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Electron microscopist’s view of the Alzheimer’s plaque 电子显微镜下的阿尔茨海默病斑块
Pub Date : 2012-12-31 DOI: 10.14748/BMR.V23.25
K. Dikranian
Alzheimer's disease (AD) is characterized by extracellular aggregation and deposition of Amyloid-beta peptide in the form of diffuse and fibrillar plaques. More than 50 years ago electron microscopic studies in humans have characterized the structure of the amyloid plaque and neurofibrillary tangles. More recently animal models of AD-type amyloidosis have provided excellent opportunities to study plaque structure during the development and expression of AD-type pathology. Ultrastructural data from a variety of transgenic mice overexpressing mutant amyloid precursor proteins, mutant presenilins, with or without human ApoE knock-in isoforms, are highly comparable to classical electron microscopic findings in AD. This review is an attempt to evaluate, from an electron microscopist’s point of view, the structural identity of AD type pathology, and the mature amyloid plaque in particular. Biomedical Reviews 2012; 23: 9-17.
阿尔茨海默病(AD)的特点是细胞外淀粉样蛋白-肽以弥漫性和纤维状斑块的形式聚集和沉积。50多年前,人类的电子显微镜研究已经确定了淀粉样斑块和神经原纤维缠结的结构。最近,ad型淀粉样变性的动物模型为研究ad型病理发展和表达过程中的斑块结构提供了极好的机会。来自各种过表达突变淀粉样前体蛋白的转基因小鼠的超微结构数据,突变的早老素,具有或不具有人类ApoE敲入异构体,与AD的经典电子显微镜结果高度相似。这篇综述试图从电子显微镜的角度来评估AD型病理的结构特征,特别是成熟的淀粉样斑块。生物医学评论2012;23:上行线。
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引用次数: 2
Tissue engineering and growth factors: updated evidence 组织工程和生长因子:最新证据
Pub Date : 2012-12-31 DOI: 10.14748/BMR.V23.26
P. Hassanzadeh
In difficult-to-treat disorders, the traditional pharmacological agents or medical devices alleviate the symptoms but do not reverse the condition. In recent years, the increasing interest into the field of tissue engineering has generated different strategies for tissue growth in vitro or the enhanced repair of damaged tissues in vivo. The core approach of tissue engineering for either therapeutic or diagnostic applications is the ability to exploit living cells in a variety of ways. In this context, identification of the ideal cells and development of biomaterials including the scaffolds for potential applications in the repair, replacement, or regeneration of damaged tissues appear crucial. Meanwhile, successful tissue engineering is often dependent on the delivery of growth factors to the regenerating tissues. Growth factors are multifunctional peptides which play fundamental roles in a wide variety of physiological processes including cell proliferation, chemotaxis, intercellular signalling, angiogenesis and the formation of extracellular matrix, also the re-establishment of tissue integrity. In order to mimic the endogenous profile of growth factor production during the natural tissue morphogenesis or regeneration, the sophisticated mechanisms of growth factor delivery should be developed. This review highlights the general aspects of tissue engineering along with the approaches taken to incorporate growth factors within the biomaterials and their delivery to injured tissue. Biomedical Reviews 2012; 23: 19-35.
在难以治疗的疾病中,传统的药物或医疗器械可以减轻症状,但不能逆转病情。近年来,对组织工程领域的兴趣日益浓厚,产生了不同的体外组织生长或体内损伤组织的增强修复策略。组织工程治疗或诊断应用的核心方法是以多种方式利用活细胞的能力。在这种情况下,理想细胞的鉴定和生物材料的开发,包括用于修复、替换或再生受损组织的支架的潜在应用,显得至关重要。同时,成功的组织工程往往依赖于将生长因子输送到再生组织中。生长因子是一种多功能肽,在细胞增殖、趋化、细胞间信号、血管生成、细胞外基质形成以及组织完整性重建等多种生理过程中发挥着重要作用。为了模拟自然组织形态发生或再生过程中生长因子产生的内源性特征,需要开发复杂的生长因子传递机制。这篇综述强调了组织工程的一般方面,以及将生长因子纳入生物材料及其递送到损伤组织的方法。生物医学评论2012;23: 19-35。
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引用次数: 13
Homage to Rita Levi-Montalcini, the queen of modern neuroscience 向现代神经科学女王丽塔·列维-蒙塔尔奇尼致敬
Pub Date : 2012-12-31 DOI: 10.14748/BMR.V23.24
G. Chaldakov, L. Aloe
The first cell growth factor, nerve growth factor (NGF), was discovered by Rita Levi-Montalcini (RLM) in the early 1950's in Washington University in Saint Louis, Missouri, USA. Originally identified as neurite outgrowth-stimulating factor, later studies revealed that non-neuronal cells, including immune cells, endothelial cells, cardiomyocytes, pancreatic beta cells, prostate epithelial cells and adipose tissue cells, are also targets for and/or sources of NGF. Nerve growth factor is well recognized at present to mediate multiple biological phenomena, ranging from the neurotrophic through immunotrophic and epitheliotrophic to metabotrophic effects. Consequently, NGF and other members of the neurotrophin family are implicated in the pathogenesis of a large spectrum of neuronal and non-neuronal diseases, ranging from Alzheimer's and other neurodegenerative diseases to atherosclerosis and other cardiometabolic diseases. Recent studies demonstrated the therapeutic potentials of NGF in these diseases including ocular and cutaneous diseases. Whereas NGF TrkA receptor antagonists emerged as novel drugs for pain, prostate and breast cancer, and urinary bladder syndromes. Here we briefly describe (i) the "unpredictable" ideogenesis of the discovery of NGF, and (ii) our scientific and human experience working in RML's laboratory for 15 years (GNC) and over 40 years (LA). Biomedical Reviews 2012; 23: 1-7.
第一个细胞生长因子——神经生长因子(NGF),是由Rita Levi-Montalcini (RLM)于20世纪50年代初在美国密苏里州圣路易斯的华盛顿大学发现的。最初被确定为神经突生长刺激因子,后来的研究表明,非神经元细胞,包括免疫细胞、内皮细胞、心肌细胞、胰腺β细胞、前列腺上皮细胞和脂肪组织细胞,也是NGF的靶点和/或来源。神经生长因子介导多种生物现象,从神经营养、免疫营养、上皮营养到代谢营养。因此,NGF和神经营养蛋白家族的其他成员参与了一系列神经元和非神经元疾病的发病机制,从阿尔茨海默氏症和其他神经退行性疾病到动脉粥样硬化和其他心脏代谢疾病。最近的研究表明,神经生长因子在包括眼部和皮肤疾病在内的这些疾病中具有治疗潜力。而NGF TrkA受体拮抗剂则成为治疗疼痛、前列腺癌和乳腺癌以及膀胱综合征的新药。在这里,我们简要描述(i)发现NGF的“不可预测”的意识形态,以及(ii)我们在RML实验室工作了15年(GNC)和40多年(LA)的科学和人类经验。生物医学评论2012;23: 1 - 7。
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引用次数: 1
Pathogenesis of amyotrophic lateral sclerosis 肌萎缩侧索硬化的发病机制
Pub Date : 2011-12-31 DOI: 10.14748/BMR.V22.31
M. Kuźma-Kozakiewicz
Amyotrophic lateral sclerosis is a devastating neurodegenerative disease affecting both upper and lower motor neuron. Despite extensive research the primary cause of the disease has not been indentified and the causative treatment is lacking. The present article describes mechanisms involved in the disease development and progression, including oxidative stress, excitotoxicity, mitochondrial dysfunction, protein aggregation, RNA processing, alterations of cytoskeleton functions and axonal transport, glial cell involvement and programmed cell death. Biomedical Reviews 2011; 22: 7-14.
肌萎缩侧索硬化症是一种影响上下运动神经元的破坏性神经退行性疾病。尽管进行了广泛的研究,但该疾病的主要原因尚未确定,也缺乏病因治疗。本文描述了疾病发生和发展的机制,包括氧化应激、兴奋毒性、线粒体功能障碍、蛋白质聚集、RNA加工、细胞骨架功能和轴突运输的改变、胶质细胞的参与和程序性细胞死亡。生物医学评论2011;22日:7 - 14。
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引用次数: 56
A linkage of mind and brain: Sir John Eccles and modern dualistic interactionism 心灵与大脑的联系:约翰·埃克尔斯爵士与现代二元互动论
Pub Date : 2011-12-31 DOI: 10.14748/BMR.V22.38
Danko D. Georgiev
Our minds, constituted by conscious experiences, are both the most familiar and most mysterious aspect of our lives. Despite the large amount of clinical evidence suggesting an intimate relationship between the brain function and the mind, the nature of this relationship remains poorly understood. In this Commentary we discuss some of the problems faced by the classical mind-brain identity theory and explain how the quantum dualistic interactionism proposed by Sir John Eccles could resolve these problems. Biomedical Reviews 2011; 22: 81-84.
我们的思想,由有意识的经验构成,是我们生活中最熟悉和最神秘的方面。尽管大量的临床证据表明大脑功能和心智之间存在着密切的关系,但人们对这种关系的本质仍然知之甚少。在这篇评论中,我们讨论了经典的心脑同一性理论所面临的一些问题,并解释了约翰·埃克尔斯爵士提出的量子二元论相互作用论如何解决这些问题。生物医学评论2011;22日:81 - 84。
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引用次数: 5
Metallosis: metal ion release from metal-on-metal joint surface replacement - current concerns and future problems 金属病:金属对金属关节表面置换的金属离子释放——当前关注的问题和未来的问题
Pub Date : 2011-12-31 DOI: 10.14748/BMR.V22.35
S. R. Manning
Since its innovation, joint replacement surgery has offered relief from the pain and functional limitation of destructive or degenerate joint disease. The search for the ideal material continues over 120 years later. Recently, using metal-on-metal bearings for younger patients has become the trend to avoid excess wear in high demand patients in the hope of reducing the need to revision surgery. Initial evidence suggested these prostheses offered a durable, functional safe joint that was less likely to be revised than the standard metal and polyethylene joint. A body of evidence is growing rapidly to suggest that metal-on-metal joints are associated with local tissue reactions - metallosis - cellular toxicity, increased serum metal ion concentrations, organ deposition of metal ions, higher rather than lower rates of revision surgery and no functional advantage over any other type of joint replacement. We will consider the reasons for metal ion release; the cellular, local tissue and systemic effects of metal ions and the patient risk and presentation. From the evidence reviewed, serious consideration should be given to the future use of metal-on-metal joint bearings and a suggested follow up plan for patients with such joints is identified and reproduced. Biomedical Reviews 2011; 22: 57-64.
自创新以来,关节置换手术已经缓解了破坏性或退行性关节疾病的疼痛和功能限制。120多年后,对理想材料的探索仍在继续。最近,为年轻患者使用金属对金属轴承已成为趋势,以避免高需求患者的过度磨损,希望减少翻修手术的需要。初步证据表明,这些假体提供了一个耐用、功能安全的关节,与标准的金属和聚乙烯关节相比,不太可能被修改。越来越多的证据表明,金属对金属关节与局部组织反应-金属中毒-细胞毒性,血清金属离子浓度增加,金属离子器官沉积,更高而不是更低的翻修手术率有关,并且与任何其他类型的关节置换术相比没有功能优势。我们将考虑金属离子释放的原因;金属离子对细胞、局部组织和全身的影响以及患者的风险和表现。从所审查的证据来看,应该认真考虑将来使用金属对金属关节轴承,并确定和复制有这种关节的患者的建议随访计划。生物医学评论2011;22: 57 - 64。
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引用次数: 0
From bone marrow to brain: stem cells in neuroprotection, plasticity, and neuroregeneration 从骨髓到大脑:干细胞在神经保护、可塑性和神经再生中的作用
Pub Date : 2011-12-31 DOI: 10.14748/BMR.V22.30
M. Penkowa
At present, curative therapies for neurological diseases are limited, even though they are prevalent worldwide. So far, molecular strategies developed for brain disorders act through one single molecular mechanism, yet, these diseases are multifactorial and highly complex, as to why a successful therapy likely calls for a more multifaceted and cell-based approach. The bone marrow contains a mixed stem and progenitor cell population including hematopoietic stem cells (HSC) and mesenchymal stromal stem cells (MSC), which are potential endogenous candidates for cell-based therapy in various brain disorders like stroke, trauma, and neurodegeneration. Unlike the neural stem cells (NSC), bone marrow HSC are readily isolated, mobilized and expanded by means of treatment with granulocyte-colony stimulating factor (G-CSF) and CXCR4-antagonist plerixafor. Once in the blood circulation, the cells preferentially home to injured tissues including the brain. Bone marrow cells may convey neuroprotection, plasticity, and neuroregeneration by different mechanisms of action, which include either transdifferentiation or cell-cell fusion with resident brain cells. Bone marrow cells also benefit the injured brain by secreting bioactive factors, which in a paracrine manner convey intrinsic repair and enhance neurogenesis. Furthermore, transplanted MSC may activate the astrocytes leading to increased glial secretion of neurotrophic growth factors and enhanced proliferation and migration of the resident NSC. These neuroregenerative mechanisms of action are not mutually exclusive, in fact they may provide a multifaceted therapeutic approach, which is requested in order to move neurorestorative and protective strategies into the clinic. Biomedical Reviews 2011; 22: 1-6.
目前,神经系统疾病的治疗方法是有限的,尽管它们在世界范围内很普遍。到目前为止,针对大脑疾病开发的分子策略通过单一的分子机制起作用,然而,这些疾病是多因素和高度复杂的,这就是为什么成功的治疗可能需要更多方面和基于细胞的方法。骨髓包含混合的干细胞和祖细胞群,包括造血干细胞(HSC)和间充质基质干细胞(MSC),它们是潜在的内源性候选细胞,用于各种脑部疾病,如中风、创伤和神经变性。与神经干细胞(NSC)不同,骨髓HSC很容易通过粒细胞集落刺激因子(G-CSF)和cxcr4拮抗剂plerixafor进行分离、动员和扩增。一旦进入血液循环,这些细胞就会优先回到受伤的组织,包括大脑。骨髓细胞可能通过不同的作用机制来传递神经保护、可塑性和神经再生,这些机制包括转分化或与常驻脑细胞的细胞-细胞融合。骨髓细胞还通过分泌生物活性因子使受损的大脑受益,这些生物活性因子以旁分泌的方式传递内在修复并促进神经发生。此外,移植的间充质干细胞可能激活星形胶质细胞,导致神经营养生长因子的胶质分泌增加,并增强常驻NSC的增殖和迁移。这些神经再生机制的作用并不是相互排斥的,事实上,它们可能提供多方面的治疗方法,这是为了将神经修复和保护策略带入临床所需要的。生物医学评论2011;22: 1 - 6。
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引用次数: 1
towards pragmatic and functional unit of mind-and-brain in rEsponsE to danko gEorgiEv's "a linkagE of mind and brain: sir john EcclEs and modErn dualistic intEractionism" 论心灵与大脑的语用和功能单位——对danko gEorgiEv《心灵与大脑的联系:约翰·埃克尔斯爵士与现代二元互动论》的回应
Pub Date : 2011-12-31 DOI: 10.14748/BMR.V22.39
Rayito Rivera-Hernández, D. Stoyanov
Consciousness is an enigma, perhaps the greatest enigma of philosophy of science. It can be described as a multilevel phenomenon, where transition (from unconsciousness to consciousness) is not a compromise OFF/ON in neuronal activity, but involves a complex change in nerve function, which is mediated by the environment. For the analysis of consciousness, the Australian philosopher David J. Chalmers distinguishes the easy problem of the hard problem of consciousness. The easy problem to analyze issues such as discrimination between sensory stimuli, the integration of information to guide behavior, verbalization of internal states, the integration of sensory information with past experience, how to focus attention, and what distinguishes waking from sleep. On the other hand, the "hard problem" of consciousness is to explain how the physical brain gives rise to consciousness. This analysis deals with the latter. Biomedical Reviews 2011; 22: 85-89.
意识是一个谜,也许是科学哲学中最大的谜。它可以被描述为一个多层次的现象,其中转换(从无意识到意识)不是神经元活动的妥协关闭/打开,而是涉及神经功能的复杂变化,这是由环境介导的。对于意识的分析,澳大利亚哲学家大卫·查默斯(David J. Chalmers)将意识的简单问题与困难问题区分开来。容易分析的问题包括:感官刺激之间的区别,信息的整合以指导行为,内部状态的语言化,感官信息与过去经验的整合,如何集中注意力,以及清醒与睡眠的区别。另一方面,意识的“难题”是解释物理大脑如何产生意识。本文分析的是后者。生物医学评论2011;22日:85 - 89。
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引用次数: 0
G protein-coupled sphingosine-1-phosphate receptors: potential molecular targets for angiogenic and anti-angiogenic therapies G蛋白偶联鞘氨醇-1-磷酸受体:血管生成和抗血管生成治疗的潜在分子靶点
Pub Date : 2011-12-31 DOI: 10.14748/BMR.V22.32
N. Takuwa, Y. Okamoto, K. Yoshioka, Y. Takuwa
Sphingosine-1-phosphate (S1P) is a plasma lipid mediator with pleiotropic activities; it is constitutively produced in red blood cells and vascular endothelial cells through phosphorylation of sphingosine by one of two S1P synthesizing enzymes, sphingosine kinase 1 and 2 (SphK 1, 2), and exported into plasma to bind to high density lipoprotein and albumin. Sphingosine-1-phosphate acts through five members of the G protein-coupled S1P receptors (S1PR1-S1PR5) to exert diverse actions, which include vascular maturation in embryonic stage and postnatal angiogenesis, maintenance of functional integrity of vascular endothelium, regulation of vascular tonus, and lymphocyte trafficking. Sphingosine-1-phosphate is unique in its ability to regulate cell migration either positively or negatively by acting through different receptor subtypes. S1PR1 and S1PR3 mediate chemotactic cell migration toward S1P via Gi/Rac pathway, whereas S1PR2 mediates S1P inhibition of chemotaxis via G12/13/Rho-dependent inhibition of Rac. Sphingosine-1-phosphate positively or negatively regulates tumor cell migration, invasion in Matrigel, and hematogenous metastasis in manners strictly dependent on S1P receptor subtypes expressed in tumor cells. S1PR1 (and S1PR3) also mediates activation of Gi/phosphatidylinositol 3-kinase (PI3K)/Akt and stimulation of cell proliferation/survival, whereas S1PR2 could mediate suppression of cell proliferation/survival through G12/13/Rho/Rho kinase/PTEN-dependent Akt inhibition. S1PR1 (and S1PR3) expressed in endothelial cells mediates angiogenic action of S1P by stimulating endothelial cell migration, proliferation and tube formation. In a mouse model of hindlimb ischemia after femoral artery resection, repeated local administration or sustained delivery of S1P, or transgenic overexpression of SphK1, accelerates post-ischemic angiogenesis, through the S1P actions on both endothelial cells and bone marrow-derived myeloid cells (BMDCs). In tumor cells, SphK1 is upregulated especially in advanced stages, through mechanisms involving both activating Ras mutation and hypoxia, which leads to increased S1P production and also decreased cellular content of pro-apoptotic sphingolipid ceramide, a metabolic precursor of S1P. Apoptotic tumor cells also produce S1P through SphK2 activation, thus implicated in tumor angiogenesis by acting on endothelial cells through S1PR1/S1PR3, as well as tumor-infiltrating macrophages and BMDCs. Inhibition of S1PR1 function by either an anti-S1P antibody or FTY720 inhibits tumor angiogenesis and tumor growth. Differently from S1PR1, S1PR2 expressed in host cells mediates inhibition of tumor angiogenesis and tumor growth, through mechanisms involving the suppression of endothelial cell migration, proliferation and tube formation, and inhibition of BMDC recruitment to tumor stroma with suppressed expression of pro-angiogenic factor and matrix metalloprotease 9. These findings provide the molecular basis for S1P receptor subty
鞘氨醇-1-磷酸(S1P)是一种多效性的血浆脂质介质;S1P合成酶sphingosine kinase 1和2 (sphk1,2)中的一种磷酸化sphingosine,从而在红细胞和血管内皮细胞中组成性地产生sphingosine,并输出到血浆中与高密度脂蛋白和白蛋白结合。鞘氨醇-1-磷酸通过G蛋白偶联S1P受体的5个成员(S1PR1-S1PR5)发挥多种作用,包括胚胎期血管成熟和出生后血管生成、维持血管内皮功能完整性、调节血管张力和淋巴细胞运输。鞘氨醇-1-磷酸通过不同的受体亚型积极或消极地调节细胞迁移的能力是独一无二的。S1PR1和S1PR3通过Gi/Rac途径介导趋化细胞向S1P迁移,而S1PR2通过G12/13/ rho依赖的Rac抑制作用介导S1P趋化。鞘氨醇-1-磷酸正或负调节肿瘤细胞的迁移、侵袭基质和血行转移,其方式严格依赖于肿瘤细胞中表达的S1P受体亚型。S1PR1(和S1PR3)也介导Gi/磷脂酰肌醇3-激酶(PI3K)/Akt的激活和刺激细胞增殖/存活,而S1PR2可以通过G12/13/Rho/Rho激酶/ pten依赖性Akt抑制介导细胞增殖/存活的抑制。内皮细胞中表达的S1PR1(和S1PR3)通过刺激内皮细胞迁移、增殖和成管,介导S1P的血管生成作用。在股动脉切除后后肢缺血小鼠模型中,反复局部给药或持续递送S1P,或转基因过表达SphK1,通过S1P对内皮细胞和骨髓源性髓样细胞(bmdc)的作用,加速缺血后血管生成。在肿瘤细胞中,SphK1表达上调,尤其是在晚期,其机制包括激活Ras突变和缺氧,从而导致S1P的产生增加,并降低细胞中促凋亡鞘脂神经酰胺(S1P的代谢前体)的含量。凋亡的肿瘤细胞也通过活化SphK2产生S1P,从而通过S1PR1/S1PR3作用于内皮细胞,以及肿瘤浸润性巨噬细胞和BMDCs参与肿瘤血管生成。通过抗s1p抗体或FTY720抑制S1PR1功能可抑制肿瘤血管生成和肿瘤生长。与S1PR1不同,宿主细胞中表达的S1PR2通过抑制促血管生成因子和基质金属蛋白酶9的表达,抑制内皮细胞的迁移、增殖和管的形成,抑制BMDC向肿瘤基质的募集,从而抑制肿瘤血管生成和肿瘤生长。这些发现为S1P受体亚型选择性靶向策略针对闭塞性外周动脉疾病的血管生成治疗,以及抗血管生成和抗肿瘤治疗癌症提供了分子基础。生物医学评论2011;22: 15 - 29。
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引用次数: 3
REGULATION OF GLUCOSE METABOLISM BY CENTRAL INSULIN ACTION 中枢胰岛素作用对葡萄糖代谢的调节
Pub Date : 2011-12-31 DOI: 10.14748/BMR.V22.33
H. Inoue
Insulin has been known to act on the hypothalamus, in particular the arcuate nucleus, in the central nervous system. Such central insulin action is not only involved in the regulation of energy metabolism via the regulation of food intake and heat production, but also plays an important role in glucose metabolism by regulating hepatic glucose production and glucose uptake by skeletal muscles. Studies on the intracerebroventricular administration of PI-3K inhibitors or sulfonylureas have demonstrated that hyperpolarization of agouti-related protein neurons induced by the activation of PI-3K signaling/KATP channels in the hypothalamic arcuate nucleus plays an important role in the suppression of hepatic glucose production mediated by central insulin action. Cutting of the vagus nerve overrides the suppression of hepatic glucose production by intracerebroventricular insulin administration, which suggests the involvement of autonomic nerves in central insulin action in the liver. The central insulin action-mediated suppression of hepatic glucose production is associated with decreased gene expression of enzymes involved in hepatic gluconeogenesis, and both increased interleukin-6 expression in hepatic non-parenchymal cells induced by central insulin action and associated activation of hepatic STAT3 play an important role in the suppression of gene expression of hepatic gluconeogenesis-related enzymes. In animal models of obesity and insulin resistance, the central insulin action-mediated hepatic glucose production control mechanism is impaired in both the hypothalamus and liver. Increased hepatic gluconeogenesis in obesity and type-2 diabetes has been attributed to impaired hepatic insulin signaling and increased expression of enzymes involved in hepatic gluconeogenesis due to hyperglycemia, but may also be partially attributed to the impairment of the central insulin action-mediated suppression of hepatic gluconeogenesis. Biomedical Reviews 2011; 22: 31-39.
已知胰岛素作用于中枢神经系统的下丘脑,特别是弓状核。这种胰岛素中枢作用不仅通过调节食物摄入和产热参与能量代谢的调节,还通过调节肝脏葡萄糖生成和骨骼肌葡萄糖摄取在葡萄糖代谢中发挥重要作用。脑室内给药PI-3K抑制剂或磺脲类药物的研究表明,下丘脑弓状核PI-3K信号通路/KATP通道激活诱导的刺痛症相关蛋白神经元的超极化在中枢胰岛素作用介导的肝糖生成的抑制中起重要作用。迷走神经的切断超过了脑室注射胰岛素对肝脏葡萄糖产生的抑制,这表明自主神经参与了肝脏的中枢胰岛素作用。中枢胰岛素作用介导的肝糖生成抑制与肝糖异生相关酶基因表达的降低有关,而中枢胰岛素作用诱导的肝非实质细胞白介素-6表达的增加和相关的肝STAT3的激活在抑制肝糖异生相关酶基因表达中起重要作用。在肥胖和胰岛素抵抗的动物模型中,中枢胰岛素作用介导的肝脏葡萄糖生成控制机制在下丘脑和肝脏中都受到损害。肥胖和2型糖尿病患者肝脏糖异生增加归因于高血糖导致的肝脏胰岛素信号通路受损和参与肝脏糖异生的酶表达增加,但也可能部分归因于胰岛素作用介导的肝糖异生中枢抑制功能受损。生物医学评论2011;22: 31 - 39。
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引用次数: 0
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Biomedical Reviews
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