Energy Deprivation Research Articles

Abstract 4135531: The Ubiquitin-Specific Protease 30 Inhibitor, MTX652, Attenuates Cardiac Dysfunction And Remodelling In a Murine Model Of Transverse Aortic Constriction

Introduction: Mitochondrial abnormalities are a characteristic of heart failure leading to energy deprivation and disease worsening. The mitochondrial deubiquitinating enzyme USP30, removes ubiquitin and represses PINK1/PARKIN-mediated mitophagy leading to accumulation of dysfunctional mitochondria. In this study we investigated the role of MTX652, a clinical stage USP30 inhibitor, in a mouse model of cardiac hypertrophy using transverse aortic constriction (TAC). Hypothesis: Inhibition of USP30 will promote mitophagy resulting in clearance of dysfunctional mitochondria and improved cellular health leading to cardioprotective effects. Aims: To determine if MTX652 can protect from TAC induced cardiac hypertrophy and remodelling. Methods: Male C57BL/6 mice, 8 weeks old, were subjected to sham surgeries or TAC using a 26G needle to induce cardiac pressure overload. MTX652 (1.5 or 5 mg/kg, n =12-13) or vehicle ( n =11) was administered orally, twice daily, starting 2 days post-surgery. Captopril (30 mg/kg/d, n =13) was also included as a positive control. After 4 weeks, echocardiography assessed left ventricle (LV) function and morphology. Cell based assays assessed MTX652 target engagement and TOM20 ubiquitination in vitro. Results: LV hypertrophy and wall thickening was observed in TAC animals. Treatment with MTX652 decreased systolic LV volume (1.5 mg/kg p<0.05 and 5 mg/kg p<0.01) and diameter (1.5 mg/kg p<0.01 and 5 mg/kg p<0.05,) demonstrating comparable effects to Captopril. A reduction in anterior wall thickness in diastole was also observed with MTX652 (5 mg/kg, p<0.01). Cardiac dysfunction was also evident in TAC animals with MTX652 showing improvements in both ejection fraction (1.5 mg/kg and 5 mg/kg, p<0.0001) and fractional shortening (1.5 mg/kg and 5 mg/kg, p<0.0001). Cellular target engagement for MTX652 was confirmed in HeLa-YFP-Parkin cells with an EC 50 of 2.7 nM ( n =2). Furthermore, the USP30 substrate TOM20 was ubiquitinated following MTX652 treatment in vitro (EC 50 =6.1 nM, n =4) providing evidence of mitophagy activation, a finding also confirmed in mouse heart tissue (MTX652, 5mg/kg). Conclusions: The USP30 inhibitor, MTX652 significantly protected mice from TAC induced cardiac hypertrophy and LV dysfunction. Furthermore, MTX652 potentiates ubiquitylation of TOM20 as a mechanism to promote mitophagy. These data suggest our clinical stage molecule could provide a novel therapeutic approach for the treatment of cardiac hypertrophy and heart failure.

Integrated transcriptomic hypothalamic-pituitary-ovarian axis network analysis reveals the role of energy availability on egg production in layers

Energy is a crucial component for maintaining egg production in layers. The hypothalamic-pituitary-ovarian (HPO) axis is an energy-sensitive functional axis for follicle development, synthesis, and secretion of reproductive hormones, and plays a key role in modulating sustained ovulation in layers. To investigate the mechanism of integrated network regulation of the HPO axis under energy fluctuation, ninety Hy-line brown layers (265-day-old, 1.92 ± 0.02 kg) were randomly divided into three groups for an 17-day experiment: a control group (Con group) fed ad libitum from days 1 to 17, an energy deprived group (ED group) that was fed ad libitum from days 1 to 12 and then underwent a fasting period from days 13 to 17 to induce a pause in laying, and a re-fed group (Rf group) that fasted for seven days (specifically, days 1 to 5, day 7, and day 9), had ad libitum access to feed on days 6 and 8, and were continuously fed from days 10 to 17. Each treatment consisted of 10 replicates with 3 birds per replicate. The study found that energy deprivation significantly decreased reproductive performance such as egg laying rate, ovarian index, number of small yellow follicles (SYF), and normal hierarchical follicles (NHIE) (P < 0.05), which recovered after refeeding, indicating the importance of energy availability for sustained ovulation in layers. In addition, estradiol (E2), estradiol/progesterone ratio (E2/P4), and luteinizing hormone (LH) displayed changes similar to follicle number, whereas follicle-stimulating hormone (FSH) exhibited a contrasting pattern. Transcriptome analysis revealed that energy deprivation downregulated genes related to energy and appetite-regulated neurotransmitter receptors and neuropeptides in the hypothalamus. These signals combined to inhibit gonadotropin-releasing hormone (GnRH) secretion and subsequently downregulated the crucial genes responsible for synthesizing gonadotropins, gonadotropin releasing hormone receptor (GnRHR), and glycoprotein hormones alpha chain (CGA). Consequently, this suppression of the hypothalamus and pituitary affected ovarian function through ovarian steroidogenesis and the extracellular matrix (ECM)-receptor interaction. These findings suggest that energy deprivation inhibits the function of the HPO axis, leading to impaired follicle development and reduced egg production and that refeeding can partially restore these indicators.

Rice sucrose non-fermenting related protein kinase (SnRK1) has a limited role in defense against Fall armyworm (Spodoptera frugiperda)

Sucrose non-fermenting (SNF) related protein kinase 1 (SnRK1) is a master regulator of energy deprivation signaling and has also been implicated in abiotic and biotic stress regulation. SnRK1 promotes stress tolerance through metabolic and transcriptional changes and plays important roles in innate immunity against various pathogens. However, whether it plays a role against insect herbivory is not understood. To test this, using the wild type (with SnRK1) and snrk1 mutant lines in rice, we examined the potential role of SnRK1 in rice against the ruinous pest, Fall armyworm (FAW), Spodoptera frugiperda. We also investigated the response of FAW towards these lines at different time intervals after exogenous application of plant hormone, Jasmonic acid (JA), and a JA blocker (Ibuprofen). Additional experiments by feeding FAW with leaf infused diet, fresh leaves, and a short-term exposure of FAW to the lines were also carried out. FAW mass gain, growth and development, and host ecophysiological traits were observed. In addition, we also quantified the major surface defenses- trichomes, and wax before and after herbivory. Our results show that FAW response did not vary between mutants and wild type rice. Meanwhile, we found plant hormonal application influenced the ecophysiological traits regardless of mutants and wild type rice. Collectively, we show that while defense against FAW in rice is JA mediated, SnRK1 has a limited role as observed through manipulative experiments with the wild type and snrk1 mutant rice lines.

A precision intelligent nanomissile for inhibiting tumor metastasis, boosting energy deprivation and immunotherapy

The epithelial-mesenchymal transition (EMT), tumor stroma and local metabolic alterations cooperate to establish a unique tumor microenvironment (TME) that fosters tumor progression and metastasis. To tackle this challenge, a precision intelligent nanomissile named HA@AT-Pd has been designed for dual-pronged cancer-associated fibroblast (CAF) transformation and tumor cell elimination. It is observed that HA@AT-Pd inhibits the production of cancer stem cells (CSCs) by blocking the TGF-β/Smad signaling pathway-mediated EMT and reversing activated CAFs to quiescence. Notably, HA@AT-Pd induces energy depletion in breast cancer cells through simultaneously suppressing cellular oxidative phosphorylation and glycolysis. The inhibition of glycolysis results in reduced lactic acid production, thereby converting an immunosuppressive TME into an immune-activating environment. Furthermore, the photothermal effect generated by HA@AT-Pd evokes immunogenic cell death, which can further enhance the anti-tumor immune response. Overall, this multifunctional combination strategy unveils potential therapeutic avenues to inhibit tumor progression and metastasis.

Functional remodeling of gut microbiota and liver in laying hens as affected by fasting and refeeding after fasting.

Animals will experience energy deprivation processes such as moulting, clutching, migration and long-distance transportation under natural survival conditions and in production practices, and the body will trigger a series of adaptive metabolic changes during these processes. Fasting and refeeding after fasting can induce remodeling of nutrients and energy metabolism. This study aims to investigate the mechanisms by which the gut microbiota and liver of poultry respond to energy deprivation under specific conditions. Ninety 252-day-old laying hens were randomly divided into 3 groups: (1) fed ad libitum (control group); (2) fasted from day 13 to day 17 (fasting group); (3) fasted from day 1 to day 5, then refed on a specific feeding way (refeeding group). After that, the serum, liver, jejunum tissues, and cecum contents were sampled and sent for metabolome, transcriptome, morphology, and 16S rDNA sequencing analyses, respectively. Results showed that food deprivation not only observably decreased the body weight, liver index, and the villus height and villus/crypt ratio of jejunum, but also significantly changed the gut microbiota compositions, serum metabolic profiles, and the hepatic gene expression patterns of laying hens, whereas these changes were effectively reversed by the following refeeding operation. At the same time, metabolome combined transcriptome analysis revealed that both serum differential metabolites and hepatic differential expressed genes (DEGs) were consistently enriched in the lipid and amino metabolism pathways, and strong correlations were synchronously found between the differential metabolites and both of the differential gut microbial genera and DEGs, suggesting the crosstalks among gut, liver and their resulting serum metabolic products. The results suggested that the organism might coordinate to maintain metabolic homeostasis under energy deprivation through a combination of changes in gut microbial composition and hepatic gene expression.

A potent nano-strategy for dual energy deprivation to inhibit pancreatic cancer progression

Pancreatic cancer is a highly malignant tumor that poses significant threats to public health, and glycolysis plays a crucial role in its energy metabolism. Here, glycolysis was confirmed to be directly associated with poor prognosis through the use of clinical samples from 130 patients with pancreatic ductal adenocarcinoma (PDAC), and the effectiveness of zinc ions (Zn2+) in inhibiting glycolysis-related genes was further validated. Therefore, polyvinyl pyrrolidone (PVP)-modified zinc sulfide nanomedicines (ZnS-PVP) were developed for dual energy suppression by targeting glycolysis and mitochondrial respiration in pancreatic cancer. On the one hand, the released Zn2+ efficiently inhibited glycolysis in pancreatic cancer cells through the PI3K-Akt-mTOR-HIF-1α signaling axis. On the other hand, acid-responsive release of hydrogen sulfide (H2S) gas damaged mitochondria and further reduced energy compensation by inhibiting oxidative phosphorylation. This two-pronged energy deprivation nano-strategy effectively eliminated pancreatic cancer cells and was proven to overcome chemotherapeutic resistance. Moreover, ZnS-PVP administration combined with immune checkpoint blockade (ICB) therapy significantly suppressed tumor progression in mouse orthotopic pancreatic tumor models, as also demonstrated in a pancreatic cancer patient-derived xenograft (PDX) model. Our work highlights the positive role of bioactive metal ions in targeting tumor energy metabolism and the great potential of nano-strategy for energy deprivation in the treatment of pancreatic cancer.

Hostile Environments: Housing and Asylum Policies as Drivers of Energy Deprivation Among UK Refugee Communities

ABSTRACT Although refugees in the UK are highly susceptible to the triad of factors – low income, poor housing and high energy bills – that produce vulnerability to energy deprivation, literature on this issue is rare. We therefore propose a framework towards understanding the role of “non-energy” policies as drivers of energy deprivation among UK refugees, using the conceptual lenses of deservingness, welfare chauvinism and domicide to demonstrate how the condition has been deliberately produced under the UK government’s Hostile Environment approach. We argue that this approach not only damages the physical materiality of housing and the emotional space of home, but also deleteriously impacts upon refugees’ ability to access adequate energy services. Energy deprivation thus emerges as a hidden consequence of policies that normalize precarious housing, a denial of rights, and inadequate incomes, in which “home” becomes a site of exclusion that achieves the Hostile Environment’s goal – making everyday life unbearable.

Two-Dimensional Layered Nano-MoS2 Induces Earthworm Immune Cell Apoptosis by Regulating Lysosomal Maintenance and Function: Toward Unbiased Screening and Validation of Suspicious Pathways.

Molybdenum-based nanosheets (NSMoS2) are increasingly applied in various fields and undergoing relevant risk evaluations on subjectively hypothesized toxicity pathways. However, risk assessment should be unbiased and focus on appropriate end points to avoid biased prescreening. Here, we developed an adverse biological outcome screening strategy based on nontargeted functional protein profiles in earthworm (Eisenia fetida) immune cells exposed to NSMoS2 and their ionic counterpart (Na2MoO4). Through this framework, the apoptosis-related processes with distinct mechanisms were rapidly identified and thoroughly validated phenotypically. Specifically, upon exposure to 50 μg Mo/mL Na2MoO4, cellular signaling and energy homeostasis were disrupted within the transcription-translation biological chain. The autophagic pathway was activated, which, together with energy deprivation, phenotypically induced significant autophagy that ultimately led to apoptosis. In contrast, NSMoS2, tested at the same concentration, caused a reprogramming of apoptotic gene and protein expressions. Transcriptome plasticity facilitated the endocytic-adaptive transcriptional profile characterized by cytoskeleton remodeling and lysosome organization/movement under NSMoS2 exposure. Subcellular dynamics further revealed NSMoS2-induced lysosomal damage with a time-sensitive physiological window, ultimately mediating apoptosis. These findings provide a mechanistic and visual understanding of the distinct risk profile of NSMoS2 compared to molybdate, highlighting the importance of integrating nontargeted screening and phenotypic validation in early risk warning.

Water and energy deprivation: Addressing the problem of essential utility services poverty in Mayotte

Among the 17 sustainable development goals adopted by the United Nations in 2015 are ensuring “availability and sustainable management of water and sanitation” and “access to modern energy sources”. One problem for Mahorais households is access to safe, clean and affordable essential utility services, such as electricity, water and sewerage. Moreover, Mayotte, a French oversea department, is experiencing an unprecedented drought. The island, which is sinking into a severe water crisis, has been depriving its inhabitants of running water two days out of three since the beginning of September 2023. We define a new concept of utility services poverty (basic utility services deprivation) based on the theoretical capabilities framework of Sen and Nussbaum. Using a latent class model, we identify households that are poor in utility services and characterize four household profiles. One main advantage of this methodology is replicability in many Low and Middle Income Countries’ (LMICs). We demonstrate that access to water is more discriminatory than access to electricity in Mayotte. The top priority in fighting utility services poverty should be access to water and sanitary facilities. Public policies should be implemented not according to income but to facilitate water and energy access and improve basic hygiene conditions notably through social housing.

Targeted regulation of autophagy using sorafenib-loaded biomineralization nanoenzyme for enhanced photodynamic therapy of hepatoma

Sorafenib (SF), a multi-targeted tyrosine kinase inhibitor, serves as a primary therapeutic modality for advanced liver cancer. Nonetheless, its clinical efficacy is hindered by various obstacles, such as limited bioavailability and inadequate accumulation. This study introduces a novel biomimetic mineralization enzyme, known as BSA@Pt/Ce6/SF@M (PCFM). The PCFM incorporates platinum (Pt) as a catalytic agent, SF as a molecular-targeted therapeutic agent, and Ce6 as a photosensitizer within liver cancer cell membranes. This strategy enables the combination of various anti-tumor treatments, such as photodynamic therapy (PDT) and autophagy induction, leading to increased bioavailability of SF and achieving a multidimensional synergistic anticancer effect. The PDT effect produced by Ce6 in PCFM greatly enhances SF-induced autophagy, effectively promoting autophagic cell death. Furthermore, Pt dissociates from the biomineralization process, acquiring peroxidase properties through chemokinetic reactions. This facilitates the catalysis of significant oxygen generation, addressing the challenge of hypoxia in the tumor microenvironment and improving the efficacy of PDT. Moreover, the SF further enhances therapeutic efficacy by inducing autophagy in response to energy deprivation, as indicated by the reduced levels of HIF-1α, p62, along with increased levels of ROS and LC3-Ⅱ/Ι. This biomineralization-based nanoenzyme exhibits strong anti-tumor characteristics, offering a novel strategy for overcoming challenges in liver cancer treatment.

“Internal Trouble and Outside Aggression” Strategy: Energy Deprivation Synergized With cGAS‐STING Pathway Activation for Stimuli‐Responsive Photodynamic‐Metal‐Metabolic Immunotherapy

AbstractThe aberrant metabolic activities of tumor cells not only facilitate tumor proliferation but also impair immune cell function and cause an immunosuppressive tumor microenvironment (TME). Thus, reshaping the metabolic TME while activating innate immunity is highly desirable but challenging. Herein, a multifunctional immunomodulator is engineered for near‐infrared light (NIR)‐triggered photodynamic‐metal‐metabolic immunotherapy via the “internal trouble and outside aggression” strategy. Specifically, an endogenous and exogenous stimuli‐responsive nanoagent is prepared consisting of photosensitizer chlorin e6 (Ce6) modified dense silica‐coated rare earth‐doped nanoparticles (ReNPs@SiO2(Ce6)), with in situ grown ZIF‐8 on the surface for loading glucose transporter‐1 (GLUT‐1) inhibitor Fasentin and glutaminase‐1 inhibitor bis‐2‐(5‐phenylacetamido‐1,3,4‐thiadiazol‐2‐yl)ethyl sulfide (BPTES). The as‐obtained final product is denoted as ReSZ(FB). ReSZ(FB) induces‐ mitochondrial damage and releases mitochondrial DNA (mtDNA) via NIR‐mediated PDT. Subsequently, Zn2+ from ZIF‐8 collaborates with mtDNA to activate the cGAS‐STING pathway, initiating a robust tumor‐specific immune response. Concurrently, Fasentin and BPTES triggeres energy deprivation by blocking glucose uptake and inhibiting glutamine decomposition, thereby reprogramming the metabolic TME, and alleviating immunosuppression. Tumor cells are damaged and trapped into “internal trouble” by combining PDT and energy deprivation, while the sharply enhanced immune cell lethality exposes cancer cells to “outside aggression”. Overall, this photodynamic‐metal‐metabolic immunotherapy provides a promising paradigm for cancer therapy.

Remote ischemic preconditioning prevents high-altitude cerebral edema by enhancing glucose metabolic reprogramming.

Incidence of acute mountain sickness (AMS) ranges from 40%-90%, with high-altitude cerebral edema (HACE) representing a life-threatening end stage of severe AMS. However, practical and convenient preventive strategies for HACE are lacking. Remote ischemic preconditioning (RIPC) has demonstrated preventive effects on ischemia- or hypoxia-induced cardiovascular and cerebrovascular diseases. This study aimed to investigate the potential molecular mechanism of HACE and the application of RIPC in preventing HACE onset. A hypobaric hypoxia chamber was used to simulate a high-altitude environment of 7000 meters. Metabolomics and metabolic flux analysis were employed to assay metabolite levels. Transcriptomics and quantitative real-time PCR (q-PCR) were used to investigate gene expression levels. Immunofluorescence staining was performed on neurons to label cellular proteins. The fluorescent probes Mito-Dendra2, iATPSnFR1.0, and CMTMRos were used to observe mitochondria, ATP, and membrane potential in cultured neurons, respectively. TUNEL staining was performed to detect and quantify apoptotic cell death. Hematoxylin and eosin (H&E) staining was utilized to analyze pathological changes, such as tissue swelling in cerebral cortex samples. The Rotarod test was performed to assess motor coordination and balance in rats. Oxygen-glucose deprivation (OGD) of cultured cells was employed as an invitro model to simulate the hypoxia and hypoglycemia induced by RIPC in animal experiments. We revealed a causative perturbation of glucose metabolism in the brain preceding cerebral edema. Ischemic preconditioning treatment significantly reprograms glucose metabolism, ameliorating cell apoptosis and hypoxia-induced energy deprivation. Notably, ischemic preconditioning improves mitochondrial membrane potential and ATP production through enhanced glucose-coupled mitochondrial metabolism. Invivo studies confirm that RIPC alleviates cerebral edema, reduces cell apoptosis induced by high-altitude hypoxia, and improves motor dysfunction resulting from cerebral edema. Our study elucidates the metabolic basis of HACE pathogenesis. This study provides a new strategy for preventing HACE that RIPC reduces brain edema through reprogramming metabolism, highlighting the potential of targeting metabolic reprogramming for neuroprotective interventions in neurological diseases caused by ischemia or hypoxia.

Targeting SDG7: Identifying heterogeneous energy dilemmas for socially disadvantaged groups in India using machine learning

To achieve Sustainable Development Goal (SDG) 7, prioritizing the socially disadvantaged segments of the population is imperative, given their inherent susceptibility to heightened risks of energy exclusion. However, a comprehensive understanding of the diverse energy challenges faced by households with socio-economic disparities remains elusive. This article thus addresses this gap by examining three widely acknowledged categories of marginalized households in India: racial inferiority, income poverty, and gender inequality. It notably pioneers the quantification of an umbrella pattern of energy deprivation within the SDG7 framework, encompassing energy unaffordability, energy unreliability, energy inaccessibility, and energy inequality. To do so, leveraging the latest household survey dataset and employing least squares estimates, we preliminarily capture that these three disadvantaged groups encounter significant energy barriers in the pursuit of SDG7 achievement. Given respectively selected models based on Least Absolute Shrinkage and Selection Operator (LASSO) approach, the gradient boosting model (GBM), another state-of-the-art machine learning technique, is subsequently adopted to verify feature significance and rank its importance in determining diverse energy deprivation faced by each group. The results reveal that the disadvantaged caste groups and those experiencing greater gender inequality encounter the greatest impediments to their right to reliable energy access. In comparison, energy unaffordability poses a paramount challenge for low-income households. These findings enable policymakers to design straightforward interventions that address a spectrum of socio-economic disparities, thereby fostering an just energy transition grounded in data-driven evidence.

Fasting-induced activity changes in MC3R neurons of the paraventricular nucleus of the thalamus.

The brain controls energy homeostasis by regulating food intake through signaling within the melanocortin system. Whilst we understand the role of the hypothalamus within this system, how extra-hypothalamic brain regions are involved in controlling energy balance remains unclear. Here we show that the melanocortin 3 receptor (MC3R) is expressed in the paraventricular nucleus of the thalamus (PVT). We tested whether fasting would change the activity of MC3R neurons in this region by assessing the levels of c-Fos and pCREB as neuronal activity markers. We determined that overnight fasting causes a significant reduction in pCREB levels within PVT-MC3R neurons. We then questioned whether perturbation of MC3R signaling, during fasting, would result in altered refeeding. Using chemogenetic approaches, we show that modulation of MC3R activity, during the fasting period, does not impact body weight regain or total food intake in the refeeding period. However, we did observe significant differences in the pattern of feeding-related behavior. These findings suggest that the PVT is a region where MC3R neurons respond to energy deprivation and modulate refeeding behavior.

Administration of bicarbonates through percutaneous gastrostomy with continuous nocturnal infusion in a patient with Kearns-Sayre disease: a life changing therapeutical paradigm

BackgroundMitochondrial diseases (MDs) are systemic disorders that can affect multiple organs. Renal manifestations, including renal tubular acidosis, are common because kidneys are particularly vulnerable to energy deprivation. Treatment of MDs is often complex and electrolyte replacement can be difficult especially in pediatric patients, because large and repeated amounts of oral supplements are needed but are not well tolerated.Case presentationWe describe the case of a girl affected by Kearns-Sayre disease with severe renal tubular acidosis. The management of her metabolic acidosis was challenging because she showed persistent low levels of serum bicarbonates despite a progressive incrementation of oral bicarbonates. Furthermore, as a result to the ingestion of large amounts of alkali, the girl developed an aversion to oral supplementation. After positioning a percutaneous gastrostomy (PEG) and starting enteral administration of bicarbonates (with daily boluses and continuous nocturnal infusion), she finally obtained an adequate electrolyte control, with a significant increase in her quality of life.ConclusionsIn MDs, the combination of nocturnal continuous enteral administration of alkali plus diurnal boluses may represent a valid solution to correct metabolic acidosis. It can also result in an improved patients’ quality of life, particularly in pediatric settings, where compliance to oral therapy is often lacking due to the large and repeated amounts of unpalatable bicarbonates solutions required.

Energy Poverty and Women’s Economic Well-Being in Global South: Evidence from Burkina Faso

Although the relationship between household access to energy and economic well-being has received increasing attention in recent years, studies of this link have generally focused on unidimensional measures of fuel poverty. What is the link between multidimensional energy poverty and women’s economic well-being? Using data from the Continuous Multisectoral Survey on Household Living Conditions, this paper focuses on quantifying energy poverty and its effect on the economic well-being of households, particularly women, in Burkina Faso within a multidimensional framework. The results indicate that 84% of households are in a situation of multidimensional energy poverty. These energy-poor households are deprived, on average in 67.01% of the indicators. The results of the econometric estimations show that an increase in multidimensional energy deprivation is associated with a decrease in women’s economic well-being. Given that energy poverty reduces women’s economic well-being, they should be given priority in the implementation of energy policies.

Household energy deprivation and inequality in school enrolment: evidence from Burkina Faso

Household energy deprivation and inequality in school enrolment: evidence from Burkina Faso

Energy deprivation to financial prosperity: Unveiling multidimensional energy Poverty's influence

The purpose of this research is to assess how energy poverty affects an individual's social wellbeing and financial constraints. The present research examines the effects of energy deprivation on a family's well-being, educational attainment, and economic advancement using survey data from PSLM (Pakistan Social and Living Standard Measurement). The investigation's empirical findings imply that a household's needs for energy are directly correlated with the fuel type they use and how little or expensively they rely on renewable energy. The consequent implications of energy dependence on family prosperity are significant. Energy-poor households have been shown to be more prone to experience respiratory illnesses, pay more for health care, drop out of school, and have less employment opportunities.

Dynamic linkages between human capital, natural resources, and economic growth – Impact on achieving sustainable development goals

This study examines the impact of economic growth, trade dynamics, natural resources, human capital, and sustainable development from 1990 to 2022. To capture the complexity of these factors, we utilize a Novel Dynamic Semi-parametric Additive Panel model. Additionally, we employ a Dynamic panel thresholds model to explore the sensitivity of natural resources to economic development across various indices, addressing a gap in previous nonlinear technique studies. Our findings diverge from conventional financial development and economic growth theories. While increasing money may boost trade and development, it could hinder sustainable development. Interestingly, the relationship between financial market expansion, economic improvement, and natural resource use follows an inverse “U-shaped” non-linear pattern. Furthermore, the expansion of the financial sector significantly affects the interplay between human capital and natural resources. As thresholds of growth in financial markets rise, economic growth contributes more to sustainable development, mitigating its negative impact. Several implications emerge, particularly regarding minimizing energy deprivation through global economic and developmental strategies.

Total and H-specific GDF-15 levels increase in caloric deprivation independently of leptin in humans

Mitochondrial-secreted growth differentiation factor-15 (GDF-15) promotes weight loss in animals. Its effects in humans remain unclear, due to limited research and potential measurement interference from the H202D-variant. Our post-hoc analysis investigates total (irrespective of genetic variants) and H-specific GDF-15 (detected only in H202D-variant absence) in humans under acute and chronic energy deprivation, examining GDF-15 interaction with leptin (energy homeostasis regulator) and GDF-15 biologic activity modulation by the H202D-variant. Total and H-specific GDF-15 increased with acute starvation, and total GDF-15 increased with chronic energy deprivation, compared with healthy subjects and regardless of leptin repletion. Baseline GDF-15 positively correlated with triglyceride-rich particles and lipoproteins. During acute metabolic stress, GDF-15 associations with metabolites/lipids appeared to differ in subjects with the H202D-variant. Our findings suggest GDF-15 increases with energy deprivation in humans, questioning its proposed weight loss and suggesting its function as a mitokine, reflecting or mediating metabolic stress response.