Role of Luteinizing Hormone in Regulation of the Rat Estrous Cycle

The role of luteinizing hormone (LH) in regulation of secretionof ovarian steroids during the preovnlatory phase of the ratestrous cycle has been discussed. Evidence indicating an involvementof these steroids in control of the uterine growth, vaginalcornification, mating behavior and LH secretion which occurduring this phase has been reviewed. A positive feedback controlsystem has been proposed in which both ovarian and adrenal steroidsparticipate to initiate the preovulatory "LH surge" which culminatesin ovulation and luteinization     

Effect of Cold Exposure on Thyroid Hormone Metabolism and Nuclear Binding in Rat Brain

In this study we examined whether adult rat brain tissue (cerebral hemispheres) would under cold exposure respond with changes in the local metabolism and nuclear binding of thyroid hormones (T₃, T₄). Adult, control rats kept at 22°C and cold exposed (4°C, 20 h) rats were injected with trace of ¹²⁵I-T₄ or ¹²⁵I-T₃ returned to their respective environment and sacrificed four hours later. The radioactive hormonal forms were identified and quantified in the cytoplasmic and nuclear fractions. It was found that in cold exposed rats injected with ¹²⁵I-T₄, the total cytoplasmic radioactivity was higher than that of controls. This increase was not associated with ¹²⁵I-T₄ but it reflected an increase (88 %) in its deiodination product ¹²⁵I-T₃ (¹²⁵I-T₃ (T₄)). Although total cytoplasmic ¹²⁵I-T₄ did not change, there was a decrease (28%) in its protein free cytoplasmic fraction. ¹²⁵I-T₃ (T₄) and ¹²⁵I-T₄ bound to the nuclear fraction were found to decrease by 58 and 46% respectively. Cold exposed animals injected with ¹²⁵I-T₃ also showed an increase in cytoplasmic ¹²⁵I-T₃ (81%) and a decrease in ¹²⁵I^– (40%) whereas ¹²⁵I-T₃ bound to the nuclear fraction decreased by 64%. These results indicate that cold exposure of rats decreases brain local T₃ metabolism and nuclear binding while it does not effect local T₄ metabolism.     

Excess Thyroid Hormone and Carbohydrate Metabolism

ObjectiveTo review the pertinent basic and clinical research describing the complex effects of excess thyroid hormone on carbohydrate metabolism.MethodsWe performed a MEDLINE search of the English-language literature using a combination of words (ie, “thyrotoxicosis and diabetes,” “diabetic ketoacidosis and thyroid storm,” “carbohydrate metabolism and hyperthyroid,” “glucose homeostasis and thyrotoxicosis”) to identify key articles addressing various aspects of the thyroid’s influence on carbohydrate metabolism.ResultsThyroid hormone affects glucose homeostasis via its actions on a variety of organs including increased hepatic glucose output, increased futile cycling of glucose degradation products between the skeletal muscle and the liver, decreased glycogen stores in the liver and skeletal muscle, altered oxidative and nonoxidative glucose metabolism, decreased active insulin output from the pancreas, and increased renal insulin clearance. Thyroid hormone also affects adipokines and adipose tissue, further predisposing the patient to ketosis.ConclusionsThyrotoxicosis can alter carbohydrate metabolism in a type 2 diabetic patient to such an extent that diabetic ketoacidosis develops if untreated. Based on the current understanding of this relationship, all diabetic patients should be screened for thyroid dysfunction because correcting hyperthyroidism can profoundly affect glucose homeostasis. Similarly, patients presenting in diabetic ketoacidosis should undergo a thyroid function assessment. (Endocr Pract. 2009;15:254-262)     

Thyroid Hormone Receptors in the Developing Rat Brain

It is widely believed that the adult mammalian brain is insensitiveto thyroid hormones unlike the neonatal brain which is criticallydependent on these hormones for the development of normal structureand function. Recent studies have demonstrated the presenceof limited capacity, high affinity, triiodothyronine (T3) bindingnuclear sites in tissues that are considered responsive to thyroidhormones. Furthermore, there is evidence from studies on peripheraltissues that these T3 binding sites act as true receptors ininitiating thyroid hormone action. This report examines whetherthe higher sensitivity of neonatal brain to thyroid hormonesand the purported decline in sensitivity in adulthood are relatedto changes in the concentration and affinity characteristicsof thyroid hormone receptors in rat cerebral nuclei. Analysisof Scatchard plots of in vitro T3 binding data indicate thatcerebral nuclei from adult rats contain T3 specific nuclearbinding sites at a concentration comparable to that presentduring the period when the brain is critically dependent onthe presence of thyroid hormones and exceed that in the liver,a tissue generally considered thyroid sensitive. Neonatal thyroidectomysignificantly increased the number of binding sites. The resultsshow that the apparent unresponsiveness of the cerebral cortexof adult rats to thyroid hormones is not due to the absenceor a low density of T3 nuclear binding sites. The significanceof these results is discussed.     

硒缺乏与甲状腺激素代谢及功能

Ｉ型脱碘酶为含硒酶,缺硒时,该酶活性下降,使循环Ｔ４增高,外周组织Ｔ３水平下降。缺硒可加速甲状腺组织碘的耗竭,并加重某些缺碘的生物学效应,缺硒还可能与碘缺乏病的发生发展有关。以缺硒为主要病因的克山病存在甲状腺激素代谢异常,其心肌呼吸酶活性变化与缺碘引起的甲状腺功能低下相似,缺碘可缺硒引起的甲状腺激素代谢改变与克山病的发生可能有关。     

Regulation of Resistin by Gonadal,Thyroid Hormone,and Nutritional Status

Objective: Resistin was recently identified as a hormone secreted by adipocytes that is under hormonal and nutritional control. This hormone has been suggested to be the link between obesity and type 2 diabetes. The aim of this study was to assess the influence of gender, gonadal status, thyroid hormones, pregnancy, and food restriction on resistin mRNA levels in adipose tissue of rats. Research Methods and Procedures: We have determined resistin mRNA expression by Northern blot analysis in all experimental sets. Results: Resistin mRNA expression is influenced by age, with the highest hormone levels existing at 45 days after birth and decreasing thereafter. Resistin mRNA expression is higher in men than in women. Moreover, we studied the effect of orchidectomy and ovariectomy in rats of different ages and showed that gonadal hormones increase adipose tissue resistin mRNA expression in male rats. Resistin is also regulated by thyroid hormones; it is severely decreased in hyperthyroid rats. Our results clearly show that chronic food restriction (30% of ad libitum food intake) led to a decrease in adipose tissue mRNA levels in normal cycling female rats and pregnant rats. In pregnancy, resistin mRNA levels were enhanced particularly at midgestation. Discussion: Our observations indicate that resistin is influenced by gender, gonadal status, thyroid hormones, and pregnancy. These findings suggest that resistin could explain the decreased insulin sensitivity during puberty and could be the link between sex steroids and insulin sensitivity. Moreover, resistin could mediate the effect of thyroid hormones on insulin resistance and the state of insulin resistance present during pregnancy.     

Thyroid Hormone Mediates Syndecan Expression in Rat Neonatal Cerebellum

Thyroid hormone (T₃) plays an essential role in the central nervous system development. Astrocytes mediate many of the T₃ effects in the growth and differentiation of cerebellum. In culture, T₃ induces cerebellar astrocytes to secrete growth factors, mainly FGF₂, and alters the expression and organization of the extracellular matrix (ECM) proteins, laminin, and fibronectin. In addition, T₃-treated astrocytes promote neuronal differentiation. In this study, we have investigated whether other ECM molecules, such as syndecans, are involved in T₃ action. Thus, we analyzed the expression of syndecans (1–4) by RT-PCR in astrocyte cultures from cerebellum, cortex, and hippocampus of newborn rats. Our results showed that syndecans (1–4) are expressed in astrocytes of cerebellum and cortex, whereas in hippocampus only syndecans 2 and 4 were detected. Semi-quantitative RT-PCR analysis revealed the reduced expression of syndecans 1, 2, and 4, and increased expression of syndecan 3 in hypothyroid cerebellum, when compared to the euthyroid tissue. Furthermore, we observed a reduced expression of syndecans 2 and 3 in T₃-treated cerebellar astrocytes, when compared to control cultures. This balance of proteoglycans may be involved in T₃ action mediated by FGF₂ signaling, possibly affecting the formation of the trimeric signaling receptor complex composed by syndecan/FGF/FGF-receptor (FGFR), which is essential for FGFR dimerization, activation, and subsequent cell signaling.     

甲状腺激素在两栖动物变态过程中的作用

两栖动物的幼体变态是研究甲状腺激素调节组织和器官重构的理想模式。本文主要综述了近年来两栖动物甲状腺激素合成过程中3种脱碘酶D1、D2和D3的特点及其生物学功能;甲状腺激素受体的蛋白结构、类型和机能;以及甲状腺激素对两栖动物幼体变态过程中各个类型组织和器官重构的调节;甲状腺激素、甲状腺激素受体和脱碘酶的互作,并展望了今后的研究方向。     

植物萜类化合物的天然合成途径及其相关合酶

文章概述植物萜类次生代谢产物的生物代谢途径及与其相关关键酶的研究进展。     

果实中糖的运输、代谢与积累及其调控

叶片光合产物向果实运输的主要形态是蔗糖,但在木本蔷薇科果树中,光合产物的主要运输形态为山梨醇.糖从质外体空间跨膜运入共质体的过程由糖运输蛋白介导,而糖运输蛋白的基因表达伴随着果实糖的积累而增强.蔗糖代谢酶参与了细胞内外4个与糖运输有关的无效循环.己糖代谢抑制是果实糖快速积累的前提.在木本蔷薇科果实中,蔗糖代谢酶活力仍非常活跃,表明蔗糖可能与山梨醇在果实生长发育中都起重要的作用.糖作为信号分子,调节了承担糖运输与代谢的基因的表达.自然环境因子和栽培措施能有效调控糖运输、代谢与积累.反义抑制Ivr基因表达能提高番茄果实含糖量的实验结果表明遗传工程调控糖积累的潜力.阐明糖信号与其它信号互作对糖运输与代谢的调控机制是今后研究的重点.     

Glucose Transport in Astrocytes: Regulation by Thyroid Hormone

Primary cultures of astrocytes from newborn rat brain showed evidence of a substrate-saturable process for glucose transport. The system shows a relatively high affinity for the substrate, with an apparent Km of approximately 1 mM. Maintenance of the cells in medium containing thyroid-hormone-free serum for 3, 6, or 9 days resulted in significantly reduced rates of hexose transport. Addition of exogenous triiodothyronine to the transport incubation medium of these "hypothyroid" cells markedly increased the net rate of 2-deoxyglucose uptake within 60 s to values equal to or above those of control cultures (cells maintained in normal serum). These findings support a key role for thyroid hormone in the transport of glucose across plasma membranes of brain cells and demonstrate the presence of this regulatory system in astrocytes.     

Thyroid Hormone Influences Antioxidant Defense System in Adult Rat Brain

The objective of the current study was to find out whether thyroid hormone influences antioxidant defense parameters of rat brain. Several oxidative stress and antioxidant defense parameters of mitochondrial (MF) and post-mitochondrial (PMF) fractions of cerebral cortex (CC) of adult rats were compared among euthyroid (control), hypothyroid [6-n-propylthiouracil (PTU)-challenged], and hyperthyroid (T3-treatment to PTU-challenged rats) states. Oxidative stress parameters, such as thiobarbituric acid-reactive substances (TBA-RS) and protein carbonyl content (PC), in MF declined following PTU challenge in comparison to euthyroid rats. On the other hand, when PTU-challenged rats were treated with T3, a significant increase in the level of oxidative stress parameters in MF was recorded. Hydrogen peroxide content of MF as well as PMF of CC was elevated by PTU-challenge and brought to normal level by subsequent treatment of T3. Although mitochondrial glutathione (reduced or oxidized) status did not change following PTU challenge, a significant reduction in oxidized glutathione (GSSG) level was noticed in PMF following the treatment. T3 administration to PTU-challenged rats had no effect on mitochondrial glutathione status. Total and CN-resistant superoxide dismutase (SOD) activities in MF of CC augmented following PTU challenge. CN-resistant SOD activity did not change when PTU-challenged rats were treated with T3. Although CN-sensitive SOD activity of PMF remained unaltered in response to PTU challenge, its activity increased when PTU-challenged rats were treated with T3. Catalase activity in PMF of CC of PTU-challenged rats increased, whereas the activity was decreased when hypothyroid rats were treated with T3. Similarly, total and Se-dependent glutathione peroxidase (GPx) activities of MF increased following PTU challenge and reduced following administration of T3. Se-independent GPx activity of MF and PMF and glutathione reductase activity of PMF decreased following PTU challenge and did not change further when rats were treated with T3. On the other hand, glutathione S-transferase activity of MF and PMF of CC did not change following PTU challenge but decreased below detectable level following T3 treatment. Results of the current investigation suggest that antioxidant defense parameters of adult rat brain are considerably influenced by thyroid states of the body.     

Developmental Role of Juvenile Hormone Metabolism in Lepidoptera

SYNOPSIS. Lepidopteran juvenile hormone (JH) esterase appearsto have a functional role in the regulation of embryogenesis,larval growth and development, and adult reproduction. In preovipositionaland newly laid eggs of the tobacco hornworm, Manduca sexta,JH esterase activity was elevated presumably to metabolize maternalJHs, and then declined after blastoderm formation. Also, a singlepeak in hemolymph JH esterase activity was found prior to ecdysisin the second through the fourth instar of M. sexta, the functionof which is unclear. However, in the last instar, elevated hemolymphJH esterase activity was noted prior to wandering and againprior to ecdysis to scavenge the last traces of JH necessaryfor normal development. The hemolymph JH esterase is likelyof multiple tissue origin for the prewandering peak with thefat body excluded as a source for the prepupal peak; an inhibitoryfactor from the brain and JH regulate JH esterase biosynthesis.In adult cabbage loopers, Trichoplusia ni, elevated hemolymphJH esterase activity appeared to be important in reducing theJH titer and preventing egg maturation. Structure/activity datawith trifluoromethylketones were incorporated into the designof a novel, JH esterase inhibitor, the sulfone and hydrate ofoctylthio-1,1,1- trifluoropropan-2-one, with selective and persistent,in vivo inhibitory activity. The topical application of thiscompound to last instar larvae and virgin adults of T. ni producedjuvenizing effects (delayed pupation and induced egg maturation/oviposition,respectively) providing direct evidence of a functional rolefor JH esterase in lepidopteran development.     

Gene Regulation by Thyroid Hormone During Amphibian Metamorphosis: Implications on the Role of Cell-Cell and Cell-Extracellular Matrix Interactions

SYNOPSIS. Amphibian metamorphosis is the developmental processinitiated by thyroid hormone which transforms a tadpole intoa frog. This transformation requires extensive remodeling ofalmost every tissue in the animal. One of the more well-studiedtadpole tissues that undergoes remodeling is the small intestine.This tissue requires a shortening in length as well as internalanatomical restructuring to function in the adult frog. Briefly,the tadpole epithelial cells undergo programmed cell death (orapoptosis) and are replaced by a layer of newly formed adultepithelium. About 20 thyroid hormone-regulated genes participatingin this intestinal remodeling have been identified. These genescan be divided into several groups based on the proposed functionsof their products. One of these groups contains several secretedand/or signaling molecules. Most prominent among these are theXenopus homologs of the hedgehog and stromelysin-3 genes. Basedon the expression profiles and cellular localization, hedgehogappears to be involved in adult epithelial morphogenesis. Stromelysin-3may participate in basal lamina modification which is potentiallyinvolved in the apoptosis of the larval epithelium and developmentof the adult epithelium. Here we will review in detail the potentialroles for these secreted factors as well as the proposed molecularmechanisms responsible for their physiological functions. Furthermore,we will examine the effect of these proteins on the extracellularenvironment and how this impacts upon cellular processes involvedin intestinal remodeling.     

The Impact of Iodine Excess on Thyroid Hormone Biosynthesis and Metabolism in Rats

Thyroid function ultimately depends on appropriate iodine supply to the gland. There is a complex series of checks and balances that the thyroid uses to control the orderly utilization of iodine for hormone synthesis. The aim of our study is to evaluate the mechanism underlying the effect of iodine excess on thyroid hormone metabolism. Based on the successful establishment of animal models of normal-iodine (NI) and different degrees of high-iodine (HI) intake in Wistar rats, the content of monoiodotyrosine (MIT), diiodotyrosine (DIT), T₄, and T₃ in thyroid tissues, the activity of thyroidal type 1 deiodinase (D1) and its (Dio1) mRNA expression level were measured. Results showed that, in the case of iodine excess, the biosynthesis of both MIT and DIT, especially DIT, was increased. There was an obvious tendency of decreasing in MIT/DIT ratio with increased doses of iodine intake. In addition, iodine excess greatly inhibited thyroidal D1 activity and mRNA expression. T₃ was greatly lower in the HI group, while there was no significant difference of T₄ compared with NI group. The T₃/T₄ ratio was decreased in HI groups, antiparalleled with increased doses of iodine intakes. In conclusion, the increased biosyntheses of DIT relative to MIT and the inhibition of thyroidal Dio1 mRNA expression and D1 activity may be taken as an effective way to protect an organism from impairment caused by too much T₃. These observations provide new insights into the cellular regulation mechanism of thyroid hormones under physiological and pathological conditions.     

大鼠脑α_1型甲状腺激素受体基因的cDNA克隆及序列分析

使用ＲＴ－ＰＣＲ方法克隆了Ｗｉｓｔａｒ大鼠脑α_１型甲状腺激素受体的ｃＤＮＡ,得到包含起始及终止密码子共１２３３ｂｐ、编码４０９个氨基酸的受体全长编码序列．酶切分析后,将此特异ＤＮＡ片段重组入质粒ｐＵＣ系统,得重组质粒ｐＴＲＡ．双脱氧末端终止法测定了全部核苷酸顺序,结果与文献报导的ＳＤ大鼠的结果一致,同时对长片段ＤＮＡ的ＲＴ－ＰＣＲ扩增进行了方法学的探讨。     

Characterization of the Thyroid Hormone Transport System of Cerebrocortical Rat Neurons in Primary Culture

Abstract: The uptake of 3',3,5-triiodo- l -thyronine (T₃) and l -thyroxine (T₄) by primary cultures derived from rat brain hemispheres was studied under initial velocity conditions, at 25°C. Uptake of both hormones was carrier mediated and obeyed simple Michaelis-Menten kinetics. The K _m of T₃ uptake was very similar to that of T₄, and did not vary significantly from day 1 to 4 in culture (310–400 n M ). The maximal velocity ( V _max) of T₃ uptake nearly doubled between day 1 and 4 of culture (41 ± 3 vs. 70 ± 5 pmol/min/mg of DNA, respectively). The V _max of T₄ uptake did not change (28 ± 8 and 31 ± 4 pmol/min/mg of DNA on days 1 and 4, respectively). The rank order of unlabeled thyroid hormone analogues to compete with labeled T₃ or T₄ uptakes were the same (T₃ > T₄ > 3',5',3-triiodo- l -thyronine > 3',3,5-triiodo- d -thyronine > triiodothyroacetic acid), indicating that the transport system is stereospecific. Unlabeled T₄ was a stronger competitor of labeled T₄ uptake than of labeled T₃ uptake, whereas unlabeled T₃ had the same potency for both processes. These results suggest that T₃ and T₄ are transported either by two distinct carriers or by the same carrier bearing separate binding sites for each hormone. They also indicate that the efficiency of T₃ uptake increases during neuronal maturation.