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.     

IRS-2 pathways integrate female reproduction and energy homeostasis

Severe dietary restriction, catabolic states and even short-term caloric deprivation impair fertility in mammals. Likewise, obesity is associated with infertile conditions such as polycystic ovary syndrome. The reproductive status of lower organisms such as Caenorhabditis elegans is also modulated by availability of nutrients. Thus, fertility requires the integration of reproductive and metabolic signals. Here we show that deletion of insulin receptor substrate-2 (IRS-2), a component of the insulin/insulin-like growth factor-1 signalling cascade, causes female infertility. Mice lacking IRS-2 have small, anovulatory ovaries with reduced numbers of follicles. Plasma concentrations of luteinizing hormone, prolactin and sex steroids are low in these animals. Pituitaries are decreased in size and contain reduced numbers of gonadotrophs. Females lacking IRS-2 have increased food intake and obesity, despite elevated levels of leptin. Our findings indicate that insulin, together with leptin and other neuropeptides, may modulate hypothalamic control of appetite and reproductive endocrinology. Coupled with findings on the role of insulin-signalling pathways in the regulation of fertility, metabolism and longevity in C. elegans and Drosophila, we have identified an evolutionarily conserved mechanism in mammals that regulates both reproduction and energy homeostasis.     

Microenvironmental regulation of stem cells in intestinal homeostasis and cancer

The identification of intestinal stem cells as well as their malignant counterparts, colon cancer stem cells, has undergone rapid development in recent years. Under physiological conditions, intestinal homeostasis is a carefully balanced and efficient interplay between stem cells, their progeny and the microenvironment. These interactions regulate the astonishingly rapid renewal of the intestinal epithelial layer, which consequently puts us at serious risk of developing cancer. Here we highlight the microenvironment-derived signals that regulate stem-cell fate and epithelial differentiation. As our understanding of normal intestinal crypt homeostasis grows, these developments may point towards new insights into the origin of cancer and the maintenance and regulation of cancer stem cells.     

AMPK regulates NADPH homeostasis to promote tumour cell survival during energy stress

Overcoming metabolic stress is a critical step for solid tumour growth. However, the underlying mechanisms of cell death and survival under metabolic stress are not well understood. A key signalling pathway involved in metabolic adaptation is the liver kinase B1 (LKB1)-AMP-activated protein kinase (AMPK) pathway. Energy stress conditions that decrease intracellular ATP levels below a certain level promote AMPK activation by LKB1. Previous studies showed that LKB1-deficient or AMPK-deficient cells are resistant to oncogenic transformation and tumorigenesis, possibly because of the function of AMPK in metabolic adaptation. However, the mechanisms by which AMPK promotes metabolic adaptation in tumour cells are not fully understood. Here we show that AMPK activation, during energy stress, prolongs cell survival by redox regulation. Under these conditions, NADPH generation by the pentose phosphate pathway is impaired, but AMPK induces alternative routes to maintain NADPH and inhibit cell death. The inhibition of the acetyl-CoA carboxylases ACC1 and ACC2 by AMPK maintains NADPH levels by decreasing NADPH consumption in fatty-acid synthesis and increasing NADPH generation by means of fatty-acid oxidation. Knockdown of either ACC1 or ACC2 compensates for AMPK activation and facilitates anchorage-independent growth and solid tumour formation in vivo, whereas the activation of ACC1 or ACC2 attenuates these processes. Thus AMPK, in addition to its function in ATP homeostasis, has a key function in NADPH maintenance, which is critical for cancer cell survival under energy stress conditions, such as glucose limitations, anchorage-independent growth and solid tumour formation in vivo.     

双供电路灯调光节能技术研究

介绍了一种基于太阳能和市网供电相结合的双电源供电的调光节能技术,采用SPWM控制方式和新型桥式整流逆变电路,可按照环境和用户需要自动调节汞灯的发光强度,具有节能效果明显、输入电流的死区范围小、起辉时间短、发光效率高等特点。     

一种新型制冷机能量调节的控制算法

研究新型混合吸收式制冷循环的能量调节的自动控制问题.采用动态矩阵预测控制算法设计多变量动态矩阵控制器,对新型混合吸收式制冷循环的能量进行自动调节,同时利用软件Matlab/Simulink对其进行仿真,结果表明该算法能有效地改善控制器的动态特性,显著提高制冷机的抗干扰性,表现出了较好的自适应能力.     

论共生系统:肠道菌群和人类健康

共生是生物界中普遍存在的一种现象,互利共生的一个典型例子就是人类和肠道菌群.人类利用肠道菌群消化食物来获得生存所需的能量和营养,而肠道菌群则获得栖息地和营养.肠道菌群与人类相互作用形成了一种与人类健康密切相关的平衡状态,打破这种平衡状态会导致人体内的许多疾病,如肥胖、高血压、炎症性肠病、癌症等.肠道菌群参与宿主新陈代谢、机体免疫、基因表达、疾病发展和药物疗效,同时它也受饮食、抗生素、生活方式、遗传和时间点的影响.作者系统地回顾了人类与肠道菌群之间的相互作用,分析了肠道菌群在人类疾病治疗中的应用现状,描述了治疗中存在的主要问题,为肠道菌群在人类疾病治疗中的应用提供了新的思路.     

利用发送速率调节无线传感器网络节点的能耗策略研究

无线传感器网络一般都采用节点逐跳转发方式进行数据传输,这一通信机制容易导致网络局部区域的节点能量消耗较快,进而导致整个网络过早死亡。根据无线传感器网络的数据传输特点建立了一种以节点跳数为基础的全新网络模型,通过分析网络的数据特征得到了节点承载的数据量模型,进而得出了传感器网络的能耗及其数据发送延迟。在此基础上,在保证应用延迟需求前提下,提出了网络寿命最大化的求解算法。这一算法通过依次降低能耗较高节点的数据发送速率来降低其能耗,同时通过升高能耗较低节点的数据传输率,最终取得最高效率的网络参数。通过理论分析、模拟实验结果及与其他算法效果的比较,文章所提出的解决法案可在很大程度上有效延长网络寿命。     

家白蚁消化系统发育与取食行为的分析

通过解剖家白蚁幼蚁、工蚁、兵蚁和若蚁的消化系统及测量其消化道的大小与消化道内半固体褐色物质的含量,分析了家白蚁消化系统的发育和取食行为以及相互之间的关系,结果表明幼蚁消化道的分化不明显,主要通过交哺行为自工蚁处获得液体食物;兵蚁后肠囊的发育不很充分,也主要是通过交哺行为获得液体食物,其中夹杂有一定的半固体褐色物质;若蚁的后肠囊还有待进一步发育,所获得的食物既有液体食物也有半固体褐色食物;成年工蚁的后肠囊相当发达,基本上被半固体褐色物质完全填充,主要是依靠自我取食的纤维素物质而生存。     

时滞反馈控制模型在能源消费系统中的应用

根据东部能源消费和西部能源输出之间相互支持、相互制约的复杂关系以及能源供需的时滞性建立了东西联动能源消费系统的时滞反馈控制模型,利用动力学的稳定性理论对这个能源供需模型进行了分析,并给出了东西部能源供需稳定的条件．通过对江苏省2000～2004年能源供需现状的分析,进一步验证了模型在一定程度上反映了我国能源供需的实际,对我国能源政策的制定具有重要的指导意义．     

Gut microbiota composition correlates with diet and health in the elderly

Alterations in intestinal microbiota composition are associated with several chronic conditions, including obesity and inflammatory diseases. The microbiota of older people displays greater inter-individual variation than that of younger adults. Here we show that the faecal microbiota composition from 178 elderly subjects formed groups, correlating with residence location in the community, day-hospital, rehabilitation or in long-term residential care. However, clustering of subjects by diet separated them by the same residence location and microbiota groupings. The separation of microbiota composition significantly correlated with measures of frailty, co-morbidity, nutritional status, markers of inflammation and with metabolites in faecal water. The individual microbiota of people in long-stay care was significantly less diverse than that of community dwellers. Loss of community-associated microbiota correlated with increased frailty. Collectively, the data support a relationship between diet, microbiota and health status, and indicate a role for diet-driven microbiota alterations in varying rates of health decline upon ageing.     

大熊猫胃肠道内分泌细胞的形态学研究

为了解大熊猫胃肠道内分泌细胞的形态特点，本文用ＰＡＰ法对两只大熊猫胃底、幽门腺区、十二指肠、空肠、回肠、结肠和直肠的五羟色胺、生长抑素、胃素、胆囊收缩素、神经降压素、胃动素、抑胃多肽、胰高血糖素、血管活性肠肽和内啡肽免疫反应阳性细胞进行了研究。     

Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease

Metabolomics studies hold promise for the discovery of pathways linked to disease processes. Cardiovascular disease (CVD) represents the leading cause of death and morbidity worldwide. Here we used a metabolomics approach to generate unbiased small-molecule metabolic profiles in plasma that predict risk for CVD. Three metabolites of the dietary lipid phosphatidylcholine--choline, trimethylamine N-oxide (TMAO) and betaine--were identified and then shown to predict risk for CVD in an independent large clinical cohort. Dietary supplementation of mice with choline, TMAO or betaine promoted upregulation of multiple macrophage scavenger receptors linked to atherosclerosis, and supplementation with choline or TMAO promoted atherosclerosis. Studies using germ-free mice confirmed a critical role for dietary choline and gut flora in TMAO production, augmented macrophage cholesterol accumulation and foam cell formation. Suppression of intestinal microflora in atherosclerosis-prone mice inhibited dietary-choline-enhanced atherosclerosis. Genetic variations controlling expression of flavin monooxygenases, an enzymatic source of TMAO, segregated with atherosclerosis in hyperlipidaemic mice. Discovery of a relationship between gut-flora-dependent metabolism of dietary phosphatidylcholine and CVD pathogenesis provides opportunities for the development of new diagnostic tests and therapeutic approaches for atherosclerotic heart disease.     

UPLC-Q-TOFMS/MS联用技术分析大鼠肠道微生物体外对小檗碱的代谢产物

采用大鼠肠道微生物和小檗碱进行体外厌氧共培养,并利用超高效液相色谱-四极杆飞行时间串联质谱联用仪(UPLC-Q-TOFMS/MS)分析小檗碱的代谢产物,探讨大鼠肠道微生物对小檗碱的生物转化过程.采用UPLC的方法,有效分离得到小檗碱及其代谢产物,再采用串联质谱对代谢产物进行结构解析及鉴定.研究结果发现,在体外条件下,大鼠肠道微生物通过脱甲基、脱羟基、去亚甲基等反应将小檗碱转化为小檗红碱,药根碱等5种代谢产物.     

Soma-germline interactions coordinate homeostasis and growth in the Drosophila gonad

The ability of organs such as the liver or the lymphoid system to maintain their original size or regain it after injury is well documented. However, little is known about how these organs sense that equilibrium is breached, and how they cease changing when homeostasis is reached. Similarly, it remains unclear how, during normal development, different cell types within an organ coordinate their growth. Here we show that during gonad development in the fruitfly Drosophila melanogaster the proliferation of primordial germ cells (PGCs) and survival of the somatic intermingled cells (ICs) that contact them are coordinated by means of a feedback mechanism composed of a positive signal and a negative signal. PGCs express the EGF receptor (EGFR) ligand Spitz, which is required for IC survival. In turn, ICs inhibit PGC proliferation. Thus, homeostasis and coordination of growth between soma and germ line in the larval ovary is achieved by using a sensor of PGC numbers (EGFR-mediated survival of ICs) coupled to a correction mechanism inhibiting PGC proliferation. This feedback loop ensures that sufficient numbers of PGCs exist to fill all the stem-cell niches that form at the end of larval development. We propose that similar feedback mechanisms might be generally used for coordinated growth, regeneration and homeostasis.