Possible Role of GnIH as a Novel Link between Hyperphagia-Induced Obesity-Related Metabolic Derangements and Hypogonadism in Male Mice

Gonadotropin-inhibitory hormone (GnIH) is a reproductive inhibitor and an endogenous orexigenic neuropeptide that may be involved in energy homeostasis and reproduction. However, whether GnIH is a molecular signal link of metabolism and the reproductive system, and thus, regulates reproductive activity as a function of the energy state, is still unknown. In the present study, we investigated the involvement of GnIH in glycolipid metabolism and reproduction in vivo, and in the coupling between these two processes in the testis level. Our results showed that chronic intraperitoneal injection of GnIH into male mice not only increased food intake and altered meal microstructure but also significantly elevated body mass due to the increased mass of liver and epididymal white adipose tissue (eWAT), despite the loss of testicular weight. Furthermore, chronic intraperitoneal administration of GnIH to male mice resulted in obesity-related glycolipid metabolic derangements, showing hyperlipidemia, hyperglycemia, glucose intolerance, and insulin resistance through changes in the expression of glucose and lipid metabolism-related genes in the pancreas and eWAT, respectively. Interestingly, the expression of GnIH and GPR147 was markedly increased in the testis of mice under conditions of energy imbalance, such as fasting, acute hypoglycemia, and hyperglycemia. In addition, chronic GnIH injection markedly inhibited glucose and lipid metabolism of mice testis while significantly decreasing testosterone synthesis and sperm quality, inducing hypogonadism. These observations indicated that orexigenic GnIH triggers hyperphagia-induced obesity-related metabolic derangements and hypogonadism in male mice, suggesting that GnIH is an emerging candidate for coupling metabolism and fertility by involvement in obesity and metabolic disorder-induced reproductive dysfunction of the testes.     

Two comparable Ba-MOFs with similar linkers for enhanced CO2 capture and separation by introducing N-rich groups

Two new different metal-organic frameworks (MOFs)[Ba(L1)(H2O)2]n·nH2O (MOF 1) and[Ba(L2)(-H2O)2]n·0.5nDMF·0.5nH2O (MOF 2) were yielded by the assembly of oxygen...     

钢水测温仪自动检测系统的研制

介绍一种钢水测温仪自动检测系统,阐述该系统的工作原理,着重介绍高精度信号源的硬件电路设计。用本检测系统输出的分辨率为1μV的mV级仿真热电偶信号对KZ-300BPR型测温仪进行了验证测试,结果表明各项测试指标(特别是动态参数)优于厂家检测沿用电位差计的性能指标。     

Growth mechanism for zinc coatings deposited by vacuum thermal evaporation

The vacuum thermal evaporation technique was used to simultaneously deposit zinc coatings onto interstitial free steel plates and single-crystal silicon wafers ...     

高层建筑钢结构柱安装测控方法

针对目前高层建筑钢结构柱安装测量控制方法中存在的一些技术盲点,提出处理方法和改进建议。     

叶绿素荧光量子产量的MODIS遥感算法

从荧光量子产量的原理出发,利用 MODIS 卫星数据建立了一种估算量子产量的算法--φ算法.通过 2006 年 3 月 23 日渤海和北黄海的 MODIS 数据计算了荧光量子产量,并与叶绿素荧光效率(cFE)产品进行了比较.结果表明,φ算法是一种更精确的荧光量子产量的估算算法,它有效地避免了 CFE 存在的几个误差来源:包括未考虑浮游植物的"包裹效应"、使用 412nm 的离水辐亮度反演的浮游植物吸收系数以及积分深度过浅.CFE在大部分海域出现负值,还出现了某些高估点;在有效数据范围内,两者存在明显的线性相关关系.φ算法估算的量子产量最高值在0.05左右,这与其它海区测量的值域范围基本一致.除辽东湾东北部和部分近岸水域外,大部分离岸水域在0.001～0.02的范围内.通过对φ算法的误差来源分析,认为发展一种新的反演 678nm 比吸收系数和平均吸收系数的波段比值算法是可行的,也是改进φ算法精度的有效方法.     

极大节旋藻(Arthrospira maxima)生物钟基因kaiC的克隆及分析

以kaiC基因簇部分已知序列为引物设计位点,采用PCR反应池法从节旋藻基因组fosmid文库中筛选到kaiC基因克隆,通过步移测序获得了kaiC基因全长序列。kaiC基因编码区长1554bo,基因GC碱基含量平均为41．76％,密码子第三位明显偏向于U。在基因上游385bp范围内发现一个可能的启动子序列和一些基因调控元件。KaiC蛋白分析发现了Walker A、DXXG、不完整的Walker B等重要模体和具有催化作用的功能位点。Southem杂交的结果证明kaiC基因在极大节旋藻中为单拷贝。极大节旋藻kaiC基因的特殊结构特征为研究kai基因簇的进化提供了重要的启示。     

Tetrandrine Inhibits Skeletal Muscle Differentiation by Blocking Autophagic Flux

Tetrandrine is well known to act as a calcium channel blocker. It is a potential candidate for a tumor chemotherapy drug without toxicity. Tetrandrine inhibits cancer cell proliferation and induces cell death through apoptosis and autophagy. As cancer patients usually experience complications with sarcopenia or muscle injury, we thus assessed the effects of tetrandrine on skeletal muscle cells. We report in this study that a low dose of tetrandrine (less than 5 μM) does not affect the proliferation of C2C12 myoblasts, but significantly inhibits myogenic differentiation. Consistently, tetrandrine inhibited muscle regeneration after BaCl₂-induced injury. Mechanistic experiments showed that tetrandrine decreased the p-mTOR level and increased the levels of LC3 and SQSTM1/p62 during differentiation. Ad-mRFP-GFP-LC3B transfection experiments revealed that the lysosomal quenching of GFP signals was suppressed by tetrandrine. Furthermore, the levels of DNM1L/Drp1, PPARGA1 and cytochrome C (Cyto C), as well as caspase 3 activation and ROS production, were decreased following tetrandrine administration, indicating that the mitochondrial network signaling was inhibited. Our results indicate that tetrandrine has dual effects on autophagic flux in myoblasts during differentiation, activation in the early stage and blockade in the late stage. The ultimate blocking of autophagic flux by tetrandrine led to the disruption of mitochondria remodeling and inhibition of myogenic differentiation. The inhibitory effects of tetrandrine on skeletal muscle differentiation may limit its application in advanced cancer patients. Thus, great attention should be paid to the clinical use of tetrandrine for cancer therapy.