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359 results for “mitochondrial function”
Metabolomics data associated with "Glial swip-10 controls systemic mitochondrial function, oxidative stress, and neuronal viability via copper ion homeostasis"
<p>Raw feature tables used for metabolomic analysis of the <em>Caenorhabditis elegans</em> mutant <em>swip-10</em>. The data were generated using liquid chromatography coupled high-resolution mass spectrometry. Two different columns were used: HILIC (+ ESI) and C18 (-ESI), coupled to a Thermo Q-Exactive Orbitrap mass spectrometer. The feature tables were generated using open-source peak peaking and alignment R packages: apLCMS and xMAanalyzer. See more details in the associated manuscript.</p>
Cross-species analysis identifies mitochondrial dysregulation as a functional consequence of the schizophrenia-associated 3q29 deletion
<p>The 1.6Mb deletion at chromosome 3q29 (3q29Del) is the strongest identified genetic risk factor for schizophrenia, but the effects of this variant on neurodevelopment are not well understood. We interrogated the developing neural transcriptome in two experimental model systems with complementary advantages: isogenic human cortical organoids and isocortex from the 3q29Del mouse model. We profiled transcriptomes from isogenic cortical organoids that were aged for 2 months and 12 months, as well as perinatal mouse isocortex, all at single-cell resolution. Systematic pathway analysis implicated dysregulation of mitochondrial function and energy metabolism. These molecular signatures were supported by analysis of oxidative phosphorylation protein complex expression in mouse brains and assays of mitochondrial function in engineered cell lines. Together these data indicate that metabolic disruption is associated with 3q29Del and is conserved across species.</p>
Data from: Mitochondrial function is enhanced by thyroid hormones during zebra finch development
<p>An organism's response to its environment is largely underpinned by changes in the energy supplied by the aerobic mitochondrial metabolism via adenosine-tri-phosphate (ATP) production. ATP is especially important under energy-demanding conditions, such as during growth. The biological mechanisms through which environmental factors feed-back on mitochondrial function, and thus growth, are poorly understood, but recent studies suggest a role of hormones. In particular, thyroid hormones (THs) are key regulators of growth and metabolism in vertebrates, which react flexibly to environmental influences, such as temperature or nutrient availability. We manipulated TH levels within physiological ranges during the main growth phase in zebra finch (Taeniopygia guttata) nestlings, to test for causal relationships with mitochondrial function and growth. Our TH-treatment accelerated skeletal growth and maximal mitochondrial working capacity, ETS – a mitochondrial trait reflecting ATP production potential. Furthermore, TH marginally elevated cellular metabolic rate and oxidative phosphorylation, the final step of ATP production. To our knowledge, this is the first study to characterize the regulation of mitochondria by TH during development in a naturalistic context and to address the implications for fitness.</p>
Cross-species analysis identifies mitochondrial dysregulation as a functional consequence of the schizophrenia-associated 3q29 deletion
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Data from: Mitochondrial function is enhanced by thyroid hormones during zebra finch development
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Flying on empty: Reduced mitochondrial function and flight capacity in food-deprived monarch butterflies
<p>Mitochondrial function is fundamental to organismal performance, health, and fitness – especially during energetically challenging events, such as migration. With this investigation, we evaluated mitochondrial sensitivity to ecologically relevant stressors. We focused on an iconic migrant, the North American monarch butterfly (Danaus plexippus), and examined the effects of two stressors: seven days of food deprivation, and infection by the protozoan parasite Ophryocystis elektroscirrha (known to reduce survival and flight performance). We measured whole-animal resting metabolic rate (RMR) and peak flight metabolic rate, and mitochondrial respiration of isolated mitochondria from the flight muscles. Food deprivation reduced mass-independent RMR and peak flight metabolic rate, whereas infection did not. Fed monarchs used mainly lipids in flight (respiratory quotient 0.73), but the respiratory quotient dropped in food-deprived individuals, possibly indicating switching to alternative energy sources, such as ketone bodies. Food deprivation decreased mitochondrial maximum oxygen consumption but not basal respiration, resulting in lower respiratory control ratio (RCR). Furthermore, food deprivation decreased mitochondrial complex III activity, but increased complex IV activity. Infection did not result in any changes in these mitochondrial variables. Mitochondrial maximum respiration rate correlated positively with mass-independent RMR and flight metabolic rate, suggesting a link between mitochondria and whole-animal performance. In conclusion, low food availability negatively affects mitochondrial function and flight performance, with potential implications for migration, fitness, and population dynamics. Although previous studies have reported poor flight performance in infected monarchs, we found no differences in physiological performance, suggesting that reduced flight capacity may be due to structural differences or low energy stores.</p>
The MicroRESUS study: An observational study to examine the effects of circulatory shock and resuscitation on microcirculatory function and mitochondrial respiration after cardiovascular surgery.
<p>Post-cardiotomy shock (PCS) occurs in up to 5% of cardiovascular surgeries and has an in-hospital mortality rate as high as 75%. Physiologic derangements are often multifactorial, including ischemic-reperfusion injury leading to low cardiac output, vasoplegia, hemorrhage, or pericardial tamponade. Resuscitation strategies often target the normalization of systemic hemodynamics, however, practices to achieve standard macrocirculatory goals often fail to reverse microcirculation abnormalities or address cytopathic hypoxia. Perioperative shock may be the result of an imbalance between oxygen delivery and oxygen demand or could be the result of impaired oxygen utilization. This study will examine differences in microcirculatory function and mitochondrial respiration in patients with circulatory shock after cardiovascular surgery.</p>
Altered mitochondria-associated ER membranes (MAM) function shifts mitochondrial metabolism in amyotrophic lateral sclerosis (ALS)
<p><span>Mitochondrial function is modulated by its functional interaction with the endoplasmic reticulum.</span><span> Recent research indicates that these contacts are disrupted in familial models of amyotrophic lateral sclerosis. We report here this impairment in the crosstalk between mitochondria and the endoplasmic reticulum impedes the use of glucose-derived pyruvate as mitochondrial fuel, causing a shift to fatty acids to sustain energy production. Over time, this deficiency alters mitochondrial electron flow and the active/dormant status of complex I in spinal cord tissues, but not in the brain. These findings suggest MAM plays a crucial role in regulating cellular glucose metabolism and that its dysfunction may underlie the bioenergetic deficits observed in ALS. The dataset includes the lipid profiles of the total homogenates and motchondrial fractions from SOD1.</span></p>
Metabolic rate increases with thermal acclimation and is associated with mitochondrial function in some tissues of threespine stickleback
<p>The metabolic rate (ṀO2) of eurythermal fishes changes in response to temperature, yet it is unclear how changes in mitochondrial function contribute to changes in ṀO2. We hypothesized that ṀO2 would increase with acclimation temperature in the threespine stickleback (Gasterosteus aculeatus) in parallel with metabolic remodeling at the cellular level but that changes in metabolism in some tissues and organs, such as liver, would contribute more to changes in ṀO2 than others. Threespine stickleback were acclimated to 5, 12 and 20°C for 21 weeks. At each temperature, standard and maximum metabolic rate (SMR and MMR, respectively), and aerobic scope (AS) were quantified, along with mitochondrial respiration rates in liver, oxidative skeletal, and cardiac muscles, and the maximal activity of citrate synthase (CS) and lactate dehydrogenase (LDH) in liver, and oxidative and glycolytic skeletal muscles. SMR, MMR and AS increased with acclimation temperature, along with rates of mitochondrial phosphorylating respiration in all tissues. Low SMR and MMR at 5°C were associated with low or undetectable rates of mitochondrial complex II activity and a greater reliance on complex I activity in liver, oxidative skeletal muscle, and heart. SMR was positively correlated with cytochrome c oxidase (CCO) activity in liver and oxidative muscle but not mitochondrial proton leak, while MMR was positively correlated with CCO in liver. Overall, the results suggest that changes in ṀO2 in response to temperature are driven by changes in some aspects of mitochondrial function in some, but not all tissues of threespine stickleback.</p>
Rapid changes in transcriptomic profile and mitochondrial function in human soleus muscle after three-day dry immersion
<p>Supplemental Tables for a study <strong>Rapid changes in transcriptomic profile and mitochondrial function in human soleus muscle after three-day dry immersion</strong></p>
Data from: Mitochondrial function declines with age within individuals but is not linked to the pattern of growth or mortality risk in zebra finch
<p>Mitochondrial dysfunction is considered a highly conserved hallmark of ageing. However, most studies in both model and non-model organisms are cross-sectional in design; therefore, little is known, at the individual level, on how mitochondrial function changes with age, its link to early developmental conditions or its relationship with survival. Here we manipulated the postnatal growth in zebra finches (<em>Taeniopygia guttata</em>) via dietary modification that induced accelerated growth without changing adult body size. In the same individuals, we examined blood cells mitochondrial functioning (mainly erythrocytes) when they were young (ca 36 weeks) and again in mid-aged (ca 91 weeks) adulthood. Mitochondrial function was strongly influenced by age but not by postnatal growth conditions. Across all groups, within individual <em>ROUTINE</em> respiration, <em>OXPHOS</em> and <em>OXPHOS</em> coupling efficiency significantly declined with age, while <em>LEAK</em> respiration increased. However, we found no link between mitochondrial function and the probability of survival into relatively old age (ca 4 years). Our results suggests that the association between accelerated growth and reduced longevity, evident in this as in other species, is not attributable to age-related changes in any of the measured mitochondrial function traits.</p>
The Effect of Linagliptin on Mitochondrial and Endothelial Function
ClinicalTrials.gov study NCT01969084. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Mitochondrial Function in Circulating Cells and Muscle Tissue
ClinicalTrials.gov study NCT02700698. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Trial of Oral Glutamine on Mitochondrial Function in CKD
ClinicalTrials.gov study NCT02838979. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Effect of a Wide Spectrum Nutritional Supplement on Mitochondrial Function in Children With Autism Spectrum Disorder
ClinicalTrials.gov study NCT03835117. IPD Sharing: NO. Countries: 1. Publications: 3.
Evaluation of Microcirculatory Function and Mitochondrial Respiration After Cardiovascular Surgery
ClinicalTrials.gov study NCT05330676. IPD Sharing: YES. Countries: 1. Publications: 1.
Effects of Acipimox on Mitochondrial Function in Obesity
ClinicalTrials.gov study NCT01488409. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Experimental demonstration of functional divergence in mitochondrial metabolism between two finch subspecies subjected to a thermal challenge
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Flying on empty: Reduced mitochondrial function and flight capacity in food-deprived monarch butterflies
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Metabolic rate increases with thermal acclimation and is associated with mitochondrial function in some tissues of threespine stickleback
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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