La importancia de la microbiota intestinal en la fisiología y rendimiento de pollos de engorda y gallinas de postura / The importance of intestinal microbiota on the physiology and performance of broiler chickens and laying hens

Resumen: El estudio de la microbiota ha adquirido un nuevo enfoque de interés, ya que interviene en diversos procesos fisiológicos involucrados en el desarrollo y rendimiento de los animales domésticos. Participa en el eje-microbiota-intestino-cerebro, con procesos que rigen el sistema nervioso hacia el intestino y viceversa. El objetivo de este trabajo fue identificar la importancia de la microbiota gastrointestinal de pollos de engorda y gallinas de postura y su relación con procesos fisiológicos que afecten el desarrollo, rendimiento, comportamiento y salud. En el tracto gastrointestinal de estas aves se han identificado alrededor de 17 filos de bacterias, con microorganismos predominantes según el sitio anatómico dentro del tracto y por ende con diferente función, por ejemplo, buche: Lactobacillus, Enterobacteriaceae; proventrículo: Clostridiaceae, Enterococcus; intestino: Escherichia, Streptococcus. Distintos factores intervienen en la colonización y desarrollo de la microbiota, desde el programa de alimentación y manejo, tipo de cama y densidad animal, entre otros. Existen microorganismos potencialmente patógenos que impactan negativamente en la microbiota y puedan llegar al consumidor, como Campylobacter jejuni, Salmonella enteritidis y Escherichia coli, de ahí su importancia al momento de trazar las directrices en las producciones pecuarias.

Abstract: There is an increasing interest in microbiota studies due to their relevance in physiological processes such as animal development and productivity. In addition, it its involved in the microbiota-intestinebrain axis that regulates the nervous system to the intestine and vice versa. This paper is aimed at identifying the importance of the broilers and laying hens' gastrointestinal microbiota and its relationship with diverse physiological processes that intervene in the development, productivity, behavior, and health. There are 17 filos of bacteria within the poultry gastrointestinal tract, which are site dependent and have specific functions (Example; crop: Lactobacillus, Enterobacteriaceae; proventriculus: Clostridiaceae, Enterococcus; intestine: Escherichia, Streptococcus). In addition, different factors affect the development of microbiota such as the feeding program, handling, kind of substrate, stocking density, among others. There are several potentially pathogenic microorganisms that impact microbiota negatively and may reach the final consumer such as Campylobacter jejuni, Salmonella enteritidis and Escherichia coli. Therefore, it is important to continue supporting poultry microbiota research and areas of opportunity to improve poultry production.

Disfunciones del metabolismo del surfactante pulmonar: caso clínico pediátrico / Pulmonary surfactant metabolism dysfunction: A pediatric clinical case report

Las enfermedades pulmonares intersticiales son patologías poco frecuentes en pediatría. Dentro de ellas, se incluyen las disfunciones del metabolismo del surfactante pulmonar, molécula anfipática cuya función es disminuir la tensión superficial y evitar el colapso alveolar. Se presenta el caso de un lactante de 6 meses, en seguimiento por bajo peso, que presentó dificultad respiratoria aguda y cianosis; la radiografía de tórax evidenció infiltrado intersticial, neumomediastino y neumotórax bilateral. Al interrogatorio, surgió antecedente materno de internación al año de vida, con requerimiento de oxigenoterapia prolongada y diagnóstico desconocido; presenta signos de hipoxia crónica. El paciente cursó internación con requerimiento de oxigenoterapia. Se realizaron estudios complementarios en búsqueda de etiología, sin resultados positivos. La tomografía de tórax evidenció opacidades en vidrio esmerilado, engrosamiento del intersticio septal y áreas de atrapamiento aéreo; con resultado de biopsia pulmonar y estudio genético se llegó al diagnóstico de disfunción del metabolismo del surfactante pulmonar.

Interstitial lung diseases are rare in pediatrics. They include dysfunctions in the metabolism of pulmonary surfactant, an amphipathic molecule that reduces surface tension and prevents alveolar collapse. Here we describe the case of a 6-month-old infant controlled for low weight, who presented with acute respiratory distress and cyanosis; his chest X-ray showed interstitial infiltrate, pneumomediastinum, and bilateral pneumothorax. During history-taking, it was noted that his mother had a history of hospitalization at 1 year old with unknown diagnosis, requiring prolonged oxygen therapy; she now shows signs of chronic hypoxia. The patient was hospitalized and required oxygen therapy. Ancillary tests were done to look for the etiology of the condition, with no positive results. A chest computed tomography showed groundglass opacities, thickening of the septal interstitium, and areas of air trapping; based on the results of a lung biopsy and a genetic study, pulmonary surfactant metabolism dysfunction was diagnosed.

Significado biológico y utilidad clínica del lactato en la sepsis / Biological significance and clinical utility of lactate in sepsis

La sepsis es un problema global de salud y la progresión hacia el shock séptico se asocia con un incremento marcado de la morbimortalidad. En este escenario, el aumento del lactato plasmático demostró ser un indicador de gravedad y un predictor de mortalidad, y suele interpretarse casi exclusivamente como marcador de baja perfusión tisular. Sin embargo, últimamente se produjo un cambio de paradigma en la exégesis del metabolismo y propiedades biológicas del lactato. En efecto, la adaptación metabólica al estrés, aun con adecuado aporte de oxígeno, puede justificar la elevación del lactato circulante. Asimismo, otras consecuencias fisiopatológicas de la sepsis, como la disfunción mitocondrial, se asocian con el desarrollo de hiperlactatemia sin que necesariamente se acompañen de baja perfusión tisular. Interpretar el origen y la función del lactato puede resultar de suma utilidad clínica en la sepsis, especialmente cuando sus niveles circulantes fundamentan las medidas de reanimación.

Sepsis is a global health problem; progression to septic shock is associated with a marked increase in morbidity and mortality. In this setting, increased plasma lactate levels demonstrated to be an indicator of severity and a predictor of mortality, and are usually interpreted almost exclusively as a marker of low tissue perfusion. However, a recent paradigm shift has occurred in the exegesis of lactate metabolism and its biological properties. Indeed, metabolic adaptation to stress, even with an adequate oxygen supply, may account for high circulating lactate levels. Likewise, other pathophysiological consequences of sepsis, such as mitochondrial dysfunction, are associated with the development of hyperlactatemia, which is not necessarily accompanied by low tissue perfusion. Interpreting the origin and function of lactate may be of great clinical utility in sepsis, especially when circulating lactate levels are the basis for resuscitative measures.

Plant-based diets and their effects on the metabolism and survival of chronic renal patients undergoing conservative treatment

Diet therapy in conservative treatment of chronic kidney disease involves protein restriction, but there is not enough evidence to recommend a particular type of protein, whether animal or plant based. However, studies suggest that plant-based diets help reduce the consumption of total and animal protein, reduce the need for nephroprotective drugs, improve complications and bring advantages in terms of disease progression and patient survival. The article considers up-to-date data on the effects of this diet and observed that when low in protein, primarily vegetable and in some cases supplemented with ketoanalogues, it can result in positive clinical outcomes, such as: delay in the decrease in the glomerular filtration rate, lower concentrations of urea, reduction of serum creatinine and phosphorus concentrations, lower metabolic acidosis, higher insulin sensitivity and lower systemic inflammation. As a whole, this dietary pattern may be able to postpone the start of dialysis with less progression of renal insufficiency. Additional research is needed to better characterize this dietary pattern.

La dietoterapia en el tratamiento conservador de la enfermedad renal crónica implica la restricción de proteínas, pero aún no hay pruebas suficientes para recomendar un tipo concreto de proteínas, ya sean animales o vegetales. Sin embargo, los estudios sugieren que las dietas basadas en plantas ayudan a reducir la ingesta de proteínas totales y animales, disminuyen la necesidad de fármacos nefroprotectores, mejoran las complicaciones y presentan ventajas con respecto a la progresión de la enfermedad y la supervivencia de los pacientes. En este artículo se consideran datos actualizados sobre los efectos de esta dieta y se observa que, cuando es hipoproteica, principalmente vegetal y en algunos casos se complementa con cetoanálogos, puede dar lugar a resultados clínicos positivos, como una disminución retardada de la tasa de filtración glomerular, concentraciones más bajas de urea, concentraciones reducidas de creatinina y fósforo séricos, menor acidosis metabólica, mayor sensibilidad a la insulina y menor inflamación sistémica. En conjunto, este patrón dietético tiene el potencial de retrasar el inicio de la diálisis con una menor progresión de la insuficiencia renal. Es necesario seguir investigando para caracterizar mejor este patrón dietético.

Could nanotechnology improve exercise performance? Evidence from animal studies

Abstract This review provides the current state of knowledge regarding the use of nutritional nanocompounds on exercise performance. The reviewed studies used the following nanocompounds: resveratrol-loaded lipid nanoparticles, folic acid into layered hydroxide nanoparticle, redox-active nanoparticles with nitroxide radicals, and iron into liposomes. Most of these nutritional nanocompounds seem to improve performance in endurance exercise compared to the active compound in the non-nanoencapsulated form and/or placebo. Nutritional nanocompounds also induced the following physiological and metabolic alterations: 1) improved antioxidant activity and reduced oxidative stress; 2) reduction in inflammation status; 3) maintenance of muscle integrity; 4) improvement in mitochondrial function and quality; 5) enhanced glucose levels during exercise; 6) higher muscle and hepatic glycogen levels; and 7) increased serum and liver iron content. However, all the reviewed studies were conducted in animals (mice and rats). In conclusion, nutritional nanocompounds are a promising approach to improving exercise performance. As the studies using nutritional nanocompounds were all conducted in animals, further studies in humans are necessary to better understand the application of nutritional nanocompounds in sport and exercise science.

Fish oil supplementation in obese rats ameliorates metabolic syndrome response

Accumulation of visceral adipose tissue is associated with metabolic syndrome (MS), insulin resistance, and dyslipidemia. Here we examined several morphometric and biochemical parameters linked to MS in a rodent litter size reduction model, and how a 30-day fish oil (FO) supplementation affected these parameters. On day 3 post-birth, pups were divided into groups of ten or three. On day 22, rats were split into control (C) and small litter (SL) until 60 days old. Then, after metabolic disturbance and obesity were confirmed, FO supplementation started for 30 days and the new groups were named control (C), FO supplemented (FO), obese (Ob), and obese FO supplemented (ObFO). Comparison was performed by Student t-test or 2-way ANOVA followed by Tukey post hoc test. At the end of the 60-day period, SL rats were hyperphagic, obese, hypoinsulinemic, normoglycemic, and had high visceral fat depot and high interleukin (IL)-6 plasma concentration. Obese rats at 90 days of age were fatter, hyperphagic, hyperglycemic, hypertriacylgliceromic, hipoinsulinemic, with low innate immune response. IL-6 production ex vivo was higher, but in plasma it was not different from the control group. FO supplementation brought all biochemical changes to normal values, normalized food intake, and reduced body weight and fat mass in obese rats. The innate immune response was improved but still not as efficient as in lean animals. Our results suggested that as soon MS appears, FO supplementation must be used to ameliorate the morpho- and biochemical effects caused by MS and improve the innate immune response.

Moderate-intensity continuous training reduces triglyceridemia and improves oxygen consumption in dyslipidemic apoCIII transgenic mice

This study aimed to investigate metabolism modulation and dyslipidemia in genetic dyslipidemic mice through physical exercise. Thirty-four male C57Bl/6 mice aged 15 months were divided into non-transgenic (NTG) and transgenic overexpressing apoCIII (CIII) groups. After treadmill adaptation, the trained groups (NTG Ex and CIII Ex) underwent an effort test to determine running performance and assess oxygen consumption (V̇O2), before and after the training protocol. The exercised groups went through an 8-week moderate-intensity continuous training (MICT) program, consisting of 40 min of treadmill running at 60% of the peak velocity achieved in the test, three times per week. At the end of the training, animals were euthanized, and tissue samples were collected for ex vivo analysis. ApoCIII overexpression led to hypertriglyceridemia (P<0.0001) and higher concentrations of total plasma cholesterol (P<0.05), low-density lipoprotein (LDL) cholesterol (P<0.01), and very low-density lipoprotein (VLDL) cholesterol (P<0.0001) in the animals. Furthermore, the transgenic mice exhibited increased adipose mass (P<0.05) and higher V̇O2peak compared to their NTG controls (P<0.0001). Following the exercise protocol, MICT decreased triglyceridemia and cholesterol levels in dyslipidemic animals (P<0.05), and reduced adipocyte size (P<0.05), increased muscular glycogen (P<0.001), and improved V̇O2 in all trained animals (P<0.0001). These findings contribute to our understanding of the effects of moderate and continuous exercise training, a feasible non-pharmacological intervention, on the metabolic profile of genetically dyslipidemic subjects.

Progress of the effect of hydroxyacyl-coenzyme A dehydrogenase in cancer development and its mechanism / 基础医学与临床

A close relationship between fatty acid metabolism and cancer development is well-established.The hydroxyacyl-coenzyme a dehydrogenase(HADH),a key enzyme in fatty acid beta-oxidation,has recently been identified as an anti-oncogenic factor in various cancers and an oncogenic factor in conditions like acute myeloid leukemia.In cancer cells,HADH not only directly catalyzes fatty acid beta-oxidation but also indirectly influences multiple signaling pathways such as PPAR,TNF-α,JAK-STAT3,PI3K/Akt,IFN-γ,MAPK,and non-canonical Wnt signaling pathways,affecting cancer cell proliferation and migration.HADH shows promise as a potential tumor biomarker for diagnosis,treatment,and prognosis in different cancer types,holding significant clinical value.

Nutlin-3a regulates mouse adipose function by inhibition of CIDEC expression / 基础医学与临床

Objective To investigate the effect of Nutlin-3a,a mouse double minute 2 homolog(MDM2)inhibitor,on lipid metabolism of mouse adipose.Methods High-fat diet-induced obesity(DIO)C57BL/6J mice were randomly divided into a control group injected with DMSO and an experimental group injected with Nutlin-3a.Then we conducted glucose tolerance(GTT)and insulin tolerance(ITT)tests.The epididymal white adipose tissue(eWAT),inguinal white adipose tissue(iWAT)and brown adipose tissue(BAT)of animals were isolated and microscopy of WATs with hematoxylin-eosin(HE)staining was performed to observe the morphological changes of adipocytes.The expression of lipid metabolism related gene cell death-inducing DFF45-like effector C(CIDEC)in eWAT were detected by qPCR and Western blot.Results Compared with the control group,Nutlin-3a was found to promote the body weight(P＜0.001),but no effect on glucose tolerance and insulin sensitivity in DIO mice.Nutlin-3a treatment decreased the size of adipocytes and fat deposition in adipose tissue and downregulated the mRNA and protein levels of CIDEC in eWAT.Conclusions Nutlin-3a inhibits the formation of lipid droplets by downregulating expression of CIDEC in white adipose tissue.

Advances in the role of lysophosphatidyl-choline acyltransferase 1 in tumors / 基础医学与临床

Lysophosphatidylcholine acyltransferase 1(LPCAT1),a key metabolic enzyme in the phosphatidyl-cho-line metabolism pathway,mediates phosphatidylcholine synthesis through deacylation-reacylation,which leads to alterations in the phospholipids composition of cell membranes and the remodelling of the cellular cytoskeleton.Ly-sophosphatidylcholine acyltransferase 1 has been shown to be highly expressed in gastric,breast and colorectal cancer,and can accelerate the alteration of the phospholipids composition of tumor cell membranes or interact with tumor driver genes,such as epidermal growth factor receptor and cell cycle-related genes.It might promote tumor development by affecting tumor cell proliferation,migration,invasion and resistance to chemotherapy.

Research progress on cholesterol metabolism in the regulation of colorectal cancer / 解放军医学杂志

Cholesterol metabolism is a hot topic in exploration of cancer treatment in recent years,and its complex mechanism of action potentially lays a molecular foundation related to lipid-cancer.However,most studies focus only on cholesterol as a product to understand and analyze the progress of cancer,ignoring the phased effects of related derivatives,regulatory proteins and immune cells in its metabolic process,so whether to find targets to regulate colorectal cancer(CRC)from the cholesterol metabolic pathway has become a research focus.This paper reviews the molecular mechanism and the role of signaling pathways in metabolic reprogramming of CRC starting from the abnormal intracellular cholesterol metabolic pathway in order to provide new ideas for the targeted cholesterol therapy of CRC.

Research Progress of Iron Death in Cardiomyopathy / 昆明医科大学学报

Cardiomyopathy is a group of heterogeneous myocardial diseases with a variety of specific phenotypes that can lead to cardiovascular death or progressive heart failure in severe cases.Because of the severity and complexity of these diseases,the search for new regulatory mechanisms to prevent and treat cardiomyopathy is particularly urgent.Iron death is a form of programmed cell death that differs from other forms of iron dependence and is characterized by the accumulation of iron-dependent lipid peroxides.Studies have shown that iron death can be involved in the occurrence and progression of cardiomyopathy through different signaling pathways.Therefore,targeted regulation of iron death is a new strategy to prevent cardiomyopathy.In this paper,the mechanism of iron death and its important role in cardiomyopathy were reviewed to find the potential relationship between iron death and cardiomyopathy and provide more ideas for the treatment of various cardiomyopathies in the future.

Research progress in ceruloplasmin regulation of lipid metabolism homeostasis / 上海交通大学学报（医学版）

Ceruloplasmin(Cp)is a crucial protein secreted by the liver and plays a vital role in regulating the distribution and transport of copper throughout the body,thereby maintaining copper homeostasis.Additionally,Cp functions as a significant enzyme known as ferroxidase,which is involved in iron metabolism within the body.Numerous studies have suggested a close relationship between Cp and metabolic disorders,such as diabetes and cardiovascular diseases.Recent research has also shed light on the involvement of Cp in the regulation of lipid metabolism.The various activities associated with lipid metabolism,including lipid synthesis,adipose hydrolysis,fatty acid oxidation,lipid transport,and absorption,collectively contribute to maintaining lipid homeostasis.Dysregulation of lipid metabolism can lead to metabolic disorders and cardiovascular complications.Cp regulates lipid metabolism through two main mechanisms.Firstly,Cp participates in the regulation of oxidative stress by modulating iron metabolism through its ferroxidase activity and involvement in redox reaction.Secondly,copper along with copper-dependent enzymes directly participates in the processes such as cholesterol metabolism,lipoprotein metabolism,and fatty acid synthesis.As a result,the role of Cp in maintaining the homeostasis of copper and iron allows it to regulate lipid metabolism by influencing copper or iron-dependent enzymes and related pathways.Although the correlation between Cp and lipid metabolism has been identified,an in-depth exploration of the precise mechanisms by which Cp governs lipid metabolism is warranted.This article provides an overview of the role of Cp in lipid metabolism and highlights the progress in related research,with the aim of providing new insights for the development and treatment of disorders related to lipid metabolism.

Exploration of the relationship between nicotinamide metabolism-related genes and osteoarthritis / 上海交通大学学报（医学版）

Objective·To explore the relationship between osteoarthritis and nicotinamide metabolism-related genes using bioinformatics analysis,and identify key genes with diagnostic value and therapeutic potential.Methods·By using"Osteoarthritis"as a search term,GSE12021,GSE55235,and GSE55457 were obtained from the GEO database,with GSE55457 being used as the validation set.After removing batch effects from the GSE12021 and GSE55235 datasets,the standardized combined dataset was obtained and used as the training dataset.Differentially expressed genes(DEGs)were identified from the training dataset.All nicotinamide metabolism-related genes(NMRGs)were obtained from the GeneCards and MSigDB databases.The intersection of DEGs and NMRGs was taken to obtain nicotinamide metabolism-related differentially expressed genes(NMRDEGs).Gene set enrichment analysis(GSEA)was performed on the training dataset,while gene ontology(GO)and Kyoto encyclopedia of genes and genomes(KEGG)analysis were performed on NMRDEGs.Key genes were selected by using least absolute shrinkage and selection operator(LASSO)and support vector machine(SVM)analysis in NMRDEGs to build an osteoarthritis diagnosis model which was validated by using the GSE55457 dataset.Single sample gene set enrichment analysis(ssGSEA)was used to analyze the immune cell infiltration type.Interactions networks and drug molecule predictions were obtained for these key genes'mRNA with the DGIdb,ENCORI,and CHIPBase databases.siRNA was used to knock down the key genes in chondrocytes,and then real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)was used to detect the expression of chondrogenesis-related genes.Results·Seven NMRDEGs,including NAMPT,TIPARP,were discovered.GO and KEGG analysis enriched some signaling pathways,such as nuclear factor-κB signaling pathway and positive regulation of interleukin-1-mediated signaling pathway.GSEA enriched pathways such as Hif1 Tfpathway and syndecan 1 pathway.Key genes NPAS2,TIPARP,and NAMPT were identified through LASSO and SVM analysis,and used to construct an osteoarthritis diagnostic model.The validated results showed that the diagnostic model had high accuracy.Immune infiltration analysis results obtained by ssGSEA showed significant differences(all P<0.05)in 15 types of immune cells,including macrophages.Seven potential small molecules targeting key genes were identified,along with 19 miRNAs with the sum of upstream and downstream>10,19 transcription factors with upstream and downstream>7,and 27 RNA binding proteins with clusterNum>19.The results of RT-qPCR showed that knocking down key genes reduced the expression of chondrogenesis-related genes.Conclusion·Through bioinformatics analysis,key genes related to nicotinamide metabolism,NPAS2,TIPARP,and NAMPT,are discovered,and an osteoarthritis diagnostic model is constructed.

The mechanism of lipid metabolism disorders promoting progression of lung cancer based on the oxLDL/LOX-1 signaling pathway / 实用医学杂志

Objective To explore the mechanism of lipid metabolism disorder promoting the progress of lung cancer based on the oxidized low density lipoprotein(ox-LDL)/human lectin-like oxidized low density lipopro-tein receptor 1(LOX-1)signaling pathway.Methods Eighty-one identified lung adenocarcinoma tissues with paired adjacent non-cancerous tissues(at least 5 cm away from the tumor)were collected from our hospital,and the expression of LOX-1 was detected by immunohistochemistry.LOX-1 was overexpressed in lung adenocarcinoma cell lines(A549 and H1299 cells).Cell invasion ability was measured by Transwell.Cells were treated with different concentrations of oxLDL,and cellular LOX-1 expression was investigated.Results LOX-1 staining in the tumor was significantly stronger than that in the non-cancerous tissue samples(99.4 vs.16.2 for median H score,P<0.001).High LOX-1 expression was significantly correlated with low survival(P<0.001).As compared with the patients without lymph node metastasis,those with lymph node metastasis had higher LOX-1 level(83.2 vs.121.1 for median H score,P<0.01).Overexpression of LOX-1 in lung cancer cells significantly promoted the number of invasive and metastatic cells(P<0.01).In addition,LOX-1 was an essential functional target for oxLDL-induced metastasis of lung cancer cells.Itatinib inhibited the metastasis of LOX-1 overexpressed A549 in vitro.Conclusions With an increase in oxLDL level,the expression of LOX-1 increases.Up-regulation of LOX-1 promotes metastasis of lung cancer,and its mechanism may be related to activation of the JAK1/STAT6 signaling pathway.

The mechanism of emodin inhibiting YAP1 and FOXD1 in gastric cancer AGS cells and its related study / 实用医学杂志

Objective To explore the possible mechanism of emodin in inhibiting proliferation,migration,and invasion of AGS cells and in suppressing the expressions of YAP1 and FOXD1.Methods Normal gastric cell GES-1 and gastric cancer cell AGS were cultured with different concentrations of emodin.CCK8 test,scratch test and Transwell assay were used to verify changes in the biological phenotype of AGS cells.TCGA database was applied to analyze expressions of HK2,YAP1 and FOXD1 in gastric cancer tissues and normal gastric tissues.Western blotting method was used to detect the impacts of emodin on HK2,YAP1 and FOXD1 proteins in AGS cells.Exogenous pyruvic acid was added to verify the changes in YAP1 and FOXD1.Results The IC50 of emodin was significantly higher in GES-1 cells than in AGS cells(P<0.05).CCK8 proliferation test,scratch test,and Transwell assay showed that emodin significantly inhibited the biological abilities of AGS(P<0.05 for comparisons).Analysis on the TCGA bioinformatics database found that the expression of key enzymes HK2 in the glycolysis pathway and oncogenes YAP1 and FOXD1 was significantly higher in gastric cancer tissues than in normal gastric tissues(P<0.05 for comparisons).Emodin significantly inhibited the protein expressions of key glycolytic enzymes HK2 and oncogenes YAP1 and FOXD1(P<0.05 for comparisons).With supplement of exogenous glycolytic metabolite pyruvate,the protein expressions of oncogenes YAP1 and FOXD1 significantly increased(P<0.05 for comparisons).Conclusions Emodin has a significant pharmacological inhibitory effect on gastric cancer AGS cells,markedly suppressing their biological phenotype.Emodin not only significantly inhibits the key enzyme HK2 in glycolysis metabolism,but also the protein expressions of oncogenes YAP1 and FOXD1.With the addition of exogenous pyruvate to enhance the glycolytic metabolic pathway,the protein expressions of oncogenes YAP1 and FOXD1 significantly increased.The above results suggest a close association of YAP1 and FOXD1 with glycolytic metabolism.Emodin may inhibit oncogenes YAP1 and FOXD1 through the glycolytic metabolism of gastric cancer AGS cells.

Correlation analysis of glucose and lipid metabolism indicators combined with antiphospholipid antibodies on prognosis of patients with atherosclerosis / 实用医学杂志

Objective To explore the correlation of glucose and lipid metabolism indicators combined with antiphospholipid antibodies with the prognosis of patients with atherosclerosis.Methods A total of 128 patients with atherosclerosis treated in our hospital from April 2021 to March 2023 were selected as study group,and 48 healthy individuals as control group.Glycolipid metabolism indexes and antiphospholipid antibody level of the two groups were compared,and the predictive value of glycolipid metabolism indexes,antiphospholipid antibodies and combined detection for the prognosis of patients with atherosclerosis were analyzed by ROC.Results TC,TG,ACL,and anti-β2-GP1 in the study group was higher than that in the control group(P＜0.05).The study group was divided into two sub-groups according to the prognosis.The expression level of TC,TG,ACL,and anti-β 2-GP1 in poor prognosis group was higher than that in good prognosis group(P＜0.05).TC,TG,ACL,and anti-β 2-GP1 was positively correlated with the poor prognosis of patients with atherosclerosis(P＜0.05).ROC curve showed that the predictive value of six combined tests for the prognosis of patients with atherosclerosis was higher than that of single test of TC,TG,ACL,and anti-β2-GP1(P＜0.05).Conclusion The combined detection of TC,TG,ACL,and anti-β2-GP1 has high predictive value for the prognosis of patients with atherosclerosis.

ROBO3 deficiency promotes chemotherapy-induced transition of macrophage to foam cell / 实用医学杂志

Objective To explore the effect of chemotherapeutic drugs doxorubicin or cisplatin on lipid metabolism of macrophages and its regulatory mechanism.Methods Macrophage RAW264.7 was treated with doxorubicin or cisplatin,and intracellular lipid level was detected by oil red O and ELISA;RNA sequence screen-ing and Western blot were used to confirm the changes of gene expression after chemotherapeutic drug treatment;The effects of silencing ROBO3 on cellular lipid metabolism were explored,and changes in key target genes of lipid metabolism were detected by Q-PCR and western blot.Results Adriamycin or cisplatin induced disturbances in macrophage cholesterol metabolism and exacerbated macrophage foaminess.Further studies showed that the expression of the axon guidance factor receptor,ROBO3,increased and then decreased during the chemotherapeutic drug-induced macrophage foaming process.Further intervention with ROBO3 exacerbates oxldl-induced cholesterol accumulation and foam formation in macrophages.Mechanistically,ROBO3 deficiency promotes the expression of cholesterol synthesis-related gene DHCR24 and inhibits the expression of cholesterol elimination-related gene ABCG1,resulting in cholesterol accumulation in macrophages.Conclusion This study found that ROBO3 plays an important regulatory role in the disruption of cholesterol metabolism and its foaming process in macrophages induced by chemotherapeutic drugs,which may provide new targets and ideas for the prevention and treatment of chemotherapy-related atherosclerosis.

Research progress in the treatment of AMPK regulating lipid accumulation in the treatment of nonalcoholic fatty liver disease / 实用医学杂志

Non-alcoholic fatty liver disease(NAFLD)is the leading cause of chronic liver disease and has posed significant challenges to global public health and medical care.Due to the unclear pathogenesis of NAFLD,lipid accumulation plays a key role in its development.AMPK,as a crucial molecule in lipid metabolism regulation,can improve lipid accumulation caused by NAFLD.This article describes the specific mechanisms of AMPK-related molecules in improving lipid accumulation and treating NAFLD,and lists the current experimental and therapeutic drugs related to AMPK.The potential of AMPK-related drugs in improving lipid accumulation and treating NAFLD is demonstrated,providing ideas and references for future research on AMPK-related drugs for treating NAFLD.