Nutrient Overload Research Articles

Review of current and new drugs for the treatment of metabolic-associated fatty liver disease.

In the past 3 decades, metabolic-associated fatty liver disease (MAFLD) has emerged as a widespread liver condition, with its global prevalence on the rise. It ranks as a leading contributor to hepatocellular carcinoma (HCC) and necessitates liver transplantation. Under the multiple parallel hits model, the pathogenesis of MAFLD stems from various liver stressors, notably nutrient overload and sedentary lifestyles. While medical management for MAFLD is well-established, encompassing non-pharmaceutical and pharmaceutical interventions, determining the most effective pharmaceutical therapy has remained elusive. This review discusses diabetic medications for MAFLD treatment, emphasizing recent studies and emerging drugs while reviewing other nondiabetic agents. Emerging evidence suggests that combination therapies hold promise for resolving MAFLD and metabolic steatohepatitis (MASH) while managing side effects. Ongoing trials play a pivotal role in elucidating the effects of mono, dual, and triple receptor agonists in individuals with MASH. With the rising burden of MAFLD/MASH and its severe consequences, the need for effective treatments is more pressing than ever. This review provides a comprehensive overview of the current landscape of pharmaceutical interventions for MAFLD and MASH, shedding light on the potential of newer drugs especially diabetic medications and the importance of ongoing research in this field.

Analysing Consequences of Aquaculture in Coastal Water Bodies of Ba Ria– Vung Tau, Vietnam on Sustainable Development Goals for Environmental Management

Aquaculture is vital for global food security and economic growth, particularly in coastal regions like Ba Ria – Vung Tau, Vietnam. This province has seen significant aquaculture growth, with production rising from 10,687 tons in 2010 to 20,486 tons in 2022. Key species farmed include brackish water shrimp, marine finfish, and mollusks, using methods such as cage culture, pond farming, and Integrated Multi-Trophic Aquaculture (IMTA). However, aquaculture poses environmental challenges, including conflicts over coastal space, waste management, and habitat degradation. Species like oysters and mussels help improve water quality and support balanced ecosystems, while marine finfish farming can cause nutrient overload and eutrophication. Sustainable practices like IMTA, waste management, and sustainable feed use are essential to mitigate these impacts. Aligning aquaculture with Sustainable Development Goals (SDGs), especially SDG 14 (Life Below Water), SDG 12 (Responsible Consumption and Production), and SDG 13 (Climate Action), is crucial for sustainable coastal management. This requires robust regulations, multi-stakeholder collaboration, and the integration of scientific research into policy. By ensuring aquaculture practices support SDGs, Ba Ria – Vung Tau can enhance environmental stewardship, economic resilience, and the sustainable coexistence of human activities with marine ecosystems.

NOX4-reactive oxygen species axis: critical regulators of bone health and metabolism.

Bone marrow stromal cells (BMSCs) play a significant role in bone metabolism as they can differentiate into osteoblasts, bone marrow adipocytes (BMAds), and chondrocytes. BMSCs chronically exposed to nutrient overload undergo adipogenic programming, resulting in bone marrow adipose tissue (BMAT) formation. BMAT is a fat depot transcriptionally, metabolically, and morphologically distinct from peripheral adipose depots. Reactive oxygen species (ROS) are elevated in obesity and serve as important signals directing BMSC fate. ROS produced by the NADPH oxidase (NOX) family of enzymes, such as NOX4, may be responsible for driving BMSC adipogenesis at the expense of osteogenic differentiation. The dual nature of ROS as both cellular signaling mediators and contributors to oxidative stress complicates their effects on bone metabolism. This review discusses the complex interplay between ROS and BMSC differentiation in the context of metabolic bone diseases.Special attention is paid to the role of NOX4-ROS in regulating cellular processes within the bone marrow microenvironment and potential target in metabolic bone diseases.

Vermicompost Effects on Soil Chemistry and Biology: Correlations with Basil's (Ocimum basilicum L.) Total Phenolic Content and Phenological Traits

This study explores the effects of vermicompost on the chemical and biological properties of soils, their nutrient content, and the impact on the growth and phenolic content of basil (Ocimum basilicum L.). Using a controlled experimental setup, we tested five dosages of vermicompost (0%, 4%, 12%, 20%, and 24%) to evaluate their influence on soil biological activity by measuring basal respiration (CO2-C), microbial biomass C (MBC-C), and dehydrogenase enzyme activity (DHA) as well as on basil's growth parameters and total phenolic content (TPC). The results show that vermicompost addition to soil enhanced soil microbial activity in direct proportion to the dose of vermicompost. The application of lower dosages of vermicompost (4% and 12%) significantly enhanced both fresh and dry weights, suggesting an improvement in nutrient uptake and soil structure, which likely facilitated better root growth and nutrient absorption. However, higher dosages (20% and 24%) were associated with reduced growth metrics, likely due to nutrient overload or salt stress. Notably, the highest vermicompost concentration (24%) led to a substantial increase in total phenolic content (TPC) in basil leaves, correlating with decreased growth metrics. This response indicates the plant's defensive mechanism against oxidative stress caused by excess nutrients or salinity from the vermicompost. A multiple regression analysis following a correlation analysis also revealed an inversely proportional relationship between phosphorus content in the soil and total phenolic content in basil leaves. Our findings illustrate that while moderate vermicompost dosages optimize plant growth and health, higher concentrations can strategically enhance phenolic content due to nutrient overload or salt-induced stress. These results offer critical insights for tailoring organic amendment applications to balance plant growth and biochemical properties in agricultural practices.

Ca2+ signaling and metabolic stress-induced pancreatic β-cell failure.

Early in the development of Type 2 diabetes (T2D), metabolic stress brought on by insulin resistance and nutrient overload causes β-cell hyperstimulation. Herein we summarize recent studies that have explored the premise that an increase in the intracellular Ca2+ concentration ([Ca2+]i), brought on by persistent metabolic stimulation of β-cells, causes β-cell dysfunction and failure by adversely affecting β-cell function, structure, and identity. This mini-review builds on several recent reviews that also describe how excess [Ca2+]i impairs β-cell function.

Decreasing Intracellular Entropy by Increasing Mitochondrial Efficiency and Reducing ROS Formation-The Effect on the Ageing Process and Age-Related Damage.

A hypothesis is presented to explain how the ageing process might be influenced by optimizing mitochondrial efficiency to reduce intracellular entropy. Research-based quantifications of entropy are scarce. Non-equilibrium metabolic reactions and compartmentalization were found to contribute most to lowering entropy in the cells. Like the cells, mitochondria are thermodynamically open systems exchanging matter and energy with their surroundings-the rest of the cell. Based on the calculations from cancer cells, glycolysis was reported to produce less entropy than mitochondrial oxidative phosphorylation. However, these estimations depended on the CO2 concentration so that at slightly increased CO2, it was oxidative phosphorylation that produced less entropy. Also, the thermodynamic efficiency of mitochondrial respiratory complexes varies depending on the respiratory state and oxidant/antioxidant balance. Therefore, in spite of long-standing theoretical and practical efforts, more measurements, also in isolated mitochondria, with intact and suboptimal respiration, are needed to resolve the issue. Entropy increases in ageing while mitochondrial efficiency of energy conversion, quality control, and turnover mechanisms deteriorate. Optimally functioning mitochondria are necessary to meet energy demands for cellular defence and repair processes to attenuate ageing. The intuitive approach of simply supplying more metabolic fuels (more nutrients) often has the opposite effect, namely a decrease in energy production in the case of nutrient overload. Excessive nutrient intake and obesity accelerate ageing, while calorie restriction without malnutrition can prolong life. Balanced nutrient intake adapted to needs/activity-based high ATP requirement increases mitochondrial respiratory efficiency and leads to multiple alterations in gene expression and metabolic adaptations. Therefore, rather than overfeeding, it is necessary to fine-tune energy production by optimizing mitochondrial function and reducing oxidative stress; the evidence is discussed in this paper.

IDF23-0273 Nutrient overload and insulin resistance can precede reductions in mitochondrial respiration in omental adipose tissue

IDF23-0273 Nutrient overload and insulin resistance can precede reductions in mitochondrial respiration in omental adipose tissue

The impact of bed rest on human skeletal muscle metabolism

Insulin sensitivity and metabolic flexibility decrease in response to bed rest, but the temporal and causal adaptations in human skeletal muscle metabolism are not fully defined. Here, we use an integrative approach to assess human skeletal muscle metabolism during bed rest and provide a multi-system analysis of how skeletal muscle and the circulatory system adapt to short- and long-term bed rest (German Clinical Trials: DRKS00015677). We uncover that intracellular glycogen accumulation after short-term bed rest accompanies a rapid reduction in systemic insulin sensitivity and less GLUT4 localization at the muscle cell membrane, preventing further intracellular glycogen deposition after long-term bed rest. We provide evidence of a temporal link between the accumulation of intracellular triglycerides, lipotoxic ceramides, and sphingomyelins and an altered skeletal muscle mitochondrial structure and function after long-term bed rest. An intracellular nutrient overload therefore represents a crucial determinant for rapid skeletal muscle insulin insensitivity and mitochondrial alterations after prolonged bed rest.

Excessive or sustained endoplasmic reticulum stress: one of the culprits of adipocyte dysfunction in obesity.

As the prevalence of obesity continues to rise globally, the research on adipocytes has attracted more and more attention. In the presence of nutrient overload, adipocytes are exposed to pressures such as hypoxia, inflammation, mechanical stress, metabolite, and oxidative stress that can lead to organelle dysfunction. Endoplasmic reticulum (ER) is a vital organelle for sensing cellular pressure, and its homeostasis is essential for maintaining adipocyte function. Under conditions of excess nutrition, ER stress (ERS) will be triggered by the gathering of abnormally folded proteins in the ER lumen, resulting in the activation of a signaling response known as the unfolded protein responses (UPRs), which is a response system to relieve ERS and restore ER homeostasis. However, if the UPRs fail to rescue ER homeostasis, ERS will activate pathways to damage cells. Studies have shown a role for disturbed activation of adipocyte ERS in the pathophysiology of obesity and its complications. Prolonged or excessive ERS in adipocytes can aggravate lipolysis, insulin resistance, and apoptosis and affect the bioactive molecule production. In addition, ERS also impacts the expression of some important genes. In view of the fact that ERS influences adipocyte function through various mechanisms, targeting ERS may be a viable strategy to treat obesity. This article summarizes the effects of ERS on adipocytes during obesity.

NADPH oxidase 4 in mouse β cells participates in inflammation on chronic nutrient overload.

By exposing mice carrying a deletion of NADPH oxidase isoform 4, NOX4, specifically in pancreatic β cells (βNOX4-/-) to nutrient excess stimulated by a high-fat diet (HFD), this study aimed to elucidate the role of β-cell redox status in the development of meta-inflammation within the diabetic phenotype. The authors performed basic phenotyping of βNOX4-/- mice on HFD involving insulin and glycemic analyses, histochemistry of adipocytes, indirect calorimetry, and cytokine analyses. To characterize local inflammation, the study used caspase-1 activity assay, interleukin-1β immunochemistry, and real-time polymerase chain reaction during coculturing of β cells with macrophages. The phenotype of βNOX4-/- mice on HFD was not associated with hyperinsulinemia and hyperglycemia but showed accumulation of excessive lipids in epididymal fat and β cells. Surprisingly, mice showed significantly reduced systemic inflammation. Decreased interleukin-1β protein levels and downregulated NLRP3-inflammasome activity were observed on chronic glucose overload in βNOX4-/- isolated islets and NOX4-silenced INS1-E cells resulting in attenuated proinflammatory polarization of macrophages/monocytes in vitro and in situ and reduced local islet inflammation. Experimental evidence suggests that NOX4 pro-oxidant activity in β cells is involved in NLRP3-inflammasome activation during chronic nutrient overload and participates in local inflammatory signaling and perhaps toward peripheral tissues, contributing to a diabetic inflammatory phenotype.

In Silico identification of novel phytochemicals that target SFRP4: An early biomarker of diabesity.

The simultaneous coexistence of complicated metabolic conditions like obesity and diabetes within an individual is known as diabesity. Obesity is the key factor for many chronic diseases, including insulin resistance and type 2 diabetes (T2D). Metabolic stress due to nutrient overload releases different inflammatory mediators. Secreted frizzled-related protein 4 (SFRP4) is also an inflammatory mediator that impairs insulin secretion. SFRP4 acts as an early biomarker for diabesity expressed with interleukin-1 beta (IL-1β) in the adipose tissues that hinder the exocytosis of insulin-secreting granules from the pancreatic β-cells and is a potential target for preserving β-cell dysfunction and the diabesity treatment. The current study aimed to screen potential bioactive compounds targeting and inhibiting the diabesity-linked SFRP4 protein through an in silico approach. The three-dimensional (3D) structure of human SFRP4 was predicted through comparative modeling techniques and evaluated by various online bioinformatics tools. The molecular docking and MD simulation investigations were carried out against phytochemicals with anti-diabetic and anti-obesity properties to shortlist the best SFRP4 inhibitor. Hesperetin, Curcumin, Isorhamnetin, Embelin, Epicatechin, and Methyl Eugenol interacted strongly with SFRP4 by displaying zero RMSD and binding affinities of -6.5, -6.4, -6.3, -5.3, -6.3 and -5.8 kcal/mol respectively. Additionally, the root mean square fluctuation and root mean square deviation graphs from the MD simulation results demonstrated that hesperetin has good variations throughout the simulation period as compared to others. This dynamic stability and control behavior of hesperetin, when it interacts with SFRP4, shows that it has the potential to modulate the function and activity of the protein. Therefore, hesperetin is identified as an effective and top drug candidate through this analysis for preserving beta-cell function and treating diabesity by targeting SFRP4. The findings of this study could be useful in the design and development of diabesity drugs.

ABHD4 regulates adipocyte differentiation in vitro but does not affect adipose tissue lipid metabolism in mice

Alpha/beta hydrolase domain-containing protein 4 (ABHD4) catalyzes the deacylation of N-acyl phosphatidyl-ethanolamine (NAPE) and lyso-NAPE to produce glycerophospho-N-acyl ethanolamine (GP-NAE). Through a variety of metabolic enzymes, NAPE, lyso-NAPE, and GP-NAE are ultimately converted into NAE, a group of bioactive lipids that control many physiological processes including inflammation, cognition, food intake, and lipolysis (i.e., oleoylethanolamide or OEA). In a diet-induced obese mouse model, adipose tissue Abhd4 gene expression positively correlated with adiposity. However, it is unknown whether Abhd4 is a causal or a reactive gene to obesity. To fill this knowledge gap, we generated an Abhd4 knockout (KO) 3T3-L1 pre-adipocyte. During adipogenic stimulation, Abhd4 KO pre-adipocytes had increased adipogenesis and lipid accumulation, suggesting Abhd4 is responding to (a reactive gene), not contributing to (not a causal gene), adiposity, and may serve as a mechanism for protecting against obesity. However, we did not observe any differences in adiposity and metabolic outcomes between whole-body Abhd4 KO or adipocyte-specific Abhd4 KO mice and their littermate control mice (both male and female) on chow or a high-fat diet. This might be because we found that deletion of Abhd4 did not affect NAE such as OEA production, even though Abhd4 was highly expressed in adipose tissue and correlated with fasting adipose OEA levels and lipolysis. These data suggest that ABHD4 regulates adipocyte differentiation in vitro but does not affect adipose tissue lipid metabolism in mice despite nutrient overload, possibly due to compensation from other NAPE and NAE metabolic enzymes.

Cell lipid droplet heterogeneity and altered biophysical properties induced by cell stress and metabolic imbalance

Lipid droplets (LD) are important regulators of lipid metabolism and are implicated in several diseases. However, the mechanisms underlying the roles of LD in cell pathophysiology remain elusive. Hence, new approaches that enable better characterization of LD are essential. This study establishes that Laurdan, a widely used fluorescent probe, can be used to label, quantify, and characterize changes in cell LD properties. Using lipid mixtures containing artificial LD we show that Laurdan GP depends on LD composition. Accordingly, enrichment in cholesterol esters (CE) shifts Laurdan GP from ∼0.60 to ∼0.70. Moreover, live-cell confocal microscopy shows that cells present multiple LD populations with distinctive biophysical features. The hydrophobicity and fraction of each LD population are cell type dependent and change differently in response to nutrient imbalance, cell density, and upon inhibition of LD biogenesis. The results show that cellular stress caused by increased cell density and nutrient overload increased the number of LD and their hydrophobicity and contributed to the formation of LD with very high GP values, likely enriched in CE. In contrast, nutrient deprivation was accompanied by decreased LD hydrophobicity and alterations in cell plasma membrane properties. In addition, we show that cancer cells present highly hydrophobic LD, compatible with a CE enrichment of these organelles. The distinct biophysical properties of LD contribute to the diversity of these organelles, suggesting that the specific alterations in their properties might be one of the mechanisms triggering LD pathophysiological actions and/or be related to the different mechanisms underlying LD metabolism.

Chitosan and Zinc Oxide Nanoparticle-Enhanced Tripolyphosphate Modulate Phosphorus Leaching in Soil

Phosphorus (P) loss from agro-ecosystems impinges upon P use efficiency by plants and thereby constitutes both agronomic and environmental nuisances. Herein, we report on the potential for controlling P leaching loss and application in crop fertilization through repurposing and nano-functionalizing tripolyphosphate (TPP) as a sole P source. The developed TPP-Chitosan and TPP-Chitosan-ZnO nanofertilizers exhibited positive surface charges, 5.8 and 13.8 mV, and hydrodynamic sizes of 430 and 301 nm, respectively. In soil, nanoformulations of TPP-Chitosan and TPP-Chitosan-ZnO significantly reduced cumulative P leaching during 72 h, reaching 91 and 97% reductions, respectively, compared to a conventional fertilizer, monoammonium phosphate (MAP). Cumulative P leaching after 72 h from these nanofertilizers was, respectively, 84 and 95% lower than from TPP alone. TPP-Chitosan-ZnO was, overall, 65% more effective in reducing P leaching, compared to TPP-Chitosan. Relative to MAP, the wheat plant height was significantly increased by TPP-Chitosan-ZnO by 33.0%. Compared to MAP, TPP-Chitosan and TPP-Chitosan-ZnO slightly increased wheat grain yield by 21 and 30%, respectively. Notably, TPP-Chitosan-ZnO significantly decreased shoot P levels, by 35.5, 47, and 45%, compared to MAP, TPP, and TPP-Chitosan, respectively. Zn release over 72 h from TPP-Chitosan-ZnO was considerably lower, compared to a control, ZnO nanoparticles, and averaged, respectively, 34.7 and 0.065 mg/L, which was 534 times higher for the former. Grain Zn was significantly higher in the TPP-Chitosan treatment, relative to MAP. TPP-Chitosan also significantly mobilized the resident K, S, Mg, and Ca from soil into the plant, helping to improve the overall nutritional quality and supporting the role of chitosan in nutrient mobilization. Taken together, our data highlight the potential for repurposing a non-fertilizer P material, TPP, for agricultural and environmental applications and the effect of applying nanotechnology on such outcomes. Broadly speaking, the reduction in P loss is critical for controlling the eutrophication of water bodies due to nutrient overload and for sustaining the dwindling global P resources.

Effect of Nutrient Improvement and Mineral Premix Supplementation on Weight, Average Daily Gain, and Metabolite Profile of Repeat Breeder Cows

Nutrient overload, deficiency, or imbalance are fundamental issues that frequently arises in breeder cows. Malnutrition in cattle can cause delayed puberty, an increased risk of pregnancy failure, and infertility. This study aimed to determine the effect of nutrient improvement and mineral premix supplementation on body weight, average daily gain, and blood metabolite profile of repeat breeder cattle. Sixteen Simmental Cross cattle aged 4 to 5 years (calved at least once) with an average S/C of 5 and an average body weight of 400 kg were used. The feed provided was forage, Profeed® concentrate, High Quality Feed Supplement (HQFS) and mineral premix. This study was initiated by selecting repeat breeder cattle of smallholder farmers. The selected cattle were reared for three months in the research cage with a predetermined feed for each group. During the research period, four weighings were carried out to determine the body weight of the cattle. Blood samples were taken for testing of the blood metabolite profile; at the beginning and end of the study. The collected samples were then analyzed in the laboratory, and the resulting data was analyzed for variance using the independent-t-test and paired t-test. The results showed that the addition of 0.5% mineral premix had no significant effect (P > 0.05) on body weight gain. In the blood metabolite profile, the improvement in nutrition had a significant effect (P<0.05) on glucose levels (H-0 and H-71). It can be concluded that the supplementation of 0.5% mineral premix has no effect on body weight and blood metabolite profiles. Repeat breeder cattle on smallholder farmers have low glucose levels, so improving nutrition (quality and quantity) is a matter of concern to support pregnancy.

Adiponectin reverses β-Cell damage and impaired insulin secretion induced by obesity.

Obesity significantly decreases life expectancy and increases the incidence of age-related dysfunctions, including β-cell dysregulation leading to inadequate insulin secretion. Here, we show that diluted plasma from obese human donors acutely impairs β-cell integrity and insulin secretion relative to plasma from lean subjects. Similar results were observed with diluted sera from obese rats fed ad libitum, when compared to sera from lean, calorically restricted, animals. The damaging effects of obese circulating factors on β-cells occurs in the absence of nutrient overload, and mechanistically involves mitochondrial dysfunction, limiting glucose-supported oxidative phosphorylation and ATP production. We demonstrate that increased levels of adiponectin, as found in lean plasma, are the protective characteristic preserving β-cell function; indeed, sera from adiponectin knockout mice limits β-cell metabolic fluxes relative to controls. Furthermore, oxidative phosphorylation and glucose-sensitive insulin secretion, which are completely abrogated in the absence of this hormone, are restored by the presence of adiponectin alone, surprisingly even in the absence of other serological components, for both the insulin-secreting INS1 cell line and primary islets. The addition of adiponectin to cells treated with plasma from obese donors completely restored β-cell functional integrity, indicating the lack of this hormone was causative of the dysfunction. Overall, our results demonstrate that low circulating adiponectin is a key damaging element for β-cells, and suggest strong therapeutic potential for the modulation of the adiponectin signaling pathway in the prevention of age-related β-cell dysfunction.

Algal Bloom Ties: Spreading Network Inference and Extreme Eco-Environmental Feedback

Coastal marine ecosystems worldwide are increasingly affected by tide alterations and anthropogenic disturbances affecting the water quality and leading to frequent algal blooms. Increased bloom persistence is a serious threat due to the long-lasting impacts on ecological processes and services, such as carbon cycling and sequestration. The exploration of eco-environmental feedback and algal bloom patterns remains challenging and poorly investigated, mostly due to the paucity of data and lack of model-free approaches to infer universal bloom dynamics. Florida Bay, taken as an epitome for biodiversity and blooms, has long experienced algal blooms in its central and western regions, and, in 2006, an unprecedented bloom occurred in the eastern habitats rich in corals and vulnerable habitats. With global aims, we analyze the occurrence of blooms in Florida Bay from three perspectives: (1) the spatial spreading networks of chlorophyll-a (CHLa) that pinpoint the source and unbalanced habitats; (2) the fluctuations of water quality factors pre- and post-bloom outbreaks to assess the environmental impacts of ecological imbalances and target the prevention and control of algal blooms; and (3) the topological co-evolution of biogeochemical and spreading networks to quantify ecosystem stability and the likelihood of ecological shifts toward endemic blooms in the long term. Here, we propose the transfer entropy (TE) difference to infer salient dynamical inter actions between the spatial areas and biogeochemical factors (ecosystem connectome) underpinning bloom emergence and spread as well as environmental effects. A Pareto principle, defining the top 20% of areal interactions, is found to identify bloom spreading and the salient eco-environmental interactions of CHLa associated with endemic and epidemic regimes. We quantify the spatial dynamics of algal blooms and, thus, obtain areas in critical need for ecological monitoring and potential bloom control. The results show that algal blooms are increasingly persistent over space with long-term negative effects on water quality factors, in particular, about how blooms affect temperature locally. A dichotomy is reported between spatial ecological corridors of spreading and biogeochemical networks as well as divergence from the optimal eco-organization: randomization of the former due to nutrient overload and temperature increase leads to scale-free CHLa spreading and extreme outbreaks a posteriori. Subsequently, the occurrence of blooms increases bloom persistence, turbidity and salinity with potentially strong ecological effects on highly biodiverse and vulnerable habitats, such as tidal flats, salt-marshes and mangroves. The probabilistic distribution of CHLa is found to be indicative of endemic and epidemic regimes, where the former sets the system to higher energy dissipation, larger instability and lower predictability. Algal blooms are important ecosystem regulators of nutrient cycles; however, chlorophyll-a outbreaks cause vast ecosystem impacts, such as aquatic species mortality and carbon flux alteration due to their effects on water turbidity, nutrient cycling (nitrogen and phosphorus in particular), salinity and temperature. Beyond compromising the local water quality, other socio-ecological services are also compromised at large scales, including carbon sequestration, which affects climate regulation from local to global environments. Yet, ecological assessment models, such as the one presented, inferring bloom regions and their stability to pinpoint risks, are in need of application in aquatic ecosystems, such as subtropical and tropical bays, to assess optimal preventive controls.

Topic: Environmental Impacts of the US-China Trade War and Possible Solutions

The US-China trade war has been in the spotlight since 2018. However, many papers have only examined the economic issues arising from the trade war without paying much attention to the impact it has on the environment. This paper focuses on the environmental impact of the trade war on the two direct participants, which are China and the United States. It is concluded that the main environmental impact suffered by China is the increase in carbon emissions. This has led to an increase in domestic temperatures, which further leads to economic and social problems for vulnerable populations. This can be addressed through two policies, which are using green premium to implement targeted policy and investing more into the research of the new energy industry. Furthermore, the decrease in soybean production in the United States has led to environmental problems of over-nutrition and increased demand for blue water, which can further lead to water scarcity, triggering a reduction in farmers' income and a decrease in GDP. In this regard, different regulatory standards set in each state to monitor water quality can protect and enhance water quality in watersheds. in addition, investing money in controlling nutrient overload and water scarcity is also an effective measure. Moreover, this paper gives policy recommendations that governments could take to deal with difficult situations, and an assessment of the different policies mentioned.

Activin receptor ALK4 promotes adipose tissue hyperplasia by suppressing differentiation of adipocyte precursors

Adipocyte hyperplasia and hypertrophy are the two main processes contributing to adipose tissue expansion, yet the mechanisms that regulate and balance their involvement in obesity are incompletely understood. Activin B/GDF-3 receptor ALK7 is expressed in mature adipocytes and promotes adipocyte hypertrophy upon nutrient overload by suppressing adrenergic signaling and lipolysis. In contrast, the role of ALK4, the canonical pan-activin receptor, in adipose tissue is unknown. Here, we report that, unlike ALK7, ALK4 is preferentially expressed in adipocyte precursors, where it suppresses differentiation, allowing proliferation and adipose tissue expansion. ALK4 expression in adipose tissue increases upon nutrient overload and positively correlates with fat depot mass and body weight, suggesting a role in adipose tissue hyperplasia during obesity. Mechanistically, ALK4 signaling suppresses expression of CEBPα and PPARγ, two master regulators of adipocyte differentiation. Conversely, ALK4 deletion enhances CEBPα/PPARγ expression and induces premature adipocyte differentiation, which can be rescued by CEBPα knockdown. These results clarify the function of ALK4 in adipose tissue and highlight the contrasting roles of the two activin receptors in the regulation of adipocyte hyperplasia and hypertrophy during obesity.

Monoacylglycerol O-acyltransferase 1 lowers adipocyte differentiation capacity in vitro but does not affect adiposity in mice.

Monoacylglycerol O-acyltransferase 1 (Mogat1), a lipogenic enzyme that converts monoacylglycerol to diacylglycerol, is highly expressed in adipocytes and may regulate lipolysis by re-esterifying fatty acids released during times when lipolytic rates are low. However, the role of Mogat1 in regulating adipocyte fat storage during differentiation and diet-induced obesity is relatively understudied. Here, adipocyte-specific Mogat1 knockout mice were generated and subjected to a high-fat diet to determine the effects of Mogat1 deficiency on diet-induced obesity. Mogat1 floxed mice were also used to develop preadipocyte cell lines wherein Mogat1 could be conditionally knocked out to study adipocyte differentiation in vitro. In preadipocytes, it was found that Mogat1 knockout at the onset of preadipocyte differentiation prevented the accumulation of glycerolipids and reduced the differentiation capacity of preadipocytes. However, the loss of adipocyte Mogat1 did not affect weight gain or fat mass induced by a high-fat diet in mice. Furthermore, loss of Mogat1 in adipocytes did not affect plasma lipid or glucose concentrations or insulin tolerance. These data suggest Mogat1 may play a role in adipocyte differentiation in vitro but not adipose tissue expansion in response to nutrient overload in mice.