Influence of body composition on energy metabolism in females with constitutional thinness
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Energy metabolism in health and diseases
Energy metabolism is indispensable for sustaining physiological functions in living organisms and assumes a pivotal role across physiological and pathological conditions. This review provides an extensive overview of advancements in energy metabolism research, elucidating critical pathways such as glycolysis, oxidative phosphorylation, fatty acid metabolism, and amino acid metabolism, along with their intricate regulatory mechanisms. The homeostatic balance of these processes is crucial; however, in pathological states such as neurodegenerative diseases, autoimmune disorders, and cancer, extensive metabolic reprogramming occurs, resulting in impaired glucose metabolism and mitochondrial dysfunction, which accelerate disease progression. Recent investigations into key regulatory pathways, including mechanistic target of rapamycin, sirtuins, and adenosine monophosphate-activated protein kinase, have considerably deepened our understanding of metabolic dysregulation and opened new avenues for therapeutic innovation. Emerging technologies, such as fluorescent probes, nano-biomaterials, and metabolomic analyses, promise substantial improvements in diagnostic precision. This review critically examines recent advancements and ongoing challenges in metabolism research, emphasizing its potential for precision diagnostics and personalized therapeutic interventions. Future studies should prioritize unraveling the regulatory mechanisms of energy metabolism and the dynamics of intercellular energy interactions. Integrating cutting-edge gene-editing technologies and multi-omics approaches, the development of multi-target pharmaceuticals in synergy with existing therapies such as immunotherapy and dietary interventions could enhance therapeutic efficacy. Personalized metabolic analysis is indispensable for crafting tailored treatment protocols, ultimately providing more accurate medical solutions for patients. This review aims to deepen the understanding and improve the application of energy metabolism to drive innovative diagnostic and therapeutic strategies.
Chemogenetic induction of CA1 hyperexcitability triggers indistinguishable autistic traits in asymptomatic mice differing in Ambra1 expression and sex
Among the genomic alterations identified as risk factors in mice models of autism spectrum disorders (ASD), heterozygous deletion of Ambra1 (Activating Molecule in Beclin1-Regulated Autophagy) triggers an ASD phenotype associated with hippocampal hyperexcitability exclusively in the female sex although Ambra1 protein is comparably expressed in the hippocampus of symptomatic females and asymptomatic males. Given the intricate relationship between Ambra1 deficiency and sex in the etiology of ASD, we took advantage of asymptomatic mice including Ambra1+/− males and wild-type (Wt) mice of both sexes to investigate whether their non-pathogenic variations in Ambra1 levels could underlie a differential susceptibility to exhibit ASD-like traits in response to experimental elevation of hippocampal excitability. Here we report that selective activation of inhibitory DREADD in CA1 parvalbumin-positive interneurons (PV-IN) reduces GABAergic currents onto pyramidal neurons (PN), causes social and attentional deficits, and augments the proportion of immature/thin spines in CA1 PN dendrites to the same extent in Ambra1+/− males and Wt mice of both sexes. Our findings show that the substantial hippocampal variations in pro-autophagic Ambra1 gene product shown by asymptomatic mice differing in mutation and/or sex do not underlie a differential reactivity to chemogenetic induction of idiopathic ASD.
The evolution and maintenance of trioecy with cytoplasmic male sterility
Trioecy, the co-existence of females, males and hermaphrodites, is a rare sexual system in plants that may be an intermediate state in transitions between hermaphroditism and dioecy. Previous models have identified pollen limitation as a necessary condition for the evolution of trioecy from hermaphroditism. In these models, the seed-production and pollen production of females and males relative to those of hermaphrodites, respectively, are compromised by self-fertilization by hermaphrodites under pollen- limitation. Here, we investigate the evolution of trioecy via the invasion of cytoplasmic male sterility (CMS) into androdioecious populations in which hermaphrodites co-occur with males and where the male determiner is linked to a (partial) fertility restorer. We show that the presence of males in a population renders invasion by CMS more difficult. However, the presence of males also facilitates the maintenance of trioecy even in the absence of pollen limitation by negative frequency-dependent selection, because males reduce the transmission of CMS by females by siring sons (which cannot transmit CMS). We discuss our results in light of empirical observations of trioecy in plants and its potential role in the evolution of dioecy.
Estimating energy consumption and GHG emissions in the U.S. food supply chain for net-zero
This work provides a database of the U.S. food system’s energy consumption and GHG emissions at the national and state levels by food supply chain (FSC) stage, fuel type, and food commodity. We estimate that the U.S. FSC consumed a total 4660 TBTU (4900 PJ) of site energy, 7130 TBTU (7500 PJ) of primary energy, and generated 970 MMT of GHG emissions in 2016. Among all the stages, on-farm production is the largest energy consumer (31% primary energy) and GHG emissions contributor (70%), largely due to raising animals. Optimizing distribution can reduce the stage’s energy consumption and GHG emissions and increase products’ shelf-life. Reducing food loss and waste is another good option, as it decreases the amount of food necessary to grow, thus impacting the overall FSC. The database can help stakeholders identify stage- and region-specific strategies and measures to curtail the environmental footprint of the U.S. food system.
A single-cell network approach to decode metabolic regulation in gynecologic and breast cancers
Cancer metabolism is characterized by significant heterogeneity, presenting challenges for treatment efficacy and patient outcomes. Understanding this heterogeneity and its regulatory mechanisms at single-cell resolution is crucial for developing personalized therapeutic strategies. In this study, we employed a single-cell network approach to characterize malignant heterogeneity in gynecologic and breast cancers, focusing on the transcriptional regulatory mechanisms driving metabolic alterations. By leveraging single-cell RNA sequencing (scRNA-seq) data, we assessed the metabolic pathway activities and inferred cancer-specific protein-protein interactomes (PPI) and gene regulatory networks (GRNs). We explored the crosstalk between these networks to identify key alterations in metabolic regulation. Clustering cells by metabolic pathways revealed tumor heterogeneity across cancers, highlighting variations in oxidative phosphorylation, glycolysis, cholesterol, fatty acid, hormone, amino acid, and redox metabolism. Our analysis identified metabolic modules associated with these pathways, along with their key transcriptional regulators. These findings provide insights into the complex interplay between metabolic rewiring and transcriptional regulation in gynecologic and breast cancers, paving the way for potential targeted therapeutic strategies in precision oncology. Furthermore, this pipeline for dissecting coregulatory metabolic networks can be broadly applied to decipher metabolic regulation in any disease at single-cell resolution.
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