雌二醇对大鼠离体脂肪组织释放游离脂肪酸的影响

将大鼠离体脂肪组织置于组织灌流肌槽中,分别加入不同浓度的雌二醇及雌二醇加心得安、异搏定或无钙液,测定离体脂肪组织所释放的游离脂肪酸(freefattyacid,FFA)的含量,观察雌二醇对大鼠离体脂肪组织释放FFA的影响,并探讨其作用机制.结果发现雌二醇促进大鼠离体脂肪组织释放FFA(P<0.01),并存在剂量效应关系(r=0.845,P<0.001);;心得安、异搏定和无钙液可不同程度地阻断雌二醇对离体脂肪组织释放FFA的促进作用.由此表明雌二醇可通过增加FFA的释放,促进离体脂肪组织的分解代谢,且其作用可能部分经肾上腺素能β受体、异搏定敏感的L型Ca2+通道及细胞外Ca2+内流介导.     

ATGL生化功能调节及与心肌肥厚的关系

脂肪甘油三酯脂肪酶是脂肪分解代谢限速酶,ATGL广泛表达于全身各组织,尤其高表达于脂肪组织、肝脏和心脏等.ATGL敲除显示动物因大量甘油三酯堆积而产生严重肥胖,心脏受累尤其严重.主要介绍ATGL功能调节及其功能失调与心肌肥厚的关系     

三种麻醉剂对大鼠离体胃肠平滑肌收缩性影响的比较研究

把大鼠离体小肠段和离体胃的浸浴液(台氏液)分别换成含不同麻醉剂的台氏液．用二道记录仪记录平滑肌的收缩曲线．以收缩频率、平均幅度、运动指数和抑制率为指标,判断三种麻醉剂对离体胃肠平滑肌收缩性的影响,并进行比较．结果表明,三种麻醉剂对大鼠离体胃肠平滑肌收缩性都有不同程度的抑制作用．氨基甲酸乙酯对离体胃平滑肌收缩性的抑制作用最大,抑制率为95．6％;水合氯醛的抑制作用最小,抑制率为56．4％;然而,水合氯醛对离体十二指肠平滑肌收缩性的抑制作用最大,抑制率为99．5％;戊巴比妥钠的抑制作用最小,抑制率为48．9％．建议如进行麻醉大鼠胃运动的中枢调控机制的研究,宜采用水合氯醛麻醉;如进行麻醉大鼠小肠运动的中枢调控机制的研究,宜采用戊巴比妥钠麻醉．     

扶桑花乙酸乙酯不溶物HR-4的生物学作用研究

扶桑花乙酸乙酯不溶物ＨＲ－４对离体子宫和心血管系统的影响．结果表明，１．ＨＲ－４对小鼠离体子宫有明显的收缩作用，该作用可被异丙嗪完全阻断；而消炎痛可部分抑制该兴奋作用．２．ＨＲ－４对离体蛙心的心肌收缩力有抑制性影响，且ＨＲ－４对心肌收缩幅度的影响较对心率的影响更为明显．     

厚网藻切段离体培养的研究

本文报导了厚网藻Pachydictyon coriaccum(Holm)Okam细胞组织离体培养的研究。藻体被切段进行离体培养时，顶端细胞能不断分裂，直接长出新藻体。一个顶端细胞能纵裂成二个或三个细胞，然后每个细胞单独长成新藻体。皮层细胞在离体培养的过程中，能形成新的生长点细胞，长出新枝。髓部细胞暴露在光照下，也能不断分裂长成新藻体。皮层细胞除了能产生新枝以外，还能长出假根。假根末端呈放射状，借此附着在器皿上。切段在离体培养过程中生长旺盛。在0．3厘米×0．5厘米大小的切段上长出四十多个新枝。这一点和自然海区生长的厚网藻大不相同．说明了切段离体培养促进了细胞组织的生长。     

紫红獐牙菜对在体及离体肠肌的影响

目的：研究紫红獐牙菜对豚鼠离体肠肌及小鼠小肠推进功能的影响。方法：采用炭末推进法、离体标本运动实验法分析紫红獐牙菜对在体及离体肠肌的作用及可能的机理。结果：两个剂量组的紫红獐牙菜对乙酰多余胆碱及组胺引起的豚鼠离体肠肌痉挛均有显著的解痉作用（P〈0．05）；高剂量的紫红獐牙菜对小鼠小肠推进运动也有明显抑制作用（P〈0．05）。结论：紫红獐牙菜对动物在体及离体肠肌的收缩均有明显的抑制作用。     

离体黄瓜子叶生根试法的应用

应用离体黄瓜子叶生根试法对十一种天然及合成的化合物进行了生根活性的测定,实验结果表明：吲哚乙酸和乙烯释放物质乙烯利显著促进离体黄瓜子叶的生根,而激动素、赤霉素及脱落酸则抑制离体黄瓜子叶生根;植物生长延缓剂中的多效唑、矮壮素、丁酰肼显著促进生根;含氮化合物硫酸铵、精胶和精氨酸对离体黄瓜子叶生根也有明显的促进作用．上述结果与用绿豆和菜豆下胚轴生根试法等则得的结果一致,进一步完善了这一新的生根测定方法．     

扶桑花乙酯乙溶物HR—4的生物学作用研究

扶桑花乙酸乙酯不溶物ＩＨＲ－４对离体子宫和心血管系统的影响。结果表明，１．ＨＲ－４对小鼠离体子宫有明显的收缩作用，该作用可被异丙嗪完全阻断；而消炎痛可部分抑制该兴奋作用２．ＨＲ－４对离体硅心的心肌收缩性影响，且ＨＲ－４对心肌收缩幅度的影响较对心率的影响更为明显。     

Cu 2+ / 对离体培养下黄瓜子叶花芽分化的影响

以黄瓜子叶离体培养为实验系统,研究了Ｃｕ＾２＋对离体子叶外植体花芽分化的影响,育苗期的培养基中缺乏Ｃｕ＾２＋显著地降低离子叶外植体花芽,营养芽间接花的分化率;离体子叶外植体培养在含有不同浓度的ＣｕＳＯ４培养基中,外植体花芽和营养芽的分化率随Ｃｕ＾２＋浓度升高,其中以０．４μｍｏｌ／Ｌ为最佳;离体子叶外植体在培养的不同时期给予Ｃｕ＾２＋脉冲处理２４ｈ,发现第５天给予０．４μｍｏｌ／Ｌ脉冲处理显著地促     

白首乌离体快速繁殖的研究

本文进行了白首乌茎段的离体培养，选用不同的培养基和不同激素配比试验．结果表明，白首乌茎段在改良ＭＳ＋ＩＢＡ０．５ｍｇ／Ｌ培养基下．能继代和繁殖，繁殖周期为２５天，每周期繁殖倍数为３以上．试管苗移栽在椰糠或河沙基质中成活率可达８５％以上．故本方法可用于离体快繁．     

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。     

AMPK细胞能量感受器研究进展

腺苷酸活化蛋白激酶(AMPK)作为体内能量感受器能感知能量改变情况.阐述了AMPK在外周组织、肝脏组织、骨骼肌和脂肪组织中的能量代谢调节及在下丘脑中枢中的神经调节等相关作用机制.     

Adipocytes as regulators of energy balance and glucose homeostasis

Adipocytes have been studied with increasing intensity as a result of the emergence of obesity as a serious public health problem and the realization that adipose tissue serves as an integrator of various physiological pathways. In particular, their role in calorie storage makes adipocytes well suited to the regulation of energy balance. Adipose tissue also serves as a crucial integrator of glucose homeostasis. Knowledge of adipocyte biology is therefore crucial for understanding the pathophysiological basis of obesity and metabolic diseases such as type 2 diabetes. Furthermore, the rational manipulation of adipose physiology is a promising avenue for therapy of these conditions.     

瘦素与能量平衡

通过对瘦素的研究分析,了解到瘦素受体广泛存在于下丘脑、肺、肾脏、肌肉和脂肪组织等中。瘦素是由ob基因编码、在脂肪组织合成分泌的蛋白质类激素,含有146个氨基酸,主要功能是调控进食、能量及体重。瘦素和其他激素一样,需要与特异的受体结合才能发挥其生物学作用。总之,瘦素的发现,为进一步研究肥胖的发生机制,以及预防和治疗肥胖开辟了一条崭新的途径。     

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。     

Roles of a sustained activation of NCED3 and the synergistic regulation of ABA biosynthesis and catabolism in ABA signal production in Arabidopsis

ABA, acting as a stress signal, plays crucial roles in plant resistance to water stress. Because ABA signal production is based on ABA biosynthesis, the regulation of NCED, a key enzyme in the ABA biosynthesis pathway, is normally thought of as the sole factor controlling ABA signal production. Here we demonstrate that ABA catabolism in combination with a synergistic regulation of ABA biosynthesis plays a crucial role in governing ABA signal production. Water stress induced a significant accumulation of ABA, which exhibited different patterns in detached and attached leaves. ABA catabolism followed a temporal trend of exponential decay for both basic and stress ABA, and there was little difference in the catabolic half-lives of basic ABA and stress ABA. Thus, the absolute rate of ABA catabolism, i.e. the amount of ABA catabolized per unit time, increases with increased ABA accumulation. From the dynamic processes of ABA biosynthesis and catabolism, it can be inferred that stress ABA accumulation may be governed by a synergistic regulation of all the steps in the ABA biosynthesis pathway. Moreover, to maintain an elevated level of stress ABA sustained activation of NCED3 should be required. This inference was supported by further findings that the genes encoding major enzymes in the ABA biosynthesis pathway, e.g. NCED3, AAO3 and ABA3 were all activated by water stress, and with ABA accumulation progressing, the expressions of NCED3, AAO3 and ABA3 remained activated. Data on ABA catabolism and gene expression jointly indicate that ABA signal production is controlled by a sustained activation of NCED3 and the synergistic regulation of ABA biosynthesis and catabolism.     

A PPARγ-FGF1 axis is required for adaptive adipose remodelling and metabolic homeostasis

Although feast and famine cycles illustrate that remodelling of adipose tissue in response to fluctuations in nutrient availability is essential for maintaining metabolic homeostasis, the underlying mechanisms remain poorly understood. Here we identify fibroblast growth factor 1 (FGF1) as a critical transducer in this process in mice, and link its regulation to the nuclear receptor PPARγ (peroxisome proliferator activated receptor γ), which is the adipocyte master regulator and the target of the thiazolidinedione class of insulin sensitizing drugs. FGF1 is the prototype of the 22-member FGF family of proteins and has been implicated in a range of physiological processes, including development, wound healing and cardiovascular changes. Surprisingly, FGF1 knockout mice display no significant phenotype under standard laboratory conditions. We show that FGF1 is highly induced in adipose tissue in response to a high-fat diet and that mice lacking FGF1 develop an aggressive diabetic phenotype coupled to aberrant adipose expansion when challenged with a high-fat diet. Further analysis of adipose depots in FGF1-deficient mice revealed multiple histopathologies in the vasculature network, an accentuated inflammatory response, aberrant adipocyte size distribution and ectopic expression of pancreatic lipases. On withdrawal of the high-fat diet, this inflamed adipose tissue fails to properly resolve, resulting in extensive fat necrosis. In terms of mechanisms, we show that adipose induction of FGF1 in the fed state is regulated by PPARγ acting through an evolutionarily conserved promoter proximal PPAR response element within the FGF1 gene. The discovery of a phenotype for the FGF1 knockout mouse establishes the PPARγ–FGF1 axis as critical for maintaining metabolic homeostasis and insulin sensitization.     

大鳍鳠臀鳍和脂鳍的比较组织学研究

大鳍鳠臀鳍和脂鳍均是皮肤特化的产物．臀鳍的组织结构可分为表皮层、胶原纤维层、胶原下层和鳍条４部分；脂鳍可分为表皮层、胶原纤维层和脂肪层．臀鳍和脂鳍的表层均与皮肤的表皮相似，而发达的胶原纤维层与皮肤真皮的致密层相当．臀鳍的胶原下层、脂鳍的脂肪层与皮下层相当，而鳍条则是矿化的结缔组织．从特化程度来看，脂鳍的特化程度不如臀鳍高，表明脂鳍应是奇鳍褶的痕迹器官．