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Migratory birds excel in phenotypic flexibility, adapting physiologically as their life histories and environments require. Discerning the metabolic processes underlying migrants' physiology, an emergent property of multiple continuous and dynamic organism–environment interactions, is therefore challenging, particularly under natural conditions. Accordingly, analyses of snapshot‐sampled serum‐circulating metabolites, versatile and readily applicable for migrating birds, have increasingly become the method of choice for such physiologic inference. However, the atemporal nature of single sampling might obscure the links between observed metabolite concentrations and the processes producing them, necessitating an analytical decoupling of focal processes from their broader biochemical background.In the present study, we examined how variation in combined fat and muscle fuel stores, traits pivotal in migratory context, relates to the serum‐circulating metabolomes of spring‐migrating Eurasian blackcaps stopping‐over. Our analyses accounted for potential spatiotemporal influences in the form of time past night's fasting and random local conditions across three sites within the Negev Desert. We shifted the focus from compound‐level analysis of preselected metabolites towards the level of inclusive metabolome, quantifying serum‐circulating lipophilic and polar molecules via UHPLC–MS/MS untargeted metabolomic technique.Our results indicated a general relationship between fuel stores and the metabolome, comprising 16 326 lipophilic and 6923 polar compounds, among which 918 and 44 were annotated, respectively. By applying generalized latent‐variable linear modeling (GLLVM) upon concentrations of annotated metabolites, we identified several candidate biomarkers, some novel in migratory context, notably the fuel‐associated increase in serum ceramides likely derived from circulating very low‐density lipoproteins (VLDLs). Relying on estimated metabolite links with fuel and foraging time and on modeled residual covariations among metabolites, we demonstrate fuel–metabolite associations generally consistent with higher fat‐ and lower protein mobilization in birds having greater stores and with decreased fuel utilization as ingested nutrients accumulate over time, thus introducing a novel approach for the physiological study of migrating birds. [ABSTRACT FROM AUTHOR]

Simple Summary: The physiology and performance of individuals in a bee colony are directly related to the quality of nutrients available in the colony. A diet enriched with high-quality protein increases the immunity of the colony and the individual bees. In this study, we examined the effect of diets with different protein sources on dietary consumption, vitellogenin (Vg), abdominal lipid content, and hypopharyngeal gland development in adult worker bees. Our results indicate that the use of certain protein sources in bee diets can improve the parameters investigated. Honey bees play an important role in the pollination of flowering plants. When honey bee colonies are deficient in pollen, one of their main nutrients, protein supplements are required. In this study, the effects of diets with six different protein sources on the physiological characteristics of worker bees (vitellogenin (Vg), abdominal lipid content (ALC), hypopharyngeal gland (HPG)) and consumption were investigated. The protein sources of the diets (diet I, ..., diet VI) included pollen, spirulina dust (Arthrospira platensis Gomont), fresh egg yolk, lyophilized lactose-free skimmed milk powder, active fresh yeast, and ApiProtein. It was identified that consumption by worker bees was highest in the diet group supplemented with spirulina (diet II). Although there was no statistical difference regarding the Vg content in the hemolymph, numerically, the highest content was found in diet group IV (lyophilized lactose-free skimmed milk powder) (4.73 ± 0.03 ng/mL). ALC and HPG were highest in the group fed diet II. These results suggest that offering honey bees diets with certain protein sources can support their physiological traits. [ABSTRACT FROM AUTHOR]

Abstract Physical activity (PA) positively influences pregnancy, a critical period for health promotion, and affects placental structure and function in ways previously overlooked. Here, we summarize the current body of literature examining the association between PA, placenta biology, and physiology while also highlighting areas where gaps in knowledge exist. PA during pregnancy induces metabolic changes, influencing nutrient availability and transporter expression in the placenta. Hormones and cytokines secreted during PA contribute to health benefits, with intricate interactions in pro‐ and anti‐inflammatory markers. Extracellular vesicles and placental “‐omics” data suggest that gestational PA can shape placental biology, affecting gene expression, DNA methylation, metabolite profiles, and protein regulation. However, whether cytokines that respond to PA alter placental proteomic profiles during pregnancy remains to be elucidated. The limited research on placenta mitochondria of physically active gestational parents (gesP), has shown improvements in mitochondrial DNA and antioxidant capacity, but the relationship between PA, placental mitochondrial dynamics, and lipid metabolism remains unexplored. Additionally, PA influences the placenta‐immune microenvironment, angiogenesis, and may confer positive effects on neurodevelopment and mental health through placental changes, vascularization, and modulation of brain‐derived neurotrophic factor. Ongoing exploration is crucial for unraveling the multifaceted impact of PA on the intricate placental environment.

Abstract Cardiovascular disease (CVD) is the leading cause of death worldwide. Physical activity interventions improve almost all modifiable CVD risk factors, but the effect of physical activity on low density lipoprotein cholesterol (LDL‐C) is uncertain. This may be due to lack of research on the feeding status in which the physical activity is performed. The aim of this study is to investigate the effect of fasted versus fed exercise on LDL‐C concentrations in males and females. One hundred healthy participants, equal males and females, aged between 25 and 60 years will be recruited and will undergo a home‐based 12‐week exercise intervention. After baseline testing, participants will be randomized to a fasted exercise (exercise after an 8‐h fast) or fed exercise (exercise 90–180 min after ingestion of 1 g kg−1 CHO) group and will perform 50 min of moderate intensity exercise (e.g., 95% heart rate of lactate threshold 1) three times a week either before or after a high carbohydrate (1 g kg−1) meal. Participants will visit the laboratory again at week 4 and week 12 and measurements will be taken for body composition, resting blood pressure, fasting blood glucose, lipid profiles and systemic inflammation, lactate threshold, and 14‐day blood glucose control.

Abstract Background The ability of honeybees to survive and sustain honey production depends on their ability to adapt to their environment. This study evaluated the seasonal fluctuations of antioxidant activities and biochemical compositions of honeybees, Apis mellifera adansonii L. from rainforest, guinea savannah and derived savannah zones of Nigeria during three seasonal periods (onset of rain, wet season and dry season) from January to December, 2017. Honeybees were collected from fully colonized colonies of two different apiaries from each of the ecological zones during the seasonal periods. Amino acid composition was determined using high-performance liquid chromatography. Antioxidant enzymes activity, body protein, glucose and lipid profile were evaluated using standard protocols. Results Seasonal periods showed significant (p 0.05) influence on the body glucose, protein pattern, total cholesterol, activities of malondialdehyde, reduced glutathione, glutathione peroxidase and catalase. Body glucose content in the honeybees from the rainforest and guinea savannah zones was highest during the dry season. Conclusions Antioxidant activities and biochemical compositions of honeybees are differently affected by both ecological zones and seasonal fluctuations.

Temperature is one of the most important environmental conditions affecting physiological processes in ectothermic organisms like ants. Yet, we often lack information on how certain physiological traits covary with temperature across time. Here, we test predictions on how one trait—lipid content—covaries with temperature using a conspicuous, ground-dwelling harvester ant. We focus on lipid content as fat bodies are metabolically active tissues that are important for storing and releasing energy in response to demand, which could be vital for survival under variable temperatures. From March to November, we extracted lipids from surface workers of 14 colonies while simultaneously recording ground temperature. We first assessed if lipid content was highest during cooler temperatures when ants were less active and less metabolically stressed. In doing so, we found that lipid content of ants declined almost 70% from cool months (November lipid content = 14.6%) to hot months (August lipid content = 4.6%). We next assessed if lipid levels from a group of ants collected at a single time point could change by placing individuals into environmental chambers set at 10, 20, and 30°C (i.e. the approximate span of average temperatures from March to November). Temperature again had a significant impact such that after 10 days, lipid content of ants in the hottest chamber (30°C) had decreased by more than 75%. While intraspecific variation in physiological traits often follows seasonal patterns, our results suggest fluctuations in temperature may account for a portion of the variance observed in traits like lipid content. [ABSTRACT FROM AUTHOR]

Background: The ability of honeybees to survive and sustain honey production depends on their ability to adapt to their environment. This study evaluated the seasonal fluctuations of antioxidant activities and biochemical compositions of honeybees, Apis mellifera adansonii L. from rainforest, guinea savannah and derived savannah zones of Nigeria during three seasonal periods (onset of rain, wet season and dry season) from January to December, 2017. Honeybees were collected from fully colonized colonies of two different apiaries from each of the ecological zones during the seasonal periods. Amino acid composition was determined using high-performance liquid chromatography. Antioxidant enzymes activity, body protein, glucose and lipid profile were evaluated using standard protocols. Results: Seasonal periods showed significant (p < 0.05) effect on the eighteen amino acids, superoxide dismutase (SOD), triglycerides and fat-free nitrogen recorded in the honeybees. Amino acids were higher in the honeybees from the rainforest zone, regardless of the seasonal period. SOD and body protein were higher during the wet season in the three ecological zones. However, seasonal periods showed no significant (p > 0.05) influence on the body glucose, protein pattern, total cholesterol, activities of malondialdehyde, reduced glutathione, glutathione peroxidase and catalase. Body glucose content in the honeybees from the rainforest and guinea savannah zones was highest during the dry season. Conclusions: Antioxidant activities and biochemical compositions of honeybees are differently affected by both ecological zones and seasonal fluctuations. [ABSTRACT FROM AUTHOR]

Olive suffers from cold damage when introduced to high-latitude regions from its native warm climes. Therefore, this study aims to improve the adaption of olive to climates in which it is cold for part of the year. The phenotype, physiological performance, nutrient content, and gene expression of olive leaves (from two widely planted cultivars) were examined after cultivation in normal and cold stress conditions. The results showed that the cold-tolerant cultivar possessed stronger photosynthesis efficiency and higher anti-oxidase activity after cold treatment than the cold-sensitive cultivar. Alteration of gene expression and metabolites in the amino acid metabolism, glycerolipid metabolism, diterpenoid biosynthesis, and oleuropein metabolism pathways played an important role in the cold responses of olive. Furthermore, the construction of the network of genes for ubiquitination and metabolites suggested that polyubiquitination contributes most to the stable physiology of olive under cold stress. Altogether, the results of this study can play an important role in helping us to understand the cold hardiness of olive and screen cold-resistant varieties for excellent quality and yield. [ABSTRACT FROM AUTHOR]

The progression of aging affects various blood parameters, which can weaken the viability of the body. Clarification of various aspects of this process requires additional observations, especially with the use of animals. The study was conducted on 43 healthy outbred male rats aged 24 months. Also, 32 healthy outbred male rats 3 months old, which formed the control group, were taken under observation. The examined 24-month-old rats showed standard aging phenomena. In their erythrocytes, there was an increase in lipid peroxidation caused by a weakening of the activity of their antioxidant defense. In the blood of two-year-old rats, there was a decrease in the level of erythrocyte-discocytes. This was accompanied in them by an excess content of erythrocytes in the blood, which had a changed shape to varying degrees. In rats of the older group, erythrocyte aggregation was increased, as indicated by an increase in the numberof erythrocytes that entered the aggregates in the blood and an increase in the number of most erythrocyte aggregates with a decrease in the level of free erythrocytes. For two-year-old rats, low content of erythrocytesdisconcytes in the blood and an excess number of erythrocytes with a modified shape, as well as an increase in their aggregation, are characteristics. An important reason for these changes is the weakening of the antioxidant protection of erythrocytes, leading to a pronounced activation of lipid peroxidation in them. [ABSTRACT FROM AUTHOR]

Background: Metabolic changes induced by the host immune response to pathogens found in patients with community-acquired pneumonia (CAP) may provide insight into its pathogenesis. In this study, we characterized differences in the host metabolic response to common CAP-associated pathogens. Method: Targeted metabolomic profiling was performed on serum samples obtained from hospitalized CAP patients (n = 119) at admission. We quantified 347 unique metabolites across multiple biochemical classes, including amines, acylcarnitines, and signaling lipids. We evaluated if unique associations between metabolite levels and specific CAP-associated pathogens could be identified. Results: Several acylcarnitines were found to be elevated in C. burnetii and herpes simplex virus and lowered in M. pneumoniae as compared to other pathogens. Phenylalanine and kynurenine were found elevated in L. pneumophila as compared to other pathogens. S-methylcysteine was elevated in patients with M. pneumoniae, and these patients also showed lowered cortisol levels in comparison to almost all other pathogens. For the herpes simplex virus, we observed a unique elevation of eicosanoids and several amines. Many lysophosphatidylcholines showed an altered profile in C. burnetii versus S. pneumoniae, L. pneumophila, and respiratory syncytial virus. Finally, phosphatidylcholines were negatively affected by the influenza virus in comparison to S. pneumoniae. Conclusions: In this exploratory analysis, metabolites from different biochemical classes were found to be altered in serum samples from patients with different CAP-associated pathogens, which may be used for hypothesis generation in studies on differences in pathogen host response and pathogenesis of CAP.

Introduction: The role of dietary fat in the evolution of cardiometabolic disorders is highly controversial. As both dietary intake and the development of cardiometabolic risk differ by sex, we evaluated sex-specific differences in the associations between dietary fats (saturated and unsaturated) and four key cardiometabolic risk factors—lipid profiles, body fat, inflammation, and glucose regulation.Methods: We included 2391 women and men aged ≥30 years in the prospective Framingham Offspring Cohort. Weight-adjusted dietary fats (saturated, monounsaturated, and polyunsaturated fats, including omega-3 and omega-6) were derived from 3-day dietary records. Analysis of covariance was used to derive adjusted mean levels of all outcomes.Results: In both men and women, intakes of saturated and monounsaturated fats were inversely associated with TG:HDL ratio (p < 0.02 for both types of fat). In women, higher omega-3 and omega-6 PUFAs were also inversely associated with TG:HDL (p < 0.05 for both), but for men, only omega-3 PUFAs were associated (p = 0.026). All types of dietary fat were beneficially associated with larger HDL particle sizes in both men and women, while only saturated and monounsaturated fats were associated with larger LDL particles in men. In addition, saturated and monounsaturated fats were associated with statistically significantly higher concentrations of HDL and lower concentrations of LDL and VLDL particles in both sexes, while polyunsaturated fat had favorable associations in women only. Saturated fat also had beneficial associations with three measures of body fat. For example, women with the highest (vs. lowest) saturated fat intake had a lower BMI (27.7 ± 0.25 vs. 26.2 ± 0.36 kg/m2, p = 0.001); findings were similar in men (28.2 ± 0.25 vs. 27.1 ± 0.20, p = 0.002). Unsaturated fats had beneficial associations with body fat primarily in women. Finally, omega-3 PUFAs among women were inversely associated with interleukin-6 levels. There was no association between dietary fat intake and fasting glucose levels in either women or men.Discussion: In sum, we found no evidence of an adverse association between dietary fats and several surrogate markers of cardiometabolic health. This study suggests that different dietary fats may have divergent associations with cardiometabolic risk in women and men, perhaps owing to differences in food sources of the same dietary fats.

Transient receptor potential vanilloid 1 (TRPV1), a non-selective ligand-gated cation channel with high permeability for Ca2+, has received considerable attention as potential therapeutic target for the treatment of several disorders including pain, inflammation, and hyperlipidemia. In particular, TRPV1 regulates lipid metabolism by mechanisms that are not completely understood. Interestingly, TRPV1 and lipids regulate each other in a reciprocal and complex manner. This review surveyed the recent literature dealing with the role of TRPV1 in the hyperlipidemia-associated metabolic syndrome. Besides TRPV1 structure, molecular mechanisms underlying the regulatory effect of TRPV1 on lipid metabolism such as the involvement of uncoupling proteins (UCPs), ATP-binding cassette (ABC) transporters, peroxisome proliferation-activated receptors (PPAR), sterol responsive element binding protein (SREBP), and hypoxia have been discussed. Additionally, this review extends our understanding of the lipid-dependent modulation of TRPV1 activity through affecting both the gating and the expression of TRPV1. The regulatory role of different classes of lipids such as phosphatidylinositol (PI), cholesterol, estrogen, and oleoylethanolamide (OEA), on TRPV1 has also been addressed.

Yeast are a powerful material for the encapsulation of compounds. Usually, yeast used as capsules are inactivated by the encapsulation treatment, which is stressful to cells. However, if kept active, cells can bring their own activity in addition to the encapsulated compound. We have observed previously that lipid-grown Yarrowia lipolytica were more resistant to encapsulation. The objective of the present study was to identify physiological markers involved in this resistance. Cells were cultured in the presence of glucose or methyl-oleate as the sole carbon source and submitted to a - dodecalactone stress. This paper focuses on the role of intracellular lipid droplets (LDs) and of the ergosteryl content to protect cells during the lactone treatment. Lipid-grown cells were more resistant to lactone and the presence of LDs before the shock increased significantly the resistance. The ergosteryl esters from the LD pool were hydrolysed to release ergosterol able to strenghten the plasma membrane during the shock. For cells devoid of LDs, membrane ergosterols were esterified concomitantly with LDs growth, resulting in a membrane weakening. By using pox3-mutant strains, which possesse numerous and small-sized LDs, we observed the original behaviour: these mutants showed no increased resistance and their LDs exploded in the cytoplasma during the shock. These results point out the role of LDs in cell resistance to amphiphilic stresses as a storage compartment as well as in ergosterol homeostasis. [ABSTRACT FROM AUTHOR]

Background: Hyperprolactinemia is one of the most common hypothalamic-pituitary-endocrine disorders in women of reproductive age, with the highest frequency at the age of 25–44 years. In addition to influencing the reproductive system, it is important to study the effects of prolactin (PRL) on various metabolic links. Available data indicate that the effect of PRL on metabolism depends on its level. In this regard, the study of the relationship of different levels of PRL with anthropometric parameters, indicators of lipid and carbohydrate metabolism in young women is relevant.Aim: To study the frequency of metabolic syndrome (MS) and its individual components in women aged 25–45 years with different levels of prolactin.Materials and methods: Work design — cross-sectional research. A randompopulationsample of women 25–45 agedwas examined. Pregnant and breastfeeding women with macroprolactinoma, and taking antipsychotics were excluded. Information was collected using a structured ­questionnaire, including, but not limited to, the presence of pregnancies, childbirth, menstrual irregularities, and a clinical examination, anthropometric measurements, biochemical and hormonal blood analyzes were performed. Statistical data processing was carried out.Results: According to the inclusion and exclusion criteria, this analysis presents data from 401 women, the average age of the examibed was 36.14±6.19 years. There was no difference in the levels of thyroid-stimulating hormone and prolactin (PRL) in the age groups of 25–34 and 35–45 years. According to the survey, the incidence of thyroid diseases in the studied groups is comparable. Every fifth woman indicated menstrual irregularities. Among women 25–45 years old, women with low-normal PRL values (Me = 4.49 [3.52; 5.41] ng/ml) have more unfavorable metabolic indicators. Metabolic syndrome (MS) was detected in 28%,with a predominant increase in the frequency of abdominal obesity — 55%, hypercholesterolemic LDL — 63%. Women with high PRL (Me = 41.35 [34.78; 45.88] ng / ml) also have an unfavorable metabolic profile: MS was detected in 47%, abdominal obesity — 56%, hypertension — 39%.Conclusions: In women 25–45 years old, low and high PRL values are more often associated with metabolic ill health. PRL values are from 7.8 to 28 ng / ml, i.e. conditionally defined as normal, highly normal and at the level of moderate hyperprolactinemia contribute to the maintenance of a favorable metabolic profile. When deciding on the treatment of women with non-tumor etiology hyperprolactinemia, it is important to assess the metabolic status, expanding their understanding of PRL as a hormone associated only with lactation and with the pituitary-gonad axis.

Dysregulated lipid metabolism is common in infection and inflammation and is a part of the complex milieu underlying the pathophysiological sequelae of disease. Sepsis is a major cause of mortality and morbidity in the world and is characterized by an exaggerated host response to an infection. Metabolic changes, including alterations in lipid metabolism, likely are important in sepsis pathophysiology. Here, we designed an in vitro cell culture model using endothelial cells, E. coli, and neutrophils to mimic sepsis in a simplified cell model. Lipid alterations were studied in the presence of the pathogenic E. coli strain CFT073 and non-pathogenic E. coli strain JM109. We employed untargeted lipidomics to first identify lipid changes and then targeted lipidomics to confirm changes. Both unique and shared lipid signatures were identified in cocultures with these E. coli strains. In the absence of neutrophils, the CFT073 strain elicited alterations in lysophosphatidylcholine and diglyceride molecular species during coculture while both strains led to increases in phosphatidylglycerols. Lipid alterations in these cocultures changed with the addition of neutrophils. In the presence of neutrophils with E. coli and endothelial cells, triglyceride increases were a unique response to the CFT073 strain while phosphatidylglycerol and diglyceride increases occurred in response to both strains. Phosphatidylethanolamine also increased in neutrophils, E. coli and endothelial cells cocultures, and this response was greater in the presence of the CFT073 strain. We further evaluated changes in phosphatidylethanolamine in a rat model of sepsis, which showed multiple plasma phosphatidylethanolamine molecular species were elevated shortly after the induction of sepsis. Collectively, these findings demonstrate unique lipid responses by co-cultures of E. coli with endothelial cells which are dependent on the E. coli strain as well as the presence of neutrophils. Furthermore, increases in phosphatidylethanolamine levels in CFT073 urosepsis E. coli, endothelial cell, neutrophil cocultures were similarly observed in the plasma of septic rats.

Abstract Infants with neonatal cholestasis are prone to neurodevelopmental deficits, however, the underlying pathogenesis is unclear. Lipid malabsorption and accumulation of potentially neurotoxic molecules in the blood such as bile acids are important yet relatively unexplored pathways. Here, we developed a translational piglet model to understand how the molecular bile acid and lipid composition of the brain is affected by this disease and relates to motor function. Piglets (8‐days old) had bile duct ligation or sham surgery and were fed a formula diet for 3 weeks. Alongside sensory‐motor deficits observed in bile duct‐ligated animals, we found a shift toward a more hydrophilic and conjugated bile acid profile in the brain. Additionally, comprehensive lipidomics of the cerebellum revealed a decrease in total lipids including phosphatidylinositols and phosphatidylserines and increases in lysophospholipid species. This was paralleled by elevated cerebellar expression of genes related to inflammation and tissue damage albeit without significant impact on the brain transcriptome. This study offers new insights into the developing brain's molecular response to neonatal cholestasis indicating that bile acids and lipids may contribute in mediating motor deficits.

Membrane asymmetry is important for cellular physiology and established by energy‐dependent unidirectional lipid translocases, which have diverse physiological functions in plants. By contrast, the role of phospholipid scrambling (PLS), the passive bidirectional lipid transfer leading to the break‐down of membrane asymmetry, is currently still unexplored. The Arabidopsis thaliana genome contains a single gene (At1g73020) with homology to the eukaryotic TMEM16 family of Ca2+‐activated phospholipid scramblases. Here, we investigated the protein function of this Arabidopsis homolog. Fluorescent AtTMEM16 fusions localized to the ER both in transiently expressing Arabidopsis protoplasts and HEK293 cells. A putative scrambling domain (SCRD) was identified on the basis of sequence conservation and conferred PLS to transfected HEK293 cells, when grafted into the backbone of the non‐scrambling plasma membrane‐localized TMEM16A chloride channel. Finally, AtTMEM16 'gain‐of‐function' variants gave rise to cellular phenotypes typical of aberrant scramblase activity, which were reversed by the additional introduction of a 'loss‐of‐function' mutation into the SCRD. In conclusion, our data suggest AtTMEM16 works as an ER‐resident lipid scramblase in Arabidopsis. [ABSTRACT FROM AUTHOR]

Metabolic associated fatty liver disease (MAFLD) is the most common chronic liver disease worldwide due to the sedentary and overeating lifestyle. Yet, the pathophysiology of MAFLD is still unclear and no drug has been approved for MAFLD treatment. Extracellular vesicles (EVs) are heterogenous membrane-bound particles released from almost all types of cells. These nano-sized particles mediate intercellular communication through their bioactive cargos including nucleic acids, proteins, and lipids. The EVs modulate metabolic homeostasis via communication between adipose tissue and liver. The dysregulation of lipid metabolism leads to inflammation in liver and the number and compounds of EVs are changed during MAFLD. The injured hepatocytes secrete EVs to induce the migration of bone marrow-derived monocytes and the activation of macrophages in liver. The EVs secreted by different cells regulate the alteration of hepatic stellate cell (HSC) phenotypes and HSC activation gives rise to liver fibrosis. Based on the participation of EVs in MAFLD progression, we discuss the prospects of EVs as a therapeutic target and their application in drug delivery.

Background: Subclinical left ventricular diastolic dysfunction (LVDD) is an emerging consequence of increased insulin resistance, and dyslipidemia is one of the few correctable risk factors of LVDD. This study evaluated the role of mean and visit-to-visit variability of lipid measurements in risk of LVDD in a healthy population. Methods: This was a 3.7-year (interquartile range, 2.1 to 4.9) longitudinal cohort study including 2,817 adults (median age 55 years) with left ventricular ejection fraction >50% who underwent an annual or biannual health screening between January 2008 and July 2016. The mean, standard deviation (SD), coefficient of variation (CV), variability independent of the mean (VIM), and average real variability of total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein B (apoB), non-HDL-C, and triglycerides were obtained from three to six measurements during the 5 years preceding the first echocardiogram. Results: Among the 2,817 patients, 560 (19.9%) developed LVDD. The mean of no component of lipid measurements was associated with risk of LVDD. CV (hazard ratio [HR], 1.35; 95% confidence interval [CI], 1.10 to 1.67), SD (HR, 1.27; 95% CI, 1.03 to 1.57), and VIM (HR, 1.26; 95% CI, 1.03 to 1.55) of LDL-C and all the variability parameters of apoB were significantly associated with development of LVDD. The association between CV-LDL and risk of LVDD did not have significant interaction with sex, increasing/ decreasing trend at baseline, or use of stain and/or lipid-modifying agents. Conclusion: The variability of LDL-C and apoB, rather than their mean, was associated with risk for LVDD. [ABSTRACT FROM AUTHOR]

Lipids are key macromolecules that perform a multitude of biological functions ranging from maintaining structural integrity of membranes, energy storage, to signaling molecules. Unsurprisingly, variations in lipid composition and its levels can influence the functional and physiological state of the cell and its milieu. Cellular senescence is a permanent state of cell cycle arrest and is a hallmark of the aging process, as well as several age-related pathologies. Senescent cells are often characterized by alterations in morphology, metabolism, chromatin remodeling and exhibit a complex pro-inflammatory secretome (SASP). Recent studies have shown that the regulation of specific lipid species play a critical role in senescence. Indeed, some lipid species even contribute to the low-grade inflammation associated with SASP. Many protein regulators of senescence have been well characterized and are associated with lipid metabolism. However, the link between critical regulators of cellular senescence and senescence-associated lipid changes is yet to be elucidated. Here we systematically review the current knowledge on lipid metabolism and dynamics of cellular lipid content during senescence. We focus on the roles of major players of senescence in regulating lipid metabolism. Finally, we explore the future prospects of lipid research in senescence and its potential to be targeted as senotherapeutics.

Protein-lipid interactions are key regulators of ion channel function. Numerous ion channels, including hyperpolarization-activated cyclic-nucleotide gated (HCN) channels have been shown to be regulated by phosphoinositides (PIPs), with important implications in cardiac and neuronal function. Specifically, PIPs have been shown to enhance HCN activation. Using computational approaches, we aim to identify potential binding sites for HCN1-PIP interactions. Computational docking and coarse-grained simulations indicate that PIP binding to HCN1 channels is not well coordinated, but rather occurs over a broad surface of charged residues primarily in the HCN-domain, S2 and S3 helices that can be loosely organized in 2 or 3 overlapping clusters. Thus, PIP-HCN1 interactions are more resembling of electrostatic interactions that occur in myristoylated alanine-rich C kinase substrate (MARCKS) proteins, than the specifically coordinated interactions that occur in pleckstrin homology domains (PH domains) or ion channels such as inward rectifier potassium (Kir) channels. Our results also indicate that phosphatidylinositol (PI) interactions with HCN1 are even lower affinity, explaining why unphosphorylated PI have no effect on HCN1 activation unlike phosphorylated PIPs.

ObjectivesInsulin resistance (IR) has been shown to play important role in the pathogenesis of type 2 diabetes mellitus (T2DM). There is an intricate interplay between IR, dyslipidemia, and serum uric acid (SUA) in people with and without diabetes. Physical activity has a positive impact on insulin sensitivity in insulin-resistant populations. However, the effect of different intensities of physical activity on insulin levels under different lipid indices and SUA levels is unclear.MethodsTo explore the association between physical activity and insulin, we enrolled 12,982 participants aged above 18 years from the National Health and Nutrition Examination Survey (NHANES) conducted between 2009 and 2018. Next, we conducted multivariate logistic regression analyses, generated fitted smoothing curves, and visualized the data using generalized additive models.ResultsIncreased intensities of physical activity can significantly reduce insulin levels. The association between physical activity and insulin persisted even after adjusting for confounding factors, with β value (95% CI) = −17.10 (−21.64, −12.56) in moderate group, β value (95% CI) = −28.60 (−33.08, −24.11) in high group, respectively. High-intensity physical activity significantly lowered insulin levels in the lower and higher SUA tertiles, and three tertiles of LDL-c, HDL-c, and TG. Moreover, the link between physical activity and insulin was stronger in male individuals.ConclusionThis study shows that physical activity can significantly lower insulin levels, and high-intensity physical activity still has additional potential benefits for insulin levels, even in the condition of dyslipidemia and hyperuricemia.

Mammalian epidermis is a striking example of the role of lipids in tissue biology. In this stratified epithelium, highly specialized structures are formed that leverage the hydrophobic properties of lipids to form an impermeable barrier and protect the humid internal environment of the body from the dry outside. This is achieved through tightly regulated lipid synthesis that generates the molecular species unique to the tissue. Beyond their fundamental structural role, lipids are involved in the active protection of the body from external insults. Lipid species present on the surface of the body possess antimicrobial activity and directly contribute to shaping the commensal microbiota. Lipids belonging to a variety of classes are also involved in the signaling events that modulate the immune responses to environmental stress as well as differentiation of the epidermal keratinocytes themselves. Recently, high-resolution methods are beginning to provide evidence for the involvement of newly identified specific lipid molecules in the regulation of epidermal homeostasis. In this review we give an overview of the wide range of biological functions of mammalian epidermal lipids.

Melanoma, one of the most lethal cutaneous cancers, is characterized by its ability to metastasize to other distant sites, such as the bone. Melanoma cells revealed a variable in vitro propensity to be attracted toward bone fragments, and melanoma-derived exosomes play a role in regulating the osteotropism of these cells. We have here investigated the lipid profiles of melanoma cell lines (LCP and SK-Mel28) characterized by different metastatic propensities to colonize the bone. We have purified exosomes from cell supernatants by ultracentrifugation, and their lipid composition has been compared to identify potential lipid biomarkers for different migration and invasiveness of melanoma cells. Matrix-assisted laser desorption ionization-time-of-flight/mass spectrometry (MALDI-TOF/MS) lipid analysis has been performed on very small amounts of intact parental cells and exosomes by skipping lipid extraction and separation steps. Statistical analysis has been applied to MALDI mass spectra in order to discover significant differences in lipid profiles. Our results clearly show more saturated and shorter fatty acid tails in poorly metastatic (LCP) cells compared with highly metastatic (SK-Mel28) cells, particularly for some species of phosphatidylinositol. Sphingomyelin, lysophosphatidylcholine, and phosphatidic acid were enriched in exosome membranes compared to parental cells. In addition, we have clearly detected a peculiar phospholipid bis(monoacylglycero)phosphate as a specific lipid marker of exosomes. MALDI-TOF/MS lipid profiles of exosomes derived from the poorly and highly metastatic cells were not significantly different.

Although Flaviviruses such as dengue (DENV) and zika (ZIKV) virus are important human pathogens, an effective vaccine or antiviral treatment against them is not available. Hence, the search for new strategies to control flavivirus infections is essential. Several studies have shown that the host lipid metabolism could be an antiviral target because cholesterol and other lipids are required during the replicative cycle of different Flaviviridae family members. FDA-approved drugs with hypolipidemic effects could be an alternative for treating flavivirus infections. However, a better understanding of the regulation between host lipid metabolism and signaling pathways triggered during these infections is required. The metabolic pathways related to lipid metabolism modified during DENV and ZIKV infection are analyzed in this review. Additionally, the role of lipid-lowering drugs as safe host-targeted antivirals is discussed.

Saccharomyces cerevisiae, commonly known as baker’s yeast, is one of the most comprehensively studied model organisms in science. Yeast has been used to study a wide variety of human diseases, and the yeast model system has proved to be an especially amenable tool for the study of lipids and lipid-related pathophysiologies, a topic that has gained considerable attention in recent years. This review focuses on how yeast has contributed to our understanding of the mitochondrial phospholipid cardiolipin (CL) and its role in Barth syndrome (BTHS), a genetic disorder characterized by partial or complete loss of function of the CL remodeling enzyme tafazzin. Defective tafazzin causes perturbation of CL metabolism, resulting in many downstream cellular consequences and clinical pathologies that are discussed herein. The influence of yeast research in the lipid-related pathophysiologies of Alzheimer’s and Parkinson’s diseases is also summarized.

Sex differences in whole-body fat storage exist in many species. For example, Drosophila females store more fat than males. Yet, the mechanisms underlying this sex difference in fat storage remain incompletely understood. Here, we identify a key role for sex determination gene transformer (tra) in regulating the male-female difference in fat storage. Normally, a functional Tra protein is present only in females, where it promotes female sexual development. We show that loss of Tra in females reduced whole-body fat storage, whereas gain of Tra in males augmented fat storage. Tra’s role in promoting fat storage was largely due to its function in neurons, specifically the Adipokinetic hormone (Akh)-producing cells (APCs). Our analysis of Akh pathway regulation revealed a male bias in APC activity and Akh pathway function, where this sex-biased regulation influenced the sex difference in fat storage by limiting triglyceride accumulation in males. Importantly, Tra loss in females increased Akh pathway activity, and genetically manipulating the Akh pathway rescued Tra-dependent effects on fat storage. This identifies sex-specific regulation of Akh as one mechanism underlying the male-female difference in whole-body triglyceride levels, and provides important insight into the conserved mechanisms underlying sexual dimorphism in whole-body fat storage.

Odd chain fatty acids (15:0 and 17:0) from dairy fat as well as odd chain phenolic lipids (alkylresorcinols) from whole grain are commonly reviewed as candidate biomarkers for dietary analysis and their ingestion are inversely related to chronic disease risks. Therefore, low levels of dietary intake of these odd chain molecules may be related to higher risk of physiological states that cause chronic diseases or mortality. It is a prerequisite to examine and understand their main role in beneficial health effects in disease prevention. We propose odd chain fatty acids (OC‐FA) and most importantly odd chain phenolic lipids (OC‐PL) as potential essential dietary compounds since they play key roles in physiological mechanisms. This review evaluates potential roles of OC‐FA and OC‐PL in mitigating chronic diseases in vitro and in vivo studies to support our hypothesis for odd chain molecules as essential dietary lipids. Further studies are needed to investigate the relationship between reduced intake of OC‐FA‐ and OC‐PL‐containing foods and susceptibilities to chronic diseases. [ABSTRACT FROM AUTHOR]

Skeletal muscle quantity and quality decrease with older age, which is partly attributed to ectopic fat infiltration and has negative metabolic consequences. To inform efforts to preserve skeletal muscle with aging, a better understanding of biologic correlates of quantity and quality of muscle and intermuscular adipose tissue (IMAT) is needed. We used targeted lipidomics of lipoprotein subfractions among 947 Multi-Ethnic Study of Atherosclerosis participants to provide a detailed metabolic characterization of area and density of abdominal muscle and IMAT. Serum lipoprotein subfractions were measured at the first visit using 1H-Nuclear Magnetic Resonance spectroscopy. Muscle and IMAT area (cm2) and density (Hounsfield units) were estimated at visit 2 or 3 using computed tomography of the total abdominal, locomotion (psoas), and stabilization (paraspinal, oblique, rectus abdominis) muscles. We identified lipoprotein subfractions associated with body composition using linear regression adjusting for demographics, lifestyle, and multiple comparisons. Among 105 lipoprotein subfractions, 24 were associated with total muscle area (absolute standardized regression coefficient range: 0.07–0.10, p-values ≤ 0.002), whereas none were associated with total muscle density. When examining muscle subgroups, 25 lipoprotein subfractions were associated with stabilization muscle area, with associations strongest among the obliques. For total IMAT area, there were 27 significant associations with lipoprotein subfractions (absolute standardized regression coefficient range: 0.09–0.13, p-values ≤ 0.002). Specifically, 27 lipoprotein subfractions were associated with stabilization IMAT area, with associations strongest among the oblique and rectus abdominis muscles. For total IMAT density, there were 39 significant associations with lipoprotein subfractions (absolute standardized regression coefficient range: 0.10–0.19, p-values ≤ 0.003). Specifically, 28 and 33 lipoprotein subfractions were associated with IMAT density of locomotion and stabilization (statistically driven by obliques) muscles, respectively. Higher VLDL (cholesterol, unesterified cholesterol, phospholipids, triglycerides, and apolipoprotein B) and lower HDL (cholesterol and unesterified cholesterol) were associated with higher muscle area, higher IMAT area, and lower IMAT density. Several associations between lipoprotein subfractions and abdominal muscle area and IMAT area and density were strongest among the stabilization muscles, particularly the obliques, illustrating the importance of examining muscle groups separately. Future work is needed to determine whether the observed associations indicate a lipoprotein profile contributing to worse skeletal muscle with fat infiltration.

Dysferlinopathies are a group of muscle disorders caused by mutations to dysferlin, a transmembrane protein involved in membrane patching events following physical damage to skeletal myofibers. We documented dysferlin expression in vascular tissues including non-muscle endothelial cells, suggesting that blood vessels may have an endogenous repair system that helps promote vascular homeostasis. To test this hypothesis, we generated dysferlin-null mice lacking apolipoprotein E (ApoE), a common model of atherosclerosis, dyslipidemia and endothelial injury when stressed with a high fat, and cholesterol-rich diet. Despite high dysferlin expression in mouse and human atheromatous plaques, loss of dysferlin did not affect atherosclerotic burden as measured in the aortic root, arch, thoracic, and abdominal aortic regions. Interestingly, we observed that dysferlin-null mice exhibit lower plasma high-density lipoprotein cholesterol (HDL-C) levels than their WT controls at all measured stages of the disease process. Western blotting revealed abundant dysferlin expression in protein extracts from mouse livers, the main regulator of plasma lipoprotein levels. Despite abnormal lipoprotein levels, Dysf/ApoE double knockout mice responded to cholesterol absorption blockade with lower total cholesterol and blunted atherosclerosis. Our study suggests that dysferlin does not protect against atherosclerosis or participate in cholesterol absorption blockade but regulates basal plasma lipoprotein composition. Dysferlinopathic patients may be dyslipidemic without greater atherosclerotic burden while remaining responsive to cholesterol absorption blockade.

Objective: The benefits of Pilates for blood glucose and lipids remain unclear. The purpose of this study was to examine the effect of Pilates on their levels.Methods: Searches were conducted in five databases to identify relevant articles published until October 29, 2020. Paired reviewers independently screened the articles and extracted data from each included study. Meta-analysis was performed to assess the effects of Pilates on blood glucose and lipids. Subgroup analyses and sensitivity analyses were conducted to explore heterogeneity.Results: According to the inclusion and exclusion criteria, 15 randomized controlled trials (RCTs) comprising 587 participants were included in the study. Overall, the Pilates group (PG) had a significantly greater reduction in post-prandial blood glucose than the control group (CG) (MD = −22.25 mg/dL, 95% CI: [−28.34, 16.17] mg/dL, P < 0.00001, I2 = 0%); glycated hemoglobin (HbA1c) (MD = −0.78%, 95% CI: [−1.13, −0.42]%, P < 0.0001, I2 = 88%); total cholesterol (TC) (MD = −20.90 mg/dL, 95% CI: [−37.21, −4.60] mg/dL, P = 0.01, I2 = 84%); triglycerides (TG) (MD = −12.59 mg/dL, 95% CI: [−19.88, −5.29] mg/dL, P = 0.0007, I2 = 86%); and low density lipoprotein cholesterol (LDL-C) (MD = −12.39 mg/dL, 95% CI: [−16.82, −7.95] mg/dL, P < 0.00001, I2 = 45%) compared to CG, whereas no significant difference was detected between the two groups in fasting blood glucose (MD = −7.04 mg/dL, 95% CI: [−17.26, 3.17] mg/dL, P = 0.18, I2 = 93%), insulin (MD = −1.44 μU/mL, 95% CI: [−4.30, 1.41] μU/mL, P = 0.32, I2 = 0%); and high density lipoprotein cholesterol (HDL-C) (MD = −2.68 mg/dL, 95% CI: [−9.03, 3.67] mg/dL, P = 0.41, I2 = 89%). However, by subgroup analysis, we found that compared to the CG, PG showed no significant improvement in blood glucose and lipids levels for non-diabetics, while it presented a significantly greater decrease in post-prandial blood glucose, TC, TG, and LDL-C for diabetic patients. Notably, for diabetic patients, Pilates and medication treatments showed no significant reduction in fasting blood glucose (MD = −7.00 mg/dL, 95% CI: [−26.06, 12.06] mg/dL, P = 0.40) and HbA1c (MD = −0.23%, 95% CI: [−0.58, 0.13]%, P = 0.21, I2 = 0%) than medications treatment used alone, and Pilates combined with medications and dietary treatments presented no significant improvement in fasting blood glucose than a combination of medications and dietary treatments (MD = −10.90 mg/dL, 95% CI: [−32.35, 10.54] mg/dL, P = 0.32, I2 = 94%).Conclusions: Overall, Pilates could improve post-prandial blood glucose, fasting blood glucose, HbA1c, TG, TC, and LDL-C for diabetic patients, which could be influenced by its duration and intensity. Moreover, it had no significant effect on blood glucose and lipids for non-diabetic individuals. However, Pilates, as an adjunctive treatment to medications was not superior to medications used alone in lowering fasting blood glucose and HbA1c. Furthermore, Pilates combined with medications and dietary treatments showed no significant improvement in fasting blood glucose, whereas it had a greater reduction in post-prandial blood glucose and HbA1c for diabetic patients.Systematic Review Registration:https://osf.io/xgv6w.

Abstract Key differences exist between men and women in the determinants and manifestations of cardiovascular and cardiometabolic diseases. Recently, gut microbiome-host relations have been implicated in cardiovascular disease and associated metabolic conditions; therefore, gut microbiota may be key mediators or modulators driving the observed sexual dimorphism in disease onset and progression. While current evidence regarding pure physiological sex differences in gut microbiome composition is modest, robust research suggests that gut microbiome-dependent metabolites may interact with important biological pathways under sex hormone control, including toll-like receptor and flavin monooxygenase signaling. Here, we review key sex differences in gut microbiome interactions with four primary determinants of cardiovascular disease, impaired glucose regulation, dyslipidemia, hypertension, and obesity. Through this process, we propose important sex differences in downstream metabolic pathways that may be at the interface of the gut microbiome and cardiovascular disease.

Accumulating evidence highlights the importance of interactions between tumour cells and stromal cells for tumour initiation, progression, and metastasis. In tumours that contain adipocyte in their stroma, adipocytes contribute to modification of tumour microenvironment and affect metabolism of tumour and tumour progression by production of cytokines and adipokines from the lipids. The omentum and bone marrow (BM) are highly adipocyte-rich and are also common metastatic and primary tumour developmental sites. Omental adipocytes exhibit metabolic cross-talk, immune modulation, and angiogenesis. BM adipocytes secrete adipokines, and participate in solid tumour metastasis through regulation of the CCL2/CCR2 axis and metabolic interactions. BM adipocytes also contribute to the progression of hematopoietic neoplasms. Here, we here provide an overview of research progress on the cross-talks between omental/BM adipocytes and tumour cells, which may be pivotal modulators of tumour biology, thus highlighting novel therapeutic targets. Abbreviations: MCP-1, monocyte chemoattractant protein 1IL, interleukinSTAT3, signal transducer and activator of transcription 3FABP4, fatty acid binding protein 4PI3K/AKT, phosphoinositide 3-kinase/protein kinase BPPAR, peroxisome proliferator-activated receptorPUFA, polyunsaturated fatty acidTAM, tumour-associated macrophagesVEGF, vascular endothelial growth factorVEGFR, vascular endothelial growth factor receptorBM, bone marrowBMA, bone marrow adipocytesrBMA, regulated BMAcBMA, constitutive BMAUCP-1, uncoupling protein-1TNF-α, tumour necrosis factor-alphaRANKL, receptor activator of nuclear factor kappa-Β ligandVCAM-1, vascular cell adhesion molecule 1JAK2, Janus kinase 2CXCL (C–X–C motif) ligandPGE2, prostaglandin E2COX-2, cyclooxygenase-2CCL2, C-C motif chemokine ligand 2NF-κB, nuclear factor-kappa BMM, multiple myelomaALL, acute lymphoblastic leukemiaAML, acute myeloid leukemiaGDF15, growth differentiation factor 15AMPK, AMP-activated protein kinaseMAPK, mitogen-activated protein kinaseAPL, acute promyelocytic leukemiaCCR2, C-C motif chemokine receptor 2SDF-1α, stromal cell-derived factor-1 alphaFFA, free fatty acidsLPrA, leptin peptide receptor antagonistMCD, malonyl-CoA decarboxylase.

Torpor and hibernation are powerful strategies enabling animals to survive periods of low resource availability. The state of torpor results from an active and drastic reduction of an individual’s metabolic rate (MR) associated with a relatively pronounced decrease in body temperature. To date, several forms of torpor have been described in all three mammalian subclasses, i.e., monotremes, marsupials, and placentals, as well as in a few avian orders. This review highlights some of the characteristics, from the whole organism down to cellular and molecular aspects, associated with the torpor phenotype. The first part of this review focuses on the specific metabolic adaptations of torpor, as it is used by many species from temperate zones. This notably includes the endocrine changes involved in fat- and food-storing hibernating species, explaining biomedical implications of MR depression. We further compare adaptive mechanisms occurring in opportunistic vs. seasonal heterotherms, such as tropical and sub-tropical species. Such comparisons bring new insights into the metabolic origins of hibernation among tropical species, including resistance mechanisms to oxidative stress. The second section of this review emphasizes the mechanisms enabling heterotherms to protect their key organs against potential threats, such as reactive oxygen species, associated with the torpid state. We notably address the mechanisms of cellular rehabilitation and protection during torpor and hibernation, with an emphasis on the brain, a central organ requiring protection during torpor and recovery. Also, a special focus is given to the role of an ubiquitous and readily-diffusing molecule, hydrogen sulfide (H2S), in protecting against ischemia-reperfusion damage in various organs over the torpor-arousal cycle and during the torpid state. We conclude that (i) the flexibility of torpor use as an adaptive strategy enables different heterothermic species to substantially suppress their energy needs during periods of severely reduced food availability, (ii) the torpor phenotype implies marked metabolic adaptations from the whole organism down to cellular and molecular levels, and (iii) the torpid state is associated with highly efficient rehabilitation and protective mechanisms ensuring the continuity of proper bodily functions. Comparison of mechanisms in monotremes and marsupials is warranted for understanding the origin and evolution of mammalian torpor.

Background: This study examines the effects of sports drinks ingestion during high-intensity exercise for carbohydrate oxidation rate (CHO-O) among athletes.Methods: PubMed, Embase, and the Cochrane library were searched for available papers published up to November 2019. The primary outcome is the carbohydrate oxidation rate (CHO-O), and the secondary outcome is the fat oxidation rate (Fat-O). Statistical heterogeneity among the included studies was evaluated using Cochran's Q test and the I2 index. The random-effects model was used for all analyses, regardless of the I2 index.Results: Five studies are included, with a total of 58 participants (range, 8–14/study). All five studies are randomized crossover trials. Compared to the control beverages, sports drinks have no impact on the CHO-O of athletes [weighted mean difference (WMD) = 0.29; 95% CI, −0.06 to 0.65, P = 0.106; I2 = 97.4%, P < 0.001] and on the Fat-O of athletes (WMD = −0.074; 95% CI, −0.19 to 0.06, P = 0.297; I2 = 97.5%, P < 0.001). Carbohydrate–electrolyte solutions increase CHO-O (WMD = 0.47; 95% CI, 0.08–0.87, P = 0.020; I2 = 97.8%, P < 0.001) but not Fat-O (WMD = −0.14; 95% CI, −0.31 to 0.03, P = 0.103; I2 = 98.2%, P < 0.001). Caffeine has a borderline effect on Fat-O (WMD = 0.05; 95% CI, 0.00–0.10, P = 0.050).Conclusions: Compared with the control beverages, sports drinks show no significant improvement in CHO-O and Fat-O in athletes. Carbohydrate–electrolyte solutions increase CHO-O in athletes but not Fat-O.

Amyloids are implicated in many diseases, and disruption of lipid membrane structures is considered as one possible mechanism of pathology. In this paper we investigate interactions between an aggregating peptide and phospholipid membranes, focusing on the nanometer-scale structures of the aggregates formed, as well as on the effect on the aggregation process. As a model system, we use the small amyloid-forming peptide named NACore, which is a fragment of the central region of the protein α-synuclein that is associated with Parkinson’s disease. We find that phospholipid vesicles readily associate with the amyloid fibril network in the form of highly distorted and trapped vesicles that also may wet the surface of the fibrils. This effect is most pronounced for model lipid systems containing only zwitterionic lipids. Fibrillation is found to be retarded by the presence of the vesicles. At the resolution of our measurements, which are based mainly on cryogenic transmission electron microscopy (cryo-TEM), X-ray scattering, and circular dichroism (CD) spectroscopy, we find that the resulting aggregates can be well fitted as linear combinations of peptide fibrils and phospholipid bilayers. There are no detectable effects on the cross-β packing of the peptide molecules in the fibrils, or on the thickness of the phospholipid bilayers. This suggests that while the peptide fibrils and lipid bilayers readily co-assemble on large length-scales, most of them still retain their separate structural identities on molecular length-scales. Comparison between this relatively simple model system and other amyloid systems might help distinguish aspects of amyloid-lipid interactions that are generic from aspects that are more protein specific. Finally, we briefly consider possible implications of the obtained results for in-vivo amyloid toxicity.

Maintaining energy homeostasis is critical for ensuring proper growth and maximizing survival potential of all organisms. Here we review the role of somatic muscle in regulating energy homeostasis in insects. The muscle is not only a large consumer of energy, it also plays a crucial role in regulating metabolic signaling pathways and energy stores of the organism. We examine the metabolic pathways required to supply the muscle with energy, as well as muscle-derived signals that regulate metabolic energy homeostasis.

Glucocerebrosides are sphingolipid components of cell membranes that intervene in numerous cell biological processes and signaling pathways and that deregulation is implicated in human diseases such as Gaucher disease and Parkinson's disease. In the present study, we conducted a systematic review using document co-citation analysis, clustering and visualization tools to explore the trends and knowledge structure of glucocerebrosides research as indexed in the Science Citation Index Expanded database (1956—present). A co-citation network of 5,324 publications related to glucocerebrosides was constructed. The analysis of emerging categories and keywords suggested a growth of research related to neurosciences over the last decade. We identified ten major areas of research (e.g., clusters) that developed over time, from the oldest (i.e., on glucocerebrosidase protein or molecular analysis of the GBA gene) to the most recent ones (i.e., on drug resistance in cancer, pharmacological chaperones, or Parkinson's disease). We provided for each cluster the most cited publications and a description of their intellectual content. We moreover identified emerging trends in glucocerebrosides research by detecting the surges in the rate of publication citations in the most recent years. In conclusion, this study helps to apprehend the most significant lines of research on glucocerebrosides. This should strengthen the connections between scientific communities studying glycosphingolipids to facilitate advances, especially for the most recent researches on cancer drug resistance and Parkinson's disease.

Symbiosis naturally provides an opportunity for microorganisms to live together by mutual or one-way benefit. In symbiotic relationships, the microorganisms usually overcome the limitations of being free-living. Understanding the symbiotic relationships of oleaginous microorganisms provides potential route for the sustainable production of microbial-based alternative fuels. So far, several studies have been conducted in oleaginous microorganisms for the production of alternative fuels. However, some oleaginous microorganisms require high quantity of nutrients for their growth, and high level of energy and chemicals for harvest and separation of lipid bodies. Symbiotic associations can successfully be applied to address these issues. Of symbiotic associations, lichens and selective species of oleaginous endosymbiotic mucoromycotina have received substantial interest as better models to study the evolutionary relationships as well as single-cell oil production. Construction of artificial lichen system composed of cyanobacteria and oleaginous yeast has been achieved for sustainable production of lipids with minimum energy demand. Recently, endosymbiotic mucoromycotina species have been recognized as potential sources for biofuels. Studies found that endohyphal bacterium influences lipid profiling in endosymbiotic mucoromycotina species. Studies on the genetic factors related to oleaginous characteristics of endosymbiotic mucoromycotina species are scarce. In this regard, this review summarizes the different forms of symbiotic associations of oleaginous microorganisms and how symbiotic relationships are impacting the lipid formation in microorganisms. Further, the review also highlights the importance of evolutionary relationships and benefits of co-culturing (artificial symbiosis) approaches for sustainable production of biofuels. [ABSTRACT FROM AUTHOR]

The common octopus, Octopus vulgaris, has a short life cycle, growing rapidly to maturity, spawning once, and characterized by an asynchronic oocyte development and a synchronic ovulation dying after breeding. This species has a protein and amino acid metabolism and it is usually defined as an income breeder. However, most biochemical studies lack an examination of the whole reproductive cycle, in particular the spawning process. We here studied the biochemical changes and determined the energy strategy along reproduction in female O. vulgaris, and found that proteins were the main energy reserve, primarily located in the body muscle when sexually maturing and decreasing during breeding. Lipids were also an important source of energy in the ovary and digestive gland and decreased during breeding too. By contrast, glycogen had a minor contribution to the energy content and was the unique compound that increased in spawning and post-spawning females. Additionally, the most abundant fatty acids (FA) in all tissues were 16:0, 18:0, 20:1n9, 20:4n6 (ARA), 20:5n3 (EPA) and 22:6n3 (DHA), with a clear predominance of long-chain polyunsaturated FA. The FA profile of mature ovaries was compared with other life stages finding similitudes with eggs, hatchlings and juveniles but considerable differences with paralarvae which showed higher DHA/ARA and EPA/ARA ratios. Therefore, we found important biochemical changes along the reproductive cycle that determined the energetic signature in each tissue, though no significant energy trade-offs between tissues were found, suggesting that, on the one hand, female O. vulgaris obtained energy directly from food accumulated simultaneously in the somatic and reproductive tissues during sexual maturation. However, an energy reallocation from somatic to reproductive growth would occur once vitellogenesis has started, so that the rate at which body growths would decrease in favor of ovary growth. On the other hand, during breeding, a general decrease in the energy content occurred in all tissues, so that the ovary would be responsible for the spawning success, whereas muscle tissues and digestive gland would independently supply the energy needed for the body maintenance safeguarding the female survival needed for the maternal care.

It is well established that diabetes is the major cause of chronic kidney disease worldwide. Both hyperglycemia, and more recently, advanced glycation endproducts, have been shown to play critical roles in the development of kidney disease. Moreover, the renin-angiotensin system along with growth factors and cytokines have also been shown to contribute to the onset and progression of diabetic kidney disease; however, the role of lipids in this context is poorly characterized. The current study aimed to compare the effect of 20 weeks of streptozotocin-induced diabetes or western diet feeding on kidney disease in two different mouse strains, C57BL/6 mice and hyperlipidemic apolipoprotein (apo) E knockout (KO) mice. Mice were fed a chow diet (control), a western diet (21% fat, 0.15% cholesterol) or were induced with streptozotocin-diabetes (55 mg/kg/day for 5 days) then fed a chow diet and followed for 20 weeks. The induction of diabetes was associated with a 3-fold elevation in glycated hemoglobin and an increase in kidney to body weight ratio regardless of strain (p < 0.0001). ApoE deficiency significantly increased plasma cholesterol and triglyceride levels and feeding of a western diet exacerbated these effects. Despite this, urinary albumin excretion (UAE) was elevated in diabetic mice to a similar extent in both strains (p < 0.0001) but no effect was seen with a western diet in either strain. Diabetes was also associated with extracellular matrix accumulation in both strains, and western diet feeding to a lesser extent in apoE KO mice. Consistent with this, an increase in renal mRNA expression of the fibrotic marker, fibronectin, was observed in diabetic C57BL/6 mice (p < 0.0001). In summary, these studies demonstrate disparate effects of diabetes and hyperlipidemia on kidney injury, with features of the diabetic milieu other than lipids suggested to play a more prominent role in driving renal pathology.

Metabolic diseases, such as diabetes, obesity, and fatty liver disease, have now reached epidemic proportions. Receptor tyrosine kinases (RTKs) are a family of cell surface receptors responding to growth factors, hormones, and cytokines to mediate a diverse set of fundamental cellular and metabolic signaling pathways. These ligands signal by endocrine, paracrine, or autocrine means in peripheral organs and in the central nervous system to control cellular and tissue-specific metabolic processes. Interestingly, the expression of many RTKs and their ligands are controlled by changes in metabolic demand, for example, during starvation, feeding, or obesity. In addition, studies of RTKs and their ligands in regulating energy homeostasis have revealed unexpected diversity in the mechanisms of action and their specific metabolic functions. Our current understanding of the molecular, biochemical and genetic control of energy homeostasis by the endocrine RTK ligands insulin, FGF21 and FGF19 are now relatively well understood. In addition to these classical endocrine signals, non-endocrine ligands can govern local energy regulation, and the intriguing crosstalk between the RTK family and the TGFβ receptor family demonstrates a signaling network that diversifies metabolic process between tissues. Thus, there is a need to increase our molecular and mechanistic understanding of signal diversification of RTK actions in metabolic disease. Here we review the known and emerging molecular mechanisms of RTK signaling that regulate systemic glucose and lipid metabolism, as well as highlighting unexpected roles of non-classical RTK ligands that crosstalk with other receptor pathways.