冷暴露对下丘脑能量平衡基因表达的影响

下丘脑是机体能量平衡的调节中枢.冷暴露下,下丘脑内能量平衡相关激素的表达水平将发生变化,主要包括促甲状腺激素释放激素、促肾上腺皮质激素释放激素、瘦素、神经肽Y/刺鼠相关蛋白、前阿片黑素细胞皮质激素/可卡因-苯丙胺转录调节肽、N-甲基-D-天冬氨酸受体及脑源性神经营养因子.这些激素通过复杂的神经内分泌网络,改变机体的摄食和产热,从而调控机体的能量平衡.因此,研究冷暴露对下丘脑能量平衡基因表达的影响将为肥胖等代谢紊乱性疾病的治疗提供新思路.     

脂肪酸代谢异常在高血压发病机制中的作用

原发性高血压不是单纯的血流动力学紊乱，而是伴脂质等代谢障碍的疾病。文中就脂肪酸摄入和代谢异常在高血压尤其是肥胖型高血压发病机制、尚存在的问题和今后的研究方向作一综述。     

中枢食欲调节研究进展

食欲调节网络的协调性摄食活动是维持人类生命的基本生理活动,食欲调节具有复杂而精细的调节机制,而下丘脑正是接受、整合与发放食欲调节信号、维持体重稳定的重要中枢.中枢神经系统或外周组织产生的具有促/抑食欲作用的神经内分泌因子在下丘脑形成复杂的食欲调节网络和相互投射的神经环路,对食欲进行精确的调控.不断完善下丘脑食欲调节区域,不断发现新的调控因子及其作用机制,对深入了解肥胖及糖尿病的病理生理机制及设计开发各种有效控制体重和血糖的药物有重大意义.     

脂肪酸结合蛋白在防治脂肪肝中的作用

脂肪酸结合蛋白（FABPs）是细胞内运输长链脂肪酸的蛋白超级家族成员,到目前为止发现有9种不同的FABPs。作为脂肪酸的转运体,其功能已经有大量研究证实。最近几年,许多试验更直接证实了FABPs的转运脂肪酸、参与细胞内脂质代谢作用。深入研究FABPs,在脂肪肝的检测、防治中具有重要意义。     

Leptin在胃动力及胃炎中作用的研究近况

Leptin是一种新发现的通过作用下丘脑来调节食物摄入和能量平衡的激素。近一年的研究表明leptin与胃动力及Hp相关性胃炎也有密切关系。本旨在对leptin在胃动力及胃炎中的作用作一综述。     

增食欲素与能量平衡

增食欲素是一种下丘脑神经肽,在调节摄食、能量代谢平衡、睡醒周期、血压等方面有广泛作用。增食欲素神经元对血糖、血脂和瘦素、糖皮质激素有高度反应性,并通过改变摄食和代谢率来调节能量平衡。增食欲素受体1拮抗剂(SB334867)可以抑制摄食和减轻体重,成为潜在的治疗肥胖的药物。     

IKKε调节代谢平衡及其机制

炎性反应是连接肥胖和胰岛素抵抗的重要桥梁.肥胖相关的慢性低度炎性反应严重影响了胰岛素的敏感性.高脂饮食会激活炎性通路核因子-κB,从而导致该通路中的非经典激酶核因子-κB抑制蛋白激酶ε(IKKe)在肝脏和脂肪组织中持续激活.近期研究证明,IKKε在代谢平衡中扮演重要角色,通过基因敲除或药物抑制该激酶的表达能通过各种不同机制影响脂肪组织内热量的消耗,从而减轻体重,改善糖、脂代谢.这些研究提示:IKKε是一种与代谢平衡密切相关的炎性激酶,可能成为肥胖及代谢性疾病治疗的新靶点.     

脂肪酸代谢异常在高血压发病机制中的作用

原发性高血压不是单纯的血流动力学紊乱,而是伴脂质等代谢障碍的疾病.文中就脂肪酸摄入和代谢异常在高血压尤其是肥胖型高血压发病机制、尚存在的问题和今后的研究方向作一综述.     

日常饮食中能量平衡对健康的重要性分析

目的 探讨糖尿病患者日常饮食中能量平衡对健康的影响.方法 选取2013年1月-2013年12月在该院完成治疗出院的160例2型糖尿病患者为研究对象,随机平均分成两组,实验组与对照组,每组各80例.实验组患者在日常饮食中实施能量平衡管理,对照组患者饮食不作特殊干预,比较两组患者血糖水平及血脂水平的变化.结果 实验组患者各指标均较对照组有显著性降低,两组比较差异有统计学意义(P＜0.05).结论 糖尿病患者日常饮食中实施能量平衡管理可显著降低患者体重和血糖水平,改善患者的临床各检测指标,提高临床治疗效果,促进患者疾病在治疗和恢复健康,临床疗效显著.     

Lipid sensing in the brain and regulation of energy balance

Nutrient-sensitive neurons [to glucose and fatty acids (FAs)] are present at many sites throughout the brain, including the hypothalamus and brain stem, and play a key role in the neural control of energy and glucose homoeostasis. Through their neuronal output, FAs can modulate feeding behaviour as well as insulin secretion and activity. Central administration of oleate, for example, inhibits food intake and glucose production in rats. This suggests that daily variations in plasma FA concentrations could be detected by the central nervous system as a signal that contributes to regulation of energy balance. At the cellular level, subpopulations of neurons in the ventromedial and arcuate hypothalamic nuclei are selectively either inhibited or activated by FAs. Possible molecular effectors of these FA effects most likely include the chloride and potassium ion channels. While intracellular metabolism and activation of the ATP-sensitive K⁺ channels appear to be necessary for some signalling effects of FAs, at least half the FA responses in ventromedial hypothalamic neurons are mediated by interaction with fatty acid translocase (FAT)/CD36, an FA transporter/receptor that does not require intracellular metabolism to activate downstream signalling. Thus, FAs and their metabolites can modulate neuronal activity by directly monitoring the ongoing fuel availability for brain nutrient-sensing neurons involved in the regulation of energy and glucose homoeostasis. Besides these physiological effects, FA overload or metabolic dysfunction may also impair neural control of energy homoeostasis and contribute to obesity and/or type 2 diabetes in predisposed subjects.     

Influence of rosuvastatin dose on total fatty acids and free fatty acids in plasma: Correlations with lipids involved in cholesterol homeostasis

This study investigates for the first time the influence of four doses of rosuvastatin on total fatty acids (TFA) and free fatty acids (FFA) in human plasma and correlates their changes in concentration with changes in the concentration of other lipids involved in cholesterol homeostasis.This study was a placebo-controlled, randomized, double-blind, crossover experiment. The study used a single group of 16 men and consisted of 5 treatment periods lasting 4 weeks each with placebo and 4 doses of rosuvastatin (5, 10, 20, and 40 mg). Each subject changed 5 medical treatments and received in each new treatment different tablets of rosuvastatin or placebo compared to those taken in previous treatments, in a random order. Between treatment periods there was a wash-out period of 2 weeks, without treatment.Changes in TFA and FFA were significant compared to placebo and between different doses of rosuvastatin. We found a continuous logarithmic decrease in levels of TFA, FFA, low-density lipoprotein (LDL)-cholesterol, total cholesterol, triglycerides, phospholipids, and apolipoprotein B-100, and a continuous increase in levels of high-density lipoprotein (HDL)-cholesterol and apolipoprotein A-1 by increases the dose of rosuvastatin. Analysis of the correlation of TFA and FFA with the main lipids and lipoproteins in cholesterol homeostasis indicated a linear regression with high correlation coefficients and all P-values were less than .05 level.The concentrations of TFA and FFA are significantly influenced by the dose of rosuvastatin. They are strongly correlated with those of other lipids and lipoproteins involved in cholesterol homeostasis. The mechanisms of cholesterol homeostasis regulation are involved in changing the concentrations of TFA and FFA.     

Dysregulation of energy homeostasis in mice overexpressing insulin-like growth factor-binding protein 6 in the brain

Aims/hypothesis IGFs, IGF receptors and IGF binding proteins (IGFBPs) are widely expressed in the central nervous system. To investigate the physiological significance of IGFBP-6 in the brain we established two transgenic mouse lines overexpressing human (h)-IGFBP-6 under the control of glial fibrillary acidic protein promoter. Increasing evidence suggests that insulin/IGF signalling pathways could be implicated in the neuroendocrine regulation of energy homeostasis. We explored the impact of brain IGFBP-6 overexpression on the regulation of food intake and energy balance.Methods Transgenic mice were fed either a control diet or a high-fat diet for up to 3 months. Glucose and insulin tolerance tests were carried out before and after the diet period. Plasma parameters (insulin, leptin, glucose, NEFAs and triglycerides) were measured, and uncoupling protein 1 (UCP-1) expression was quantified in brown adipose tissue. Oxygen consumption was also measured in both groups.Results The transgenic mice fed a high-fat diet for 3 months developed obesity, showing increases in plasma leptin, glucose and insulin levels and mild insulin resistance. As compared with wild-type mice, no significant differences were found in the quantity of food intake. However, UCP-1 expression was down-regulated in the brown adipose tissue of the transgenic mice.Conclusions/interpretation Our results show that brain IGFBP-6 has an impact on the regulation of energy homeostasis. These transgenic h-IGFBP-6 mice may be considered a new tool for studies of the involvement of the brain IGF system in metabolism control and obesity.     

非酒精性脂肪性肝病与血小板磷脂膜脂肪酸的相关性

非酒精性脂肪性肝病(NAFLD)是一类肝组织学改变与酒精性肝病相类似,但无过量饮酒史的临床综合征,以肝实质细胞脂肪变性和脂肪贮积为特征.     

Phospholipids and fatty acids in breast cancer tissue

Summary The fatty acid composition of fractionated phospholipids and neutral lipids was analyzed in human breast cancer tissues and the surrounding, apparently healthy tissue. In the cancer tissues the relative amounts of unsaturated fatty acids were increased in all the phospholipid subclasses analyzed. The differences were more marked in phosphatidylethanolamine than in the other phospholipid fractions and, furthermore, the relative amount of phosphatidylethanolamine was increased in cancerous tissue. In blood-erythrocyte phospholipids, no differences in fatty acid composition could be found between breast cancer and control patients. The present study suggests that the lipid composition of cancerous breast tissues differs from that of the surrounding tissue and may be involved in carcinogenesis.Supported by grants from the J. Vainio Foundation and the Finnish Ministry of Forestry and Agriculture     

高脂血症性脂肪肝大鼠血清游离脂肪酸的变化及意义

为探讨血清游离脂肪酸各组分在高脂血症性脂肪肝形成过程中的变化,并为其治疗方案提供依据.通过高脂食饵性饲养建立高脂血症性脂肪肝大鼠模型,测定其血清游离脂肪酸(FFA)组分,并与对照组进行比较.结果显示,与对照组相比,高脂血症性脂肪肝模型FFA各组分中棕榈酸(C16∶0)、亚油酸(C18∶2)增高(P均<0.05),肉豆蔻酸(C14∶0)明显增高(P<0.01),而硬脂酸(C18∶0)、花生四烯酸(C20∶4)则显著降低(P均<0.01),月桂酸(C12∶0)、油酸(C18∶1)变化不明显.提示高脂血症脂肪肝血FFA组分有特征性改变,C18∶2可能无防治脂肪肝的作用.     

Expression profile of polyunsaturated fatty acids in colorectal cancer

AIM:To investigate the relationship between the metabolism of polyunsaturated fatty acids(PUFAs)andtumor-associated factors for predicting the outcome of colorectal carcinoma(CRC)in Chinese patients.METHODS:Fresh-frozen malignant and normal tissues from 82 Chinese patients with CRC were analyzed for PUFA composition using gas-liquid chromatography.The levels of vascular endothelial growth factor(VEGF),cyclooxygenase-2(COX-2),prostaglandin E2 and platelet-derived growth factor(PDGF)were measured by enzyme-linked immunosorbent assay,and the levels of VEGF,p53 and Ki-67 were measured by immunohistochemistry.RESULTS:In malignant tissue,compared with normal tissue,the levels of totalω-6 PUFAs(24.64%±3.41%vs 26.77%±3.37%,P=0.00)and linoleic acid(LA)(15.46%±3.51%vs 18.30%±2.83%,P0.01)were lower,whereas the levels of totalω-3 PUFAs(1.58%±0.74%vs 1.35%±0.60%,P0.01)and dihomo-gamma-linolenic acid(DGLA)(1.32%±0.69%vs 0.85%±0.29%,P0.01)were significantly higher.The ratios of arachidonic acid(AA)/LA(0.53±0.22 vs0.42±0.19,P0.01)and AA/totalω-6 PUFAs(0.31±0.09 vs 0.27±0.10,P0.01)were also significantly higher in malignant tissue.The levels of PDGF(353.10±148.85 pg/m L vs 286.09±104.91 pg/m L,P0.01),COX-2(125.21±70.29 ng/m L vs 67.06±42.22 ng/m L,P0.01)and VEGF(357.11±128.76 pg/m L vs211.38±99.47 pg/m L,P0.01)were also higher in malignant tissue compared to normal tissue.COX-2was inversely correlated with LA(R=-0.3244,P0.05)and positively correlated with AA/totalω-6 PUFAs(R=0.3083,P0.05)and AA/LA(R=0.3001,P0.05).The tissue level of LA was highest in poorly differentiated tumors(19.9%±6.3%,P0.05),while the ratio of AA/ω-3 PUFAs was lowest in these tumors(10.8±2.6,P0.05).In VEGF-positive tumors,the level of LA was higher(16.2%±3.7%vs 13.9%±2.7%,P0.01),while the AA/ω-3PUFA,AA/ω-6 PUFA,and AA/LA ratios were lower than in VEGF-negativetumors(5.0±1.8 vs 6.7±3.3,0.30±0.09 vs 0.34±0.09,0.50±0.21 vs 0.61±0.21,P0.01).CONCLUSION:The metabolism of PUFAs may playan important role in the evolution of inflammationdriven tumorigenesis in CRC and may be considered apotential marker for prognosis.