycolysis and fermentation pathways to maintain energy metabolism and, in addition to reducing-power consuming processes, act in the formation of adaptive structures and the maintenance of the redox status of the plant. The aim of this work was to evaluate the relative expression of genes related to soil flooding response in two contrasting soybean cultivars. Soybean plants of the sensitive (BRS 154) and tolerant (I27) cultivars at the V1 development stage were submitted to the flooding and control conditions (without flooding) for 0, 24, 48, and 96 hours. The relative expression of genes associated with flooding, including enolase (ENO), alcohol dehydrogenase 1 (ADH1), alanine aminotransferase 2 (ALAT2), hemoglobin 1 (GLB1), LOB41 domain-containing protein (LBD41), xyloglucan endotransglycosylase (XETP) and ascorbate peroxidase (APX2), was evaluated by means of RT-qPCR. The relative expression, in general, increased with flooding, especially in the root tissue. Cultivar I27 responded positively as observed by the expression of the maintenance genes of energy metabolism, structural changes and detoxification, suggesting the presence of three tolerance mechanisms in the flooding response.


PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-10 ◽  
Author(s):  
Jennifer G. Duncan ◽  
Brian N. Finck

The mammalian myocardium is an omnivorous organ that relies on multiple substrates in order to fulfill its tremendous energy demands. Cardiac energy metabolism preference is regulated at several critical points, including at the level of gene transcription. Emerging evidence indicates that the nuclear receptor PPARαand its cardiac-enriched coactivator protein, PGC-1α, play important roles in the transcriptional control of myocardial energy metabolism. The PPARα-PGC-1αcomplex controls the expression of genes encoding enzymes involved in cardiac fatty acid and glucose metabolism as well as mitochondrial biogenesis. Also, evidence has emerged that the activity of the PPARα-PGC-1αcomplex is perturbed in several pathophysiologic conditions and that altered activity of this pathway may play a role in cardiomyopathic remodeling. In this review, we detail the current understanding of the effects of the PPARα-PGC-1αaxis in regulating mitochondrial energy metabolism and cardiac function in response to physiologic and pathophysiologic stimuli.


2021 ◽  
Author(s):  
Tian-Ran Zhou ◽  
Cagla Cömert ◽  
Xiaoyu Zhou ◽  
Lin Lin ◽  
Lars Bolund ◽  
...  

Mitochondrial dysfunction plays a critical role in metabolic associated fatty liver disease (MAFLD). This study aims to characterize mitochondrial dysfunctions in a human MAFLD Huh7 cell model triggered by free fatty acid (FFA) (palmitate and oleate) overload for 24 hours. We investigate its impact on cellular energy metabolism and identify potential targets for MAFLD treatment. FFA-treated cells displayed an accumulation of lipid droplets and slightly decreased viability but no significant changes in mitochondrial superoxide levels. Bioenergetic analysis showed a shift to more respiration and less glycolytic fermentation. Comprehensive transcriptomics and proteomics analyses identified changes in the expression of genes prominently involved in fatty acid handling and metabolism. The expressions of seven genes were consistently and significantly (p<0.05) altered (4 upregulated and 3 downregulated genes) in both proteomics and transcriptomics. The FFA-treated Huh7 cell model is an appropriate in vitro model to study fatty acid metabolism and suitable to investigate the role of mitochondria, glycolysis, and multiple metabolic pathways in MAFLD. Our comprehensive analyses form a basis for drug discovery and screening using this model.


2002 ◽  
Vol 22 (1) ◽  
pp. 17-32 ◽  
Author(s):  
Fernando Goglia ◽  
Elena Silvestri ◽  
Antonia Lanni

Because of their central role in the regulation of energy-transduction, mitochondria, the major site of oxidative processes within the cell, are considered a likely subcellular target for the action that thyroid hormones exert on energy metabolism. However, the mechanism underlying the regulation of basal metabolic rate (BMR) by thyroid hormones still remains unclear. It has been suggested that these hormones might uncouple substrate oxidation from ATP synthesis, but there are no clear-cut data to support this idea. Two iodothyronines have been identified as effectors of the actions of thyroid hormones on energy metabolism: 3',3,5-triiodo-L-thyronine (T3) and 3,5-diiodo-L-thyronine (T2). Both have significant effects on BMR, but their mechanisms of action are not identical. T3 acts on the nucleus to influence the expression of genes involved in the regulation of cellular metabolism and mitochondria function; 3,5-T2, on the other hand, acts by directly influencing the mitochondrial energy-transduction apparatus. A molecular determinant of the effects of T3 could be uncoupling protein-3 (UCP-3), while the cytochrome-c oxidase complex is a possible target for 3,5-T2. In conclusion, it is likely that iodothyronines regulate energy metabolism by both short-term and long-term mechanisms, and that they act in more than one way in affecting mitochondrial functions.


Reproduction ◽  
2013 ◽  
Vol 145 (1) ◽  
pp. 33-44 ◽  
Author(s):  
V Van Hoeck ◽  
J L M R Leroy ◽  
M Arias Alvarez ◽  
D Rizos ◽  
A Gutierrez-Adan ◽  
...  

Elevated plasma nonesterified fatty acid (NEFA) concentrations are associated with negative energy balance and metabolic disorders such as obesity and type II diabetes. Such increased plasma NEFA concentrations induce changes in the microenvironment of the ovarian follicle, which can compromise oocyte competence. Exposing oocytes to elevated NEFA concentrations during maturation affects the gene expression and phenotype of the subsequent embryo, notably prompting a disrupted oxidative metabolism. We hypothesized that these changes in the embryo are a consequence of modified energy metabolism in the oocyte. To investigate this, bovine cumulus oocyte complexes were matured under elevated NEFA conditions, and energy metabolism-related gene expression, mitochondrial function, and ultrastructure evaluated. It was found that expression of genes related to REDOX maintenance was modified in NEFA-exposed oocytes, cumulus cells, and resultant blastocysts. Moreover, the expression of genes related to fatty acid synthesis in embryos that developed from NEFA-exposed oocytes was upregulated. From a functional perspective, inhibition of fatty acid β-oxidation in maturing oocytes exposed to elevated NEFA concentrations restored developmental competence. There were no clear differences in mitochondrial morphology or oxygen consumption between treatments, although there was a trend for a higher mitochondrial membrane potential in zygotes derived from NEFA-exposed oocytes. These data show that the degree of mitochondrial fatty acid β-oxidation has a decisive impact on the development of NEFA-exposed oocytes. Furthermore, the gene expression data suggest that the resulting embryos adapt through altered metabolic strategies, which might explain the aberrant energy metabolism previously observed in these embryos originating from NEFA-exposed maturing oocytes.


Endocrinology ◽  
2010 ◽  
Vol 151 (9) ◽  
pp. 4594-4594 ◽  
Author(s):  
Vincent Bombail ◽  
Douglas Gibson ◽  
Frances Collins ◽  
Sheila MacPherson ◽  
Hilary O. D. Critchley ◽  
...  

This article appears in The Journal of Clinical Endocrinology & Metabolism. 10.1210/jc.2010-0154


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