scholarly journals Correction: PHEX Mimetic (SPR4-Peptide) Corrects and Improves HYP and Wild Type Mice Energy-Metabolism

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e101192
Author(s):  
Keyword(s):  
Energy Metabolism ◽  
Wild Type

TRPV4 deficiency increases skeletal muscle metabolic capacity and resistance against diet-induced obesity

2012 ◽  
Vol 112 (7) ◽  
pp. 1223-1232 ◽  
Author(s):  
Tatsuya Kusudo ◽  
Zhonghua Wang ◽  
Atsuko Mizuno ◽  
Makoto Suzuki ◽  
Hitoshi Yamashita
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Transient Receptor Potential ◽  
Thermal Sensation ◽  
Chow Diet ◽  
Type I ◽  
Wild Type ◽  
Diet Induced Obesity ◽  
Obesity In Mice

Transient receptor potential channel V4 (TRPV4) functions as a nonselective cation channel in various cells and plays physiological roles in osmotic and thermal sensation. However, the function of TRPV4 in energy metabolism is unknown. Here, we report that TRPV4 deficiency results in increased muscle oxidative capacity and resistance to diet-induced obesity in mice. Although no difference in body weight was observed between wild-type and Trpv4−/− mice when fed a standard chow diet, obesity phenotypes induced by a high-fat diet were significantly improved in Trpv4−/− mice, without any change in food intake. Quantitative analysis of mRNA revealed the constitutive upregulation of many genes, including those for transcription factors such as peroxisome proliferator-activated receptor α and for metabolic enzymes such as phosphoenolpyruvate carboxykinase. These upregulated genes were especially prominent in oxidative skeletal muscle, in which the activity of Ca2+-dependent phosphatase calcineurin was elevated, suggesting that other Ca2+ channels function in the skeletal muscle of Trpv4−/− mice. Indeed, gene expressions for TRPC3 and TRPC6 increased in the muscles of Trpv4−/− mice compared with those of wild-type mice. The number of oxidative type I fiber also increased in the mutant muscles following myogenin gene induction. These results strongly suggested that inactivation of Trpv4 induces compensatory increases in TRPC3 and TRPC6 production, and elevation of calcineurin activity, affecting energy metabolism through increased expression of genes involved in fuel oxidation in skeletal muscle and thereby contributing to increased energy expenditure and protection from diet-induced obesity in mice.

scholarly journals OR-035 Effect of Aerobic Training on the Exercise Capacity of Apelin Knock-out Mice

2018 ◽  
Vol 1 (2) ◽  
Author(s):  
Lu Yan ◽  
Tieying Li ◽  
Ying Zhang
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Oxygen Uptake ◽  
Exercise Capacity ◽  
Aerobic Training ◽  
Movement Time ◽  
Wild Type ◽  
Running Speed ◽  
Knock Out ◽  
Knock Out Mice

Objective Aerobic training is considered to be an effective way to enhance the body’s exercise capacity which is closely related to the improvement of skeletal muscle energy metabolism. And as a new myokine, apelin has been found to play a key role in regulating the energy metabolism of skeletal muscle. However, whether the loss of apelin gene affects exercise capacity and what role aerobic training play in it remains unknown. This study was designed to investigate the effect of apelin on exercise capacity during aerobic training and to provide a theoretical basis for the mechanism of aerobic exercise affecting exercise capacity. Methods Male C57BL/6J wild type mouse(n=20) and apelin knock-out mouse(n=20) were assigned by random allocation to four groups(n=10): wild type control(WC), wild type exercised(WE), apelin knock-out control(KC) and apelin knock-out exercised(KE). Exercise training consisted of treadmill running 60 minutes/day ×6 days/week for 4 weeks. The training intensity corresponded to the 70-75% maximum oxygen uptake of mice. The running speed was 15m/min with an incline of +5° in the first 2 weeks and subsequently adjusted to 20m/min according to the maximum oxygen uptake in the last 2 weeks. On the day after training, all groups were forced to perform a incremental exercise test to exhaustion. This test was started with an incline of +5°and a speed of 10 m/min for 5 min. After this initial phase, the speed was progressively increased by 3m/min every 3 min until animal exhausted. The maximum running speed, movement time and distance were recorded during the test. Results Compared with group WC, the maximum running speed, movement time and distance of group KC were significantly decreased(P<0.01). And the maximum running speed, movement time and distance of group KE were clearly higher than those of group KC(P<0.01). There is no significant difference between group WE and group WC, and between group KE and group WE. Conclusions The exercise capacity of mice was significantly decreased because of knocking out the apelin gene, and the exercise ability of apelin knock-out mice can be clearly enhanced by aerobic training.

scholarly journals Two Nucleoporin98 homologous genes jointly participate in the regulation of starch degradation to repress senescence in Arabidopsis

2020 ◽  
Author(s):  
Long Xiao ◽  
Shanshan Jiang ◽  
Penghui Huang ◽  
Fulu Chen ◽  
Xu Wang ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Nuclear Pore Complex ◽  
Growth And Development ◽  
Double Mutant ◽  
Growth Regulation ◽  
Sugar Metabolism ◽  
Starch Degradation ◽  
Marker Genes ◽  
Nuclear Pore ◽  
Wild Type

Abstract Background: Starch is synthesized during the day for temporary storage in leaves and then degraded during the subsequent night to support plant growth and development. Impairment of starch degradation leads to stunted growth, even senescence and death. The nuclear pore complex is involved in many cellular processes, but its relationship with starch degradation is unclear until now. We previously identified that two Nucleoporin98 (Nup98) genes (Nup98a and Nup98b) redundantly regulate flowering through CONSTANS (CO) independent pathway in Arabidopsis thaliana. The nup98a-1 nup98b-1 double mutant also shows severe senescence phenotypes. Results: We find that Nucleoporin 98 (Nup98) participates in the regulation of sugar metabolism in leaves and in turn involves in senescence regulation in Arabidopsis. We show that Nup98a and Nup98b redundantly function in the different steps of starch degradation and the nup98a-1 nup98b-1 double mutant accumulates more starch than wild type plants and has a severe early senescence phenotype compared to wild type plants. The expression of marker genes related to starch degradation is impaired in the nup98a-1 nup98b-1 double mutant, and marker genes of carbon starvation and senescence express earlier and in higher abundance in the nup98a-1 nup98b-1 double mutant than in wild type plants, suggesting that abnormality of energy metabolism is the main cause of senescence of the nup98a-1 nup98b-1 double mutant. Addition of sucrose to the growth medium rescues early senescence phenotypes of the nup98a-1 nup98b-1 mutant. Conclusions: Our results provide a line of evidence on a novel role of the nuclear pore complex in energy metabolism related to growth and development, in which Nup98 functions in starch degradation conferring growth regulation in Arabidopsis.

scholarly journals Maternal Ghrelin Deficiency Compromises Reproduction in Female Progeny through Altered Uterine Developmental Programming

Endocrinology ◽  
2011 ◽  
Vol 152 (5) ◽  
pp. 2060-2066 ◽  
Author(s):  
J. Ryan Martin ◽  
Sarah B. Lieber ◽  
James McGrath ◽  
Marya Shanabrough ◽  
Tamas L. Horvath ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Reproductive Tract ◽  
Embryo Implantation ◽  
Developmental Programming ◽  
In Utero ◽  
In Utero Exposure ◽  
Corpora Lutea ◽  
Wild Type ◽  
Female Progeny ◽  
Endometrial Proliferation

Ghrelin has a well-known role in the regulation of appetite, satiety, energy metabolism, and reproduction; however ghrelin has not been implicated in reproductive tract development. We examined the effect of ghrelin deficiency on the developmental programming of female fertility. We observed that female wild-type mice born of ghrelin heterozygote dams (i.e. exposed in utero to ghrelin deficiency) had diminished fertility and produced smaller litters. We demonstrate that exposure to in utero ghrelin deficiency led to altered developmental programming of the reproductive tract. The number of ovarian follicles, corpora lutea, and embryos produced were identical in both exposed and unexposed mice. However wild-type embryos transferred to uteri of mice exposed to in utero ghrelin deficiency had a 60% reduction in the rate of embryo implantation compared with those transferred to wild-type unexposed uteri. We identified significant alterations in the uterine expression of four genes critical for implantation and a defect in uterine endometrial proliferation. Taken together, these results demonstrate that the mechanism of subfertility was abnormal endometrial function. In utero exposure to decreased levels of ghrelin led to defects in developmental programming of the uterus and subsequent subfertility in wild-type offspring.

scholarly journals REDUCED CHLOROPLAST COVERAGE genes from Arabidopsis thaliana help to establish the size of the chloroplast compartment

2016 ◽  
Vol 113 (8) ◽  
pp. E1116-E1125 ◽  
Author(s):  
Robert M. Larkin ◽  
Giovanni Stefano ◽  
Michael E. Ruckle ◽  
Andrea K. Stavoe ◽  
Christopher A. Sinkler ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Energy Metabolism ◽  
Gene Family ◽  
Unknown Function ◽  
Cell Expansion ◽  
Mutant Allele ◽  
Eukaryotic Cells ◽  
Wild Type ◽  
Photosynthetic Organisms ◽  
Cellular Volume

Eukaryotic cells require mechanisms to establish the proportion of cellular volume devoted to particular organelles. These mechanisms are poorly understood. From a screen for plastid-to-nucleus signaling mutants in Arabidopsis thaliana, we cloned a mutant allele of a gene that encodes a protein of unknown function that is homologous to two other Arabidopsis genes of unknown function and to FRIENDLY, which was previously shown to promote the normal distribution of mitochondria in Arabidopsis. In contrast to FRIENDLY, these three homologs of FRIENDLY are found only in photosynthetic organisms. Based on these data, we proposed that FRIENDLY expanded into a small gene family to help regulate the energy metabolism of cells that contain both mitochondria and chloroplasts. Indeed, we found that knocking out these genes caused a number of chloroplast phenotypes, including a reduction in the proportion of cellular volume devoted to chloroplasts to 50% of wild type. Thus, we refer to these genes as REDUCED CHLOROPLAST COVERAGE (REC). The size of the chloroplast compartment was reduced most in rec1 mutants. The REC1 protein accumulated in the cytosol and the nucleus. REC1 was excluded from the nucleus when plants were treated with amitrole, which inhibits cell expansion and chloroplast function. We conclude that REC1 is an extraplastidic protein that helps to establish the size of the chloroplast compartment, and that signals derived from cell expansion or chloroplasts may regulate REC1.

scholarly journals Gene Expression Analysis of Energy Metabolism Mutants of Desulfovibrio vulgaris Hildenborough Indicates an Important Role for Alcohol Dehydrogenase

2003 ◽  
Vol 185 (15) ◽  
pp. 4345-4353 ◽  
Author(s):  
Shelley A. Haveman ◽  
Véronique Brunelle ◽  
Johanna K. Voordouw ◽  
Gerrit Voordouw ◽  
John F. Heidelberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Energy Metabolism ◽  
Carbon Source ◽  
Alcohol Dehydrogenase ◽  
Sulfate Reduction ◽  
Electron Donor ◽  
Desulfovibrio Vulgaris ◽  
Wild Type ◽  
Reading Frame ◽  
Metabolic Conditions

ABSTRACT Comparison of the proteomes of the wild-type and Fe-only hydrogenase mutant strains of Desulfovibrio vulgaris Hildenborough, grown in lactate-sulfate (LS) medium, indicated the near absence of open reading frame 2977 (ORF2977)-coded alcohol dehydrogenase in the hyd mutant. Hybridization of labeled cDNA to a macroarray of 145 PCR-amplified D. vulgaris genes encoding proteins active in energy metabolism indicated that the adh gene was among the most highly expressed in wild-type cells grown in LS medium. Relative to the wild type, expression of the adh gene was strongly downregulated in the hyd mutant, in agreement with the proteomic data. Expression was upregulated in ethanol-grown wild-type cells. An adh mutant was constructed and found to be incapable of growth in media in which ethanol was both the carbon source and electron donor for sulfate reduction or was only the carbon source, with hydrogen serving as electron donor. The hyd mutant also grew poorly on ethanol, in agreement with its low level of adh gene expression. The adh mutant grew to a lower final cell density on LS medium than the wild type. These results, as well as the high level of expression of adh in wild-type cells on media in which lactate, pyruvate, formate, or hydrogen served as the sole electron donor for sulfate reduction, indicate that ORF2977 Adh contributes to the energy metabolism of D. vulgaris under a wide variety of metabolic conditions. A hydrogen cycling mechanism is proposed in which protons and electrons originating from cytoplasmic ethanol oxidation by ORF2977 Adh are converted to hydrogen or hydrogen equivalents, possibly by a putative H2-heterodisulfide oxidoreductase complex, which is then oxidized by periplasmic Fe-only hydrogenase to generate a proton gradient.

scholarly journals Thioredoxin-deficient mice, a novel phenotype sensitive to ambient air and hypersensitive to hyperoxia-induced lung injury

2015 ◽  
Vol 308 (5) ◽  
pp. L429-L442 ◽  
Author(s):  
Kumuda C. Das
Keyword(s):  
Energy Metabolism ◽  
Lung Injury ◽  
Nadh Dehydrogenase ◽  
Oxygen Toxicity ◽  
Ambient Air ◽  
Genotoxic Stress ◽  
Clinical Problem ◽  
Dominant Negative ◽  
Wild Type ◽  
Mitochondrial Energy Metabolism

Pulmonary oxygen toxicity is a major clinical problem for patients undergoing supplemental oxygen therapy. Thioredoxin (Trx) is an endogenous antioxidant protein that regenerates oxidatively inactivated proteins. We examined how Trx contributes to oxygen tolerance by creating transgenic mice with decreased levels of functional thioredoxin (dnTrx-Tg) using a dominant-negative approach. These mice showed decreased Trx activity in the lung although the expression of mutant protein is three times higher than the wild-type mice. Additionally, we found that these mice showed increased oxidation of endogenous Trx in room air. When exposed to hyperoxia (>90% O2) for 4 days, they failed to recover and showed significant mortality. Even in normal oxygen levels, these mice displayed a significant decrease in aconitase and NADH dehydrogenase activities, decreased mitochondrial energy metabolism, increased p53 and Gadd45α expression, and increased synthesis of proinflammatory cytokines. These effects were further increased by hyperoxia. We also generated mice overexpressing Trx (Trx-Tg) and found they maintained lung redox balance during exposure to high oxygen and thus were resistant to hyperoxia-induced lung injury. These mice had increased levels of reduced Trx in the lung in normoxia as well as hyperoxia. Furthermore, the levels of aconitase and NADH dehydrogenase activities were maintained in these mice concomitant with maintenance of mitochondrial energy metabolism. The genotoxic stress markers such as p53 or Gadd45α remained in significantly lower levels in hyperoxia compared with dnTrx-Tg or wild-type mice. These studies establish that mice deficient in functional Trx exhibit a phenotype of sensitivity to ambient air and hypersensitivity to hyperoxia.

scholarly journals Transcriptional and Proteomic Analysis of a Ferric Uptake Regulator (Fur) Mutant of Shewanella oneidensis: Possible Involvement of Fur in Energy Metabolism, Transcriptional Regulation, and Oxidative Stress

2002 ◽  
Vol 68 (2) ◽  
pp. 881-892 ◽  
Author(s):  
Dorothea K. Thompson ◽  
Alexander S. Beliaev ◽  
Carol S. Giometti ◽  
Sandra L. Tollaksen ◽  
Tripti Khare ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcriptional Regulation ◽  
Energy Metabolism ◽  
Type Strain ◽  
Wild Type Strain ◽  
Shewanella Oneidensis ◽  
Anaerobic Growth ◽  
Ferric Uptake Regulator ◽  
Wild Type ◽  
And Oxidative Stress

ABSTRACT The iron-directed, coordinate regulation of genes depends on the fur (ferric uptake regulator) gene product, which acts as an iron-responsive, transcriptional repressor protein. To investigate the biological function of a fur homolog in the dissimilatory metal-reducing bacterium Shewanella oneidensis MR-1, a fur knockout strain (FUR1) was generated by suicide plasmid integration into this gene and characterized using phenotype assays, DNA microarrays containing 691 arrayed genes, and two-dimensional polyacrylamide gel electrophoresis. Physiological studies indicated that FUR1 was similar to the wild-type strain when they were compared for anaerobic growth and reduction of various electron acceptors. Transcription profiling, however, revealed that genes with predicted functions in electron transport, energy metabolism, transcriptional regulation, and oxidative stress protection were either repressed (ccoNQ, etrA, cytochrome b and c maturation-encoding genes, qor, yiaY, sodB, rpoH, phoB, and chvI) or induced (yggW, pdhC, prpC, aceE, fdhD, and ppc) in the fur mutant. Disruption of fur also resulted in derepression of genes (hxuC, alcC, fhuA, hemR, irgA, and ompW) putatively involved in iron uptake. This agreed with the finding that the fur mutant produced threefold-higher levels of siderophore than the wild-type strain under conditions of sufficient iron. Analysis of a subset of the FUR1 proteome (i.e., primarily soluble cytoplasmic and periplasmic proteins) indicated that 11 major protein species reproducibly showed significant (P < 0.05) differences in abundance relative to the wild type. Protein identification using mass spectrometry indicated that the expression of two of these proteins (SodB and AlcC) correlated with the microarray data. These results suggest a possible regulatory role of S. oneidensis MR-1 Fur in energy metabolism that extends the traditional model of Fur as a negative regulator of iron acquisition systems.

Sign in / Sign up

Export Citation Format

Share Document