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#metabolism

3 posts3 participants0 posts today
Public
michael

23-Apr-2025
Remembering the cold: scientists discover how #memories control #metabolism

New multidisciplinary research led by Tomás Ryan from Trinity College Dublin shows that the brain forms memories of cold experiences and uses them to control our metabolism. This newly published study is the first to show that #cold memories form in the #brain – and map out how they subsequently drive #thermoregulation.

eurekalert.org/news-releases/1 #science

EurekAlert!Remembering the cold: scientists discover how memories control metabolismNew multidisciplinary research led by Prof. Tomás Ryan from Trinity College Dublin shows that the brain forms memories of cold experiences and uses them to control our metabolism. This newly published study is the first to show that cold memories form in the brain – and map out how they subsequently drive thermoregulation. The discovery may have important applications in therapies designed to treat a range of disorders – from obesity to cancer – in which thermoregulation and metabolism (or a lack of control in this area) plays a role, as well as opening the door to more fundamental research, which could help us better understand how memories impact our behaviour and emotions.
Public
flypapers

📰 "RNase H1 counteracts DNA damage and ameliorates SMN-dependent phenotypes in a Drosophila model of Spinal Muscular Atrophy"
biorxiv.org/content/10.1101/20
#Drosophila #Metabolism #Immunity #Larva

bioRxiv · RNase H1 counteracts DNA damage and ameliorates SMN-dependent phenotypes in a Drosophila model of Spinal Muscular AtrophySpinal Muscular Atrophy (SMA) is caused by a deficiency of the Survival Motor Neuron (SMN) protein. Mutations in SMN disrupt mRNA splicing and translation, leading to maladaptive changes in transcriptomes, proteomes, neuroinflammation, and metabolism, which drive motor neuron degeneration in SMA patients. Using a Drosophila SMA model, we found that systemic depletion of Smn leads to accumulation of RNA:DNA hybrids (Rloops), increased DNA damage, dysregulation of amino acids and sugar metabolism and activation of the innate immune response, recapitulating key pathological features reported in mammalian models and severe SMA patients. Persistent DNA damage in Smn-deficient flies alters cell proliferation rates in larval brains and induces extensive cell death in the developing eye. Importantly here, we show that stimulating the resolution of RNA:DNA hybrids with transgenic human RNAse H1 prevents the accumulation of DNA damage and attenuates the transcriptome and amino acid alterations induced by Smn depletion, mitigating the Smn-dependent cellular and developmental abnormalities, in Smn-deficient flies. Our data suggest that depletion of Smn causes an accumulation of aberrant transcripts and chronic DNA damage, which along with the altered metabolomic profiles associated with Smn deficiency trigger systemic inflammatory responses, ultimately affecting neuronal function and survival. ### Competing Interest Statement The authors have declared no competing interest.
Public
flypapers

📰 "Impairment of the blood brain barrier accelerates a negative ultraslow potential in the locust CNS"
biorxiv.org/content/10.1101/20
#Metabolism #Drosophila

bioRxiv · Impairment of the blood brain barrier accelerates a negative ultraslow potential in the locust CNSInsects provide useful models for investigating evolutionarily conserved mechanisms underlying electrical events associated with brain injury and death. Spreading depolarizations (SD) are transient events that propagate through neuropil whereas the negative ultraslow potential (NUP) is sustained and reflects accumulating damage in the tissue. We used the locust, Locusta migratoria, to investigate ion homeostasis at the blood brain barrier (BBB) during SD and NUP induced by treatment with the Na+/K+-ATPase inhibitor, ouabain. We found that sustained SD caused by the metabolic inhibitor, sodium azide, was associated with a large reduction of K+ efflux through the BBB at ganglia (= grey matter) but not at connectives (= white matter). This was accompanied by a large increase in tissue resistivity but no conductance changes of identified motoneuron dendrites in the neuropil. Males recovered more slowly from ouabain-induced SD, as previously described for anoxic SD. Impairment of barrier functions of the BBB pharmacologically with cyclosporin A or DIDS, or by cutting nerve roots, accelerated the NUP, thus promoting earlier and more frequent SD, but had no effect on the temporal parameters of SD. We conclude that the mechanisms underlying onset and recovery of SD are minimally affected by the damage associated with the NUP. We suggest that future research using tissue-specific genetic approaches in Drosophila to target identified molecular structures of the BBB are likely to be fruitful. ### Competing Interest Statement The authors have declared no competing interest.
Public
Miki :rstats:

#30DayChartChallenge Día 16: Negative Relationship FOUND! 📉🐍🐦🐢🐟

¡Lo conseguimos! Tras ajustar por masa corporal, la relación entre Tasa Metabólica Específica (W/kg) y Longevidad Máxima (años) en ~530 especies animales (AnAge DB, outliers quitados) SÍ es negativa (Pearson ρ ≈ -0.42, p < 2.2e-16). #RelationshipsWeek #Animals

El gráfico log-log muestra la tendencia: mayor intensidad metabólica por kilo se asocia con vidas más cortas. ¡Apoya la idea del "ritmo de vida"! 🔥➡️⏳ Colores por Clase Taxonómica.

Un recordatorio de la importancia de normalizar variables y limpiar datos para ver la señal correcta. ¡Ciencia en acción!

🛠 #rstats #ggplot2 #ggpubr | Data: AnAge | Theme: #theme_week3_animals
📂 Código/Viz: t.ly/ouLN0

Scatter plot log-log mostrando la relación entre Longevidad Máxima (años, eje Y) y Tasa Metabólica Basal Específica (Watts/kg, eje X) para 534 especies animales (outliers eliminados). Los puntos están coloreados por Clase taxonómica (Mammalia, Aves, Reptilia, Amphibia). Una línea de regresión lineal de color marrón oscuro con intervalo de confianza gris muestra una clara tendencia negativa. El coeficiente de correlación de Pearson (rho = -0.42, p < 2.2e-16) se muestra en la esquina superior derecha. El gráfico utiliza un tema con fondo beige claro y textos en marrón. Fuente: AnAge Database.
#Day16#Negative#dataviz
Public
flypapers

📰 "Single-Cell Multiomic Analysis of Circadian Rhythmicity in Mouse Liver"
biorxiv.org/content/10.1101/20
#Circadian
#Metabolism #Drosophila #Sleep

bioRxiv · Single-Cell Multiomic Analysis of Circadian Rhythmicity in Mouse LiverFrom bacteria to humans, most organisms showcase inherent 24-hour circadian rhythms, best exemplified by the sleep-wake cycle. These rhythms are remarkably widespread, governing hormonal, metabolic, physiological, and behavioral oscillations, and are driven by "molecular clocks" that orchestrate the rhythmic expression of thousands of genes throughout the body. Here, we generate single-cell RNA and ATAC multiomic data to simultaneously characterize gene expression and chromatin accessibility of ~33,000 mouse liver cells across the 24-hour day. Our study yields several key insights, including: (i) detecting circadian rhythmicity in both discretized liver cell types and transient sub-lobule cell states, capturing space-time RNA and ATAC profiles in a cell-type- and cell-state-specific manner; (ii) delving beyond mean cyclic patterns to characterize distributions, accounting for gene expression stochasticity due to transcriptional bursting; (iii) interrogating multimodal circadian rhythmicity, encompassing RNAs, DNA regulatory elements, and transcription factors (TFs), while examining priming and lagging effects across modalities; and (iv) inferring spatiotemporal gene regulatory networks involving target genes, TFs, and cis-regulatory elements that controls circadian rhythmicity and liver physiology. Our findings apply to existing single-cell data of mouse and Drosophila brains and are further validated by time-series single molecule fluorescence in situ hybridization, as well as vast amounts of existing and orthogonal high-throughput data from chromatin immunoprecipitation followed by sequencing, capture Hi-C, and TF knockout experiments. Altogether, our study constructs a comprehensive map of the time-series transcriptomic and epigenomic landscapes that elucidate the function and mechanism of the liver peripheral clocks. ### Competing Interest Statement The authors have declared no competing interest.
Public
flypapers

📰 "Pyruvate kinase deficiency links metabolic perturbations to neurodegeneration and axonal protection"
biorxiv.org/content/10.1101/20
#DrosophilaMelanogaster
#Metabolism #Drosophila

bioRxiv · Pyruvate kinase deficiency links metabolic perturbations to neurodegeneration and axonal protectionNeurons rely on tightly regulated metabolic networks to sustain their high-energy demands, particularly through the coupling of glycolysis and oxidative phosphorylation. Here, we investigate the role of pyruvate kinase (PyK), a key glycolytic enzyme, in maintaining axonal and synaptic integrity in the Drosophila melanogaster neuromuscular system. Using genetic deficiencies in PyK, we show that disrupting glycolysis induces progressive synaptic and axonal degeneration and severe locomotor deficits. These effects require the conserved dual leucine zipper kinase (DLK), Jun N-terminal kinase (JNK), and activator protein 1 (AP-1) Fos transcription factor axonal damage signaling pathway and the SARM1 NADase enzyme, a key driver of axonal degeneration. As both DLK and SARM1 regulate degeneration of injured axons (Wallerian degeneration), we probed the effect of PyK loss on this process. Consistent with the idea that metabolic shifts may influence neuronal resilience in context-dependent ways, we find that pyk knockdown delays Wallerian degeneration following nerve injury, suggesting that reducing glycolytic flux can promote axon survival under stress conditions. This protective effect is partially blocked by DLK knockdown and fully abolished by SARM1 overexpression. Together, our findings help bridge metabolism and neurodegenerative signaling by demonstrating that glycolytic perturbations causally activate stress response pathways that dictate the balance between protection and degeneration depending on the system's state. These results provide a mechanistic framework for understanding metabolic contributions to neurodegeneration and highlight the potential of metabolism as a target for therapeutic strategies. ### Competing Interest Statement The authors have declared no competing interest.
Public
RDN

Higher blood concentrations of acylcarnitines--fatty acid metabolites indicative of mitochondrial metabolism--are associated with more severe Alzheimer's symptoms. Acylcarnitines may be a measure of 'bioenergetic age' that categorizes susceptibility to Alzheimers.

Summary: sciencealert.com/reducing-your

Original paper: nature.com/articles/s41467-025

ScienceAlert · Reducing Your 'Bioenergetic Age' May Ward Off Alzheimer's, Study FindsYour risk of developing Alzheimer's disease depends largely on your genes and your age, but that doesn't mean it's out of your hands.
#Science#Alzheimers#Aging
Public
flypapers

📰 "Dietary restriction is evolutionary conserved on the phenotypic and mechanistic level"
biorxiv.org/content/10.1101/20
#Metabolism #Drosophila

bioRxiv · Dietary restriction is evolutionary conserved on the phenotypic and mechanistic levelThe anti-ageing response of Dietary Restriction (DR) is thought to be an ancient mechanistic response, reasoning from its phenotypic conservation in a wide range of organisms. However, DR is implemented using different diets and methods across species, and evidence for conservation at the mechanistic level remains limited. Here we tested the longevity and fecundity response to DR across eight different species of Drosophila using the same diets in a reaction norm framework. We confirm that DR is phenotypically conserved across Drosophila. Next, we used comparative transcriptomics across six species and found strongly concordant differential expression in response to DR (rs > 0.28, < 0.72, P < 0.0001). We studied the evolutionary history of the top concordantly differentially expressed orthologous genes and identified that the large majority of these genes are young genes and are Diptera specific. Our results indicate that large parts of the DR response are likely to be taxonomic specific, suggesting that the genetic basis of DR is not widely conserved. To validate this hypothesis we tested whether the 15 most conserved genes that change in transcription in response to DR using conditional in vivo RNAi. Surprisingly, we found that 12 out of 15 genes tested had a lifespan phenotype, with 9 extending lifespan. Five of these genes are related to cysteine metabolism implicating it in the mechanisms of DR, further suggesting physiological compensation to DR is ubiquitous and providing a possible biomedical target. Our findings suggest that while large parts of the DR response are taxonomically specific, some core mechanisms are conserved across divergent species. The comparative approaches we used here hold promise to identify shared mechanisms relevant to our own species and therefore ultimately anti-ageing interventions. ### Competing Interest Statement The authors have declared no competing interest.
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