简介：Gutmicrobiotaexertsasignificantroleinthepathogenesisofthemetabolicsyndrome,asconfirmedbystudiesconductedbothonhumansandanimalmodels.Gutmicrobialcompositionandfunctionsarestronglyinfluencedbydiet.Thiscomplexintestinal'superorganism'seemstoaffecthostmetabolicbalancemodulatingenergyabsorption,gutmotility,appetite,glucoseandlipidmetabolism,aswellashepaticfattystorage.Animpairmentofthefinebalancebetweengutmicrobesandhost’simmunesystemcouldculminateintheintestinaltranslocationofbacterialfragmentsandthedevelopmentof'metabolicendotoxemia',leadingtosystemicinflammationandinsulinresistance.Dietinducedweight-lossandbariatricsurgerypromotesignificantchangesofgutmicrobialcomposition,thatseemtoaffectthesuccess,ortheinefficacy,oftreatmentstrategies.Manipulationofgutmicrobiotathroughtheadministrationofprebioticsorprobioticscouldreduceintestinallowgradeinflammationandimprovegutbarrierintegrity,thus,amelioratingmetabolicbalanceandpromotingweightloss.However,furtherevidenceisneededtobetterunderstandtheirclinicalimpactandtherapeuticuse.

简介：AbstractMetabolic syndrome (MetS) describes a set of risk factors that can eventually lead to the occurrence of cardiovascular and cerebrovascular disease. A detailed understanding of the MetS mechanism will be helpful in developing effective prevention strategies and appropriate intervention tools. In this article, we discuss the relationship between the clinical symptoms of MetS and differences in the gut microbial community compared with healthy individuals, characterized by the proliferation of potentially harmful bacteria and the inhibition of beneficial ones. Interactions between gut microbiota and host metabolism have been shown to be mediated by a number of factors, including inflammation caused by gut barrier defects, short-chain fatty acids metabolism, and bile acid metabolism. However, although we can clearly establish a causal relationship between gut microbial profiles and MetS in animal experiments, the relationship between them is still controversial in humans. Therefore, we need more clinical studies to augment our understanding of how we can manipulate the gut microbiota and address the role of the gut microbiota in the prevention and treatment of MetS.

简介：1.BiochemicalstructureandmolecularactivityofmeldoniumMeldonium(commercialnameMildronate)wasoriginallysynthesizedinthemid-1970sattheInstituteofOrganicSynthesisoftheLatvianSovietSocialistRepublicAcademyofSciences.Thechemicalstructureofthiscompound(3-(2,2,2-

简介：1.TheendocannabinoidsysteminobesityandmetabolicdisordersAsobesityandassociatedmetabolicdisorders,suchastype2diabetesanddyslipidemia,arebecomingoneofthemostserioushealthproblemsworldwide,developmentofeffectivetherapiesisahighpriority.Inthesearchfortreatments,therecentlydiscoveredendocannabinoidsystem(ECS)hasbeguntogarnerattention,andawealthofresearchisnowfocusing

简介：AbstractExcessive consumption of fructose, the sweetest of all naturally occurring carbohydrates, has been linked to worldwide epidemics of metabolic diseases in humans, and it is considered an independent risk factor for cardiovascular diseases. We provide an overview about the features of fructose metabolism, as well as potential mechanisms by which excessive fructose intake is associated with the pathogenesis of metabolic diseases both in humans and rodents. To accomplish this aim, we focus on illuminating the cellular and molecular mechanisms of fructose metabolism as well as its signaling effects on metabolic and cardiovascular homeostasis in health and disease, highlighting the role of carbohydrate-responsive element-binding protein in regulating fructose metabolism.

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简介：Medicaltherapyfortype2diabetesmellitusisineffectiveinthelongtermduetotheprogressivenatureofthedisease,whichrequiresincreasingmedicationdosesandpolypharmacy.Conversely,bariatricsurgeryhasemergedasacost-effectivestrategyforobesediabeticindividuals;ithaslowcomplicationratesandresultsindurableweightloss,glycemiccontrolandimprovementsinthequalityoflife,obesity-relatedco-morbidityandoverallsurvival.Thefindingthatglucosehomeostasiscanbeachievedwithaweightloss-independentmechanismimmediatelyafterbariatricsurgery,especiallygastricbypass,hasledtotheparadigmofmetabolicsurgery.However,theprimaryfocusofmetabolicsurgeryisthealterationofthephysio-anatomyofthegastrointestinaltracttoachieveglycemiccontrol,metaboliccontrolandcardio-metabolicriskreduction.Todate,metabolicsurgeryisstillnotwelldefined,asitisusedmostfrequentlyforlessobesepatientswithpoorlycontrolleddiabetes.Themechanismofglycemiccontrolisstillincompletelyunderstood.Publishedresearchfindingsonmetabolicsurgeryarepromising,butmanyaspectsstillneedtobedefined.Thispaperexaminestheproposedmechanismofdiabetesremission,theefficacyofdifferenttypesofmetabolicprocedures,thedurabilityofglucosecontrol,andtherisksandcomplicationsassociatedwiththisprocedure.Weproposeatailoredapproachfortheselectionoftheidealmetabolicprocedurefordifferentgroupsofpatients,consideringtheindicationsandprognosticfactorsfordiabetesremission.

简介：前列腺癌症是在人的最普通的恶意之一。以前的研究决定了那雄激素剥夺治疗(ADT)可以被不利新陈代谢的侧面伴随。在这未来的研究，133个人被招募，包括经历了双边的orchiectomy并且在flutamide(ADT组)上的46个前列腺癌症病人，经历了激进的前列腺切除术(non-ADT组)的有前列腺癌症的37个人并且50个正常控制题目(控制组)。所有题目被跟随至少12个月。从基线到3个月，在ADT组的人与另外的二个组相比增加了fasting浆液胰岛素和低密度的脂蛋白的层次(P<；0.05)。没有明显的变化在另外的参数被发现(P>；0.05)。在12个月以后，在ADT组的人增加了腰的层次与另外的二个组相比的圆周，fasting浆液胰岛素和葡萄糖，全部的胆固醇，高密度的脂蛋白和低密度的脂蛋白(P<；0.05)。另外，在ADT组的新陈代谢的症候群的病态率更高(P<；0.05)与另外的二个组相比。通过为有前列腺癌症的人的外科的阉割的ADT可以与不利新陈代谢的变化被联系。治疗的好处应该对这些风险谨慎地被平衡。

简介：Hormonereplacementtherapy(HRT)isinuseformorethanahalfofcentury,butthequestionofindicationsandidealcandidatesforHRTremainsunclear.Postmenopausalwomenareapopulationwiththeincreasingrisksforcardiovasculardiseaseswhicharethemaincauseofdeathinthisgroup.Declineinoestrogenconcentrations

简介：Thetraceamines(TAs)areafamilyofendogenousamineswithstructural,metabolic,physiologicalandpharmacologicalsimilaritiestoclassicalmonoamineneurotransmitters.TheTAfamilyincludestyramine,octopamine,β-phenylethylamine(PEA),andtryptamine(Figure1).Theirpresencehasbeenwell

简介：AbstractObjective:Altered bile acid transformation induces low-grade chronic inflammation and may play an important role in the pathophysiology of polycystic ovary syndrome (PCOS). Liquiritincan regulate bile acid metabolism and anti-inflammatory properties; however, limited information is available regarding its therapeutic potential in PCOS.Methods:Female C57BL/6 mice were randomly assigned into four groups (n = 6 mice/group): the control, letrozole or dehydroepiandrosterone-induced PCOS groups, PCOS + 20 mg/kg liquiritin group, and control + liquiritin groups. After 21 days of treatment, the mice were euthanized, and the associated metabolism indications were investigated. Ovarian histological examinations were performed, and serum hormone concentration was measured. The expression of key genes involved in steroid hormone synthesis, ovarian follicle development, and ovulation was assessed.Results:Liquiritin reduced fasting blood glucose levels and increased insulin sensitivity compared to the PCOS group. Liquiritin also significantly decreased serum levels of total testosterone (P < 0.001) and dehydroepiandrosterone sulfate (P < 0.05) in the PCOS group. Histomorphological inspection of ovaries from the liquiritin group revealed fewer cystic dilated follicles than in the PCOS group. Moreover, liquiritinsignificantly (P < 0.01) decreased Cyp17a1, Cyp19a1, Fshr, Hsd3b2, Runx2, and Ccn2 mRNA expression compared to letrozole-induced PCOS.Conclusion:Liquiritin may be safe and helpful in ameliorating PCOS-associated hyperandrogenemia and hyperglycemia. However, clinical trials investigating different liquiritin dosages are needed to confirm these findings.

简介：管理生命的自然现象的内在的原则是在最近的年里收到到期的重要性的关键问题之一。没有规模的建筑学的特色是大多数连接节点(中心)的活力。这篇文章的主要目的是由在二个相互作用系统的拓扑的参数上考虑建筑上的模式和中心的移动的后果分析蛋白质蛋白质和果蝇melanogaster的新陈代谢的相互作用网络。分析证明两个相互作用网络跟随一个没有规模的模型，建立从改变的状况，很真实的世界网络遵循小世界模式的事实。平均路径长度出现了一双重并且三方面的增加(从9.42～20.93并且从5.29～17.75变化，分别地)分别地，由于中心的删除为蛋白质蛋白质和新陈代谢的相互作用联网。相反，节点的任意的消除没在蛋白质蛋白质和新陈代谢的相互作用网络的拓扑的参数显示出任何显著不同(平均路径长度：9.42+/-0.02和5.27+/-0.01，分别地)。为二个盒子的这越轨行为强调大多数连接节点的意义到网络的自然拓扑学。

简介：AbstractBackground:The most common etiologies of Cushing's syndrome (CS) are adrenocorticotropic hormone (ACTH)-producing pituitary adenoma (pitCS) and primary adrenal gland disease (adrCS), both of which burden patients with metabolic disturbance. The aim of this study was to compare the metabolic features of pitCS and adrCS patients.Methods:A retrospective review including 114 patients (64 adrCS and 50 pitCS) diagnosed with CS in 2009-2019 was performed. Metabolic factors were then compared between pitCS and adrCS groups.Results:Regarding sex, females suffered both adrCs (92.2%) and pitCS (88.0%) more frequently than males. Regarding age, patients with pitCS were diagnosed at a younger age (35.40 ± 11.94 vs. 39.65 ± 11.37 years, p = 0.056) than those with adrCS, although the difference was not statistically significant. Moreover, pitCS patients had much higher ACTH levels and more serious occurrences of hypercortisolemia at all time points (8 AM, 4 PM, 12 AM) than that in adrCS patients. Conversely, indexes, including body weight, BMI, blood pressure, serum total cholesterol, low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), triglycerides, fasting plasma glucose, and uric acid, showed no differences between adrCS and pitCS patients. Furthermore, diabetes prevalence was higher in pitCS patients than in adrCS patients; however, there were no significant differences in hypertension or dyslipidemia prevalence between the two.Conclusions:Although adrCS and pitCS had different pathogenetic mechanisms, different severities of hypercortisolemia, and different diabetes prevalences, both etiologies had similar metabolic characteristics.

简介：瓣鳃类壳的稳定的同位素的作文广泛地被用来重建palaeo气候和palaeo环境。瓣鳃类壳的同位素的作文仍然在争论的碳的气候、环境的意义，和新陈代谢的碳的加入能遮住溶解的无机的碳的碳同位素记录。这研究处理淡水瓣鳃类，Corbiculafluminea霰石壳。结果显示与主人水从平衡扔并且显示出ontogenic的瓣鳃类壳的13C价值减少，显示有新陈代谢的效果，更多的新陈代谢的碳被合并到更大的壳。壳的新陈代谢的碳的比例在19.8%和26.8%之间变化。然而，13CS能仍然被用作发生在壳生长期间的13CDIC和环境过程的质的指示物。

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简介：AbstractBackground:Obesity is a fundamental factor in metabolic disorders such as hyperlipidemia, insulin resistance, fatty liver, and atherosclerosis. However, effective preventive measures are still lacking. This study aimed to investigate different surgical protocols for removing partial adipose tissue before the onset of obesity and determine whether, and by which protocol, preliminary adipose removal could exert potent preventive effects against diet-induced metabolic disorders.Methods:Male low-density lipoprotein receptor (LDL-R) knockout (KO) mice were randomly divided into four groups and subjected to epididymal fat removal (Epi-FR) surgery, subcutaneous fat removal (suQ-FR) surgery, both subcutaneous and epididymal fat removal (Epi + suQ-FR) surgery, or sham-operation. After 1 week of recovery, all mice were given a high-fat diet (HFD) for 10 weeks to induce metabolic disorders.Results:In the Epi-FR group and the sham-operated group, the mean numbers of the residual subcutaneous fat were 28.59 mg/g and 18.56 mg/g, respectively. The expression of relative genes such as Pparg, Cebpa, Dgat2, Fabp4 and Cd36 in the residual subcutaneous fat increased 2.62, 3.90, 3.11, 2.06, 1.78 times in the Epi-FR group compared with that in the sham-operated group. Whereas in the other fat-removal groups, the residual fat depots had no significant change in either size or gene expression, as compared with those of the sham-operated group. Plasma lipid and glucose levels and insulin sensitivity, as detected by the glucose tolerance test, were not significantly alleviated in the three fat removal groups. Liver mass or lipid content was not attenuated in any of the three fat removal groups. The atherosclerosis burdens in the entire inner aorta and aortic root did not decrease in any of the three fat removal groups.Conclusions:Our data suggest that removal of epididymal adipose or subcutaneous adipose alone or in combination before the onset of obesity did not protect against hyperlipidemia, insulin resistance, fatty liver, or atherosclerosis in LDL-R KO mice fed with a HFD. Hence, adipose removal possibly does not represent a potential approach in preventing obesity-related metabolic disorders in the obesity-susceptible population.

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