刺猬正常心电图分析

经过对51只刺猬休眠期和非休眠期心电图观察记录分析,得出刺猬心电图各波各间期正常值、各波波形及其变化以及休眠期与非休眠期差别等资料。     

刺猬嗅球一氧化氮合酶阳性神经元的分布和形态

用依赖还原型辅酶Ⅱ的黄递酶（NADPH-d）组织化学方法显示NOS阳性神经元在刺猬嗅球的分布和形态，观察野生刺猬嗅球内一氧化氮合酶（NOS）阳性神经元的分布和形态．结果显示：NOS阳性神经元在刺猬嗅球内广泛分布。强阳性神经元主要位于刺猬嗅球边缘的突触小球层，小球周细胞也有NOS强阳性表达；偶见深染的NOS阳性僧帽细胞；内颗粒细胞层有大量浅染且较小的NOS阳性神经元．结论：刺猬是敏嗅动物．其嗅球中的NOS阳性神经元分布状态可能与嗅觉灵敏度相关。     

休眠期刺猬小肠运动抑制成因的研究

通过休眠期和非休眠期离体不肠在１１．５℃和３７℃条件下的运动机能比较，和这两种温度下肾上腺素，乙酰胆碱对其运动机能影响比较，结果提示刺猬休眠期小肠运动抑制的成因与神经和肾上腺髓质激素直接调节无大关系，而温度过低则是一重要因素。     

不同季节中缅树鼩脂肪细胞的流式分析

为探究不同季节下中缅树鼩脂肪组织的变化情况,利用流式细胞术分别对春夏秋冬四季中缅树鼩白色脂肪细胞进行UCP1、CD137,对褐色脂肪细胞进行UCP1抗体标记研究。结果显示:中缅树鼩白色脂肪组织细胞群夏季UCP1、CD137阳性表达最低,分别为8.98%、4.42%,冬季达到最高,分别为60.91%、35.54%;褐色脂肪组织细胞群在夏季UCP1阳性表达为22.38%,冬季则高至83.78%。以上结果表明中缅树鼩在冬季,白色脂肪组织中UCP1及CD137阳性表达均增加,诱导白色脂肪组织"褐变",可能产生米色脂肪细胞;褐色脂肪组织UCP1阳性表达增加,表明其产热活性增强。     

冷驯化下中缅树鼩脂肪组织PET/CT扫描成像研究

为了研究中缅树鼩冷驯化条件下脂肪组织的产热活性及白色脂肪组织是否会褐变,实验首次利用正电子发射断层显像/X射线计算机体层成像仪(PET/CT)对中缅树鼩脂肪组织代谢活性进行了探讨,并通过不同的药物浓度梯度实验,首次成功获取中缅树鼩的最佳注射浓度为110~160μCi,此时能够获得最有效的示踪剂辐射值。实验结果表明:随着冷驯化时间的延长,冷驯化0 d、28 d、49 d中缅树鼩褐色脂肪组织的PET/CT扫描成像差异显著。冷驯化28 d时颈部、肩胛、腋下等褐色脂肪组织的平均SUV值与对照组相比差异显著,至49 d时分别增加了10.4倍、9.8倍、13.65倍。冷驯化28 d中缅树鼩腹股沟、腹部大网膜、肠系膜等白色脂肪组织的平均SUV值与对照组相比差异显著,至49 d时分别增加了5.5倍、2.56倍、5.17倍。结果说明,在冷驯化下,中缅树鼩通过增强褐色脂肪组织产热活性,以提高产热应对冷胁迫。冷驯化使中缅树鼩白色脂肪组织增加了18F-FDG的吸收值,意味着此时树鼩白色脂肪组织中可能褐变产生了米色脂肪细胞。     

脱冷过程对高原鼠兔产热的影响

本文探讨了脱冷过程中高原鼠兔的静止代谢率，非颤抖性产热，同时观察肝脏，褐色脂肪组织线粒体蛋白等指标的变化。     

普通刺猬的解剖学研究(三)内脏

对 2 8只 (♀ 1 6,♂ 1 2 )成年普通刺猬 (Erinaceuseuropaeus)的内脏进行了大体解剖学研究。普通刺猬口腔容积大 ,口裂长 ,舌大而灵活 ,食虫型牙齿 ,单室胃、单乳头肾、双角子宫、无肓肠、无阴囊 ,有乳腺 5对 ,大小肠分化不明显 ,肠长相当于体长的 5～ 6倍 ,肝 7叶 ,肺 4叶 ,肝、脾、肾、胰、心脏和肺分别占体重的 4 1 2 %～ 5 2 3% ,0 2 9%～ 0 51 % ,0 42 %～ 0 53% ,0 45%～ 0 65% ,0 36%～ 0 51 %和0 42 %～ 0 60 % ,血液和褐色脂肪分别占体重的 7 7%～ 8 2 %和 0 75%～ 0 87% ,脑较小 ,大脑表面无沟回 ,雌雄刺猬除生殖器官重量有差异外 ,其它各脏器组分均无性别差异。普通刺猬的内脏特征 ,与刺猬的进化水平和生活习性有一定关系     

褐色脂肪组织中的解偶联蛋白

褐色脂肪组织的调节产热等方面的功能近年来一直倍受关注,尤其是存在其中的解偶联蛋白更是近年来研究的热点,本文概述了解偶联蛋白及其基因的结构、解偶联蛋白的生理作用。     

几种实验动物的组织结构之差异

<正> 实验动物的基本组织结构大体相同。但因生活习性的不同,在某些品种之间出现许多差异。根据有关资料及笔者的实观察,现将小鼠、大白鼠、土拨鼠、仓鼠、犬及兔等实验动物的组织器官的差异整理如下,供科研及教学参考之用。脂肪组织(adipose tissue):脂肪组织大体分为二种,即白色脂肪和褐色脂肪。白色     

刺狷被出卖的启迪

狐狸一直对刺猬垂涎三尺,可是刺猬身上长满了刺,没办法靠近。刺猬和乌鸦是好朋友,乌鸦说：刺猬老弟呀,我真羡慕你,你身上的保护伞就连那狡猾的狐狸也奈何不得。刺猬头脑一发热,得意洋洋地说：其实我并不是刀枪不入,当我全身蜷起来的时候,我腹部露有一个小眼,如果朝那个小眼吹一吹气,我受不了痒,就会收起身上的剌。     

Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis

All homeotherms use thermogenesis to maintain their core body temperature, ensuring that cellular functions and physiological processes can continue in cold environments. In the prevailing model of thermogenesis, when the hypothalamus senses cold temperatures it triggers sympathetic discharge, resulting in the release of noradrenaline in brown adipose tissue and white adipose tissue. Acting via the β(3)-adrenergic receptors, noradrenaline induces lipolysis in white adipocytes, whereas it stimulates the expression of thermogenic genes, such as PPAR-γ coactivator 1a (Ppargc1a), uncoupling protein 1 (Ucp1) and acyl-CoA synthetase long-chain family member 1 (Acsl1), in brown adipocytes. However, the precise nature of all the cell types involved in this efferent loop is not well established. Here we report in mice an unexpected requirement for the interleukin-4 (IL-4)-stimulated program of alternative macrophage activation in adaptive thermogenesis. Exposure to cold temperature rapidly promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to induce thermogenic gene expression in brown adipose tissue and lipolysis in white adipose tissue. Absence of alternatively activated macrophages impaired metabolic adaptations to cold, whereas administration of IL-4 increased thermogenic gene expression, fatty acid mobilization and energy expenditure, all in a macrophage-dependent manner. Thus, we have discovered a role for alternatively activated macrophages in the orchestration of an important mammalian stress response, the response to cold.     

A role for brown adipose tissue in diet-induced thermogenesis

Measurement of energy balance during voluntary overeating in rats unequivocally establishes the quantitative importance of diet-induced thermogenesis in energy balance. Like cold-induced thermogenesis, this form of heat production involves changes in the activity of the sympathetic nervous system and brown adipose tissue which suggest that this tissue may determine metabolic efficiency and resistance to obesity.     

Recent advances in brown adipose tissue biology

In mammals, white adipose tissue （WAT） store energy, whereas brown adipose tissue （BAT） burns energy. As a thermogenic organ, BAT can help maintain body temperature during cold exposure. Owing to its important roles in energy metabolism and regulating triacylglycerol levels, BAT has received great attention in treating obesity and its related diseases. Recent studies have suggested that BAT may secrete factor（s）—batokines—to regulate whole- body energy metabolism. In this review, we summarize the recent advances in the formation and function of BAT, as well as molecules that regulate the activity of BAT and beige fat.     

Atypical beta-adrenoceptor on brown adipocytes as target for anti-obesity drugs

Recent studies suggest that thermogenesis in brown adipose tissue has an important role in the regulation of energy balance. Thermogenesis is effected by noradrenaline released from sympathetic nerve endings; the noradrenaline stimulates beta-adrenoceptors, causing lipolysis, and the released fatty acids then promote the uncoupling of oxidative phosphorylation from electron transport. It has been widely accepted that mammalian beta-adrenoceptors exist as two subtypes, beta 1 and beta 2, and rat brown adipocyte beta-adrenoceptors have been classed as beta 1 or as a mixed beta 1/beta 2 population. The beta 1 subtype predominates in atria, whereas the beta 2 subtype predominates in trachea. However, we have now found a novel group of beta-adrenoceptor agonists that selectively stimulate lipolysis in brown adipocytes. In contrast, isoprenaline, fenoterol and salbutamol are less potent as stimulants of lipolysis than as stimulants of atrial rate or tracheal relaxation. Therefore, beta-adrenoceptors in rat brown adipocytes are of neither the beta 1 nor beta 2 subtypes. Compounds that selectively stimulate brown adipocyte beta-adrenoceptors should have potential as thermogenic anti-obesity agents and this has been demonstrated with BRL 26830A , BRL 33725A and BRL 35135A .     

Mice overexpressing human uncoupling protein-3 in skeletal muscle are hyperphagic and lean

Uncoupling protein-3 (UCP-3) is a recently identified member of the mitochondrial transporter superfamily that is expressed predominantly in skeletal muscle. However, its close relative UCP-1 is expressed exclusively in brown adipose tissue, a tissue whose main function is fat combustion and thermogenesis. Studies on the expression of UCP-3 in animals and humans in different physiological situations support a role for UCP-3 in energy balance and lipid metabolism. However, direct evidence for these roles is lacking. Here we describe the creation of transgenic mice that overexpress human UCP-3 in skeletal muscle. These mice are hyperphagic but weigh less than their wild-type littermates. Magnetic resonance imaging shows a striking reduction in adipose tissue mass. The mice also exhibit lower fasting plasma glucose and insulin levels and an increased glucose clearance rate. This provides evidence that skeletal muscle UCP-3 has the potential to influence metabolic rate and glucose homeostasis in the whole animal.     

心肌肥厚大鼠血管膜周脂肪组织对血管舒缩功能的影响

目的:观察正常大鼠及部分结扎腹主动脉致心肌肥厚大鼠的血管膜周脂肪组织对血管舒缩功能的影响。方法:手术部分结扎腹主动脉致心肌肥厚模型,采用血管张力记录法,观察正常大鼠及模型大鼠血管膜周脂肪组织对血管舒缩功能的影响。结果:对于正常大鼠,血管膜周脂肪组织可显著降低血管对苯肾上腺素的反应性;对于模型鼠,血管膜周脂肪组织可显著升高血管对苯肾上腺素的反应性。结论:血管膜周脂肪组织对于血管的舒缩功能有重要的调节作用。     

脂肪组织血管重塑及其与慢性炎症的相互作用

肥胖机体胰岛素抵抗会引起血管并发症已得到认同,但新近关于肥胖机体慢性炎症的研究发现,在出现胰岛素抵抗前脂肪组织脉管系统已发生功能障碍。本研究分析脂肪组织毛细血管发生变化与缺氧的关系和缺氧与慢性炎症的关系,认为肥胖机体脂肪组织毛细血管发生变化,引起脂肪组织缺氧;缺氧诱导慢性炎症,肥胖关联的炎症又引起脂肪组织血管重塑,加剧脂肪组织功能障碍和胰岛素抵抗;提出在肥胖者体内,脂肪组织血管重塑能够调控慢性炎症和全身胰岛素敏感性。     

脂肪组织功能紊乱与肥胖和糖尿病

脂肪组织是机体的重要器官,主要负责能量的储存和代谢,同时分泌多种激素和细胞因子,参与机体生理功能的调控。近年来的研究表明脂肪组织的功能紊乱与肥胖和糖尿病密切相关,为进一步探讨两者的关系,综述了脂肪组织的生理和内分泌功能以及脂肪组织功能紊乱与胰岛素抵抗、肥胖和糖尿病发生、发展的关系。