瘦素与胆结石形成的关系

瘦素(Leptin)是由脂肪细胞分泌的一种调节机体能量平衡的激素.胆结石病人血中瘦素的浓度较高,瘦素可以通过调节脂质代谢,影响胆囊的收缩性,改变胆汁蛋白的成分等机制影响结石的形成.本文就对瘦素在胆结石形成中的作用的研究进展做一综述.     

瘦素与胃肠运动

瘦素是由肥胖基因编码、脂肪细胞分泌的一种蛋白质类激素,在调节摄食、体重、能量消耗和神经内分泌方面发挥着重要的作用.研究证实,瘦素可以改变胃肠神经肌肉的反应性,从而调节胃排空及肠动力.表明瘦素是与胃肠的生理功能及胃肠疾病密切相关的一种新的胃肠激素.本文就瘦素与胃肠运动的关系进行简要综述.     

瘦素基因及其启动子-2548G／A多态性的研究现状及展望

瘦素（leptin）是瘦素基因（leptingene）的蛋白产物,是由脂肪组织分泌的循环激素,调节体内的能量平衡、体重、血糖、骨骼发育、脂肪储存及某些内分泌功能,并参与造血及生殖,具有广泛的生物学效应。大量研究结果表明,血浆瘦素水平与多种疾病密切相关,瘦素基因多态性影响着瘦素的表达。现对瘦素基因及其启动子-2548G／A多态性相关问题结合文献进行综述。     

瘦素与肠黏膜屏障

瘦素是一种主要由脂肪细胞分泌的多肽类激素,在机体具有广泛的生物学效应,具有调节能量代谢、生长发育、免疫反应、促进损伤修复等作用。近年来,对肠道瘦素及其受体研究的不断深入研究,证明瘦素作为一种新的胃肠道激素,在调节胃肠功能、维护肠黏膜屏障方面具有重要的生理功能。     

重组瘦素基因构建及其对骨髓间充质干细胞增殖分化的影响

瘦素(Leptin)是由脂肪细胞分泌的一种内分泌激素,可以使骨髓间充质干细胞(BMSCs)向成骨细胞分化,我们构建了重组真核质粒pTracer-Leptin,并转染BMSCs,研究Leptin基因对BMSCs成骨活性的影响.     

瘦素及其和美容外科相关的问题

瘦素 (ｌｅｐｔｉｎ) ,是一种主要由脂肪细胞分泌的机体能量平衡调节因子。瘦素的深入研究始于 1994年Ｚｈａｎｇ等[1 ] 对瘦素的发现 ,研究内容主要集中在内分泌及其相关领域。但瘦素的特殊来源及功能可能和美容外科的一些领域有关。一、瘦素基因 (ｏｂ)和瘦素大鼠瘦素基因有 3个外显子和 1个内含子。人类瘦素基因有 84 %和鼠同源。瘦素基因的表达有组织特异性 ,即主要在白色脂肪组织表达 ;胃肠道、胎盘、乳腺也有瘦素基因表达 ,但水平较低[2 ] 。瘦素为 16 7个氨基酸组成的分泌蛋白 ,相对分子质量为 16 0 0 0 [3] 。瘦素分泌后随血流到达…     

瘦素对骨代谢影响研究进展

瘦素及其受体在中枢和外周多个部位均有表达,具有多种生物学功能,对于骨代谢有着重要的影响作用.近来研究发现瘦素可促进人骨髓间质细胞向成骨细胞分化,抑制其向脂肪细胞分化;血清瘦素水平还与成骨细胞活性及骨骼发育相关.瘦素在外周作用于多种骨细胞促进成骨,在中枢系统则抑制骨形成.瘦素在妇女绝经后骨质疏松的发生中发挥一定作用.该文主要归纳介绍瘦素调节骨代谢基本作用及调控骨骼生长作用的一些较重要的研究发现,并对其机制作初步探讨.     

痩素对骨代谢的影响

瘦素(Leptin)是一种主要由白色脂肪组织产生的16kDa蛋白质(胎盘、胃和骨骼肌也有少量产生)，由三个外显子的ob基因编码。Leptin在血浆中的浓度与机体脂肪储备量正相关，通过下丘脑神经元来调节摄食行为、能量代谢和生殖内分泌功能。近来的研究发现瘦素不仅与物质能量代谢有关，而且对     

瘦素促进移植颗粒脂肪组织血管增生的实验研究

目的　用Wistar大鼠研究瘦素 (leptin)在颗粒脂肪移植中的促进血管增生作用。方法　取大鼠腹部脂肪 ,分别经 2 0 μg/L瘦素和生理盐水处理后 ,以颗粒脂肪的形式自体移植。移植组织在不同观察时间取出后称重 ,同时行碱性磷酸酶 (AKP)染色及α 肌动蛋白 (Actin)染色 ,用计算机图像分析技术测定血管密度。实验结果用SPSS统计分析软件进行统计学分析。结果　瘦素处理组血管面密度在移植 10d、2 0d后分别为 (0 .12± 0 .0 4 ) μm2 / μm2 、(6 .83± 1.86 )× 10 -2 μm2 / μm2 ,显著高于同一观察时间的生理盐水处理组 (P <0 .0 5 )。Actin染色强度也较高。结论　一定浓度的瘦素对移植鼠颗粒脂肪组织具有促进血管增生作用。     

瘦素对脂肪细胞的直接调节作用

目的:观察瘦素对人脂肪细胞分解代谢及脂肪蓄积的直接影响,探讨脂肪细胞的自分泌调节作用。方法:取正常成人皮下脂肪组织,常规提取和培养前脂肪细胞,待细胞融合后诱导分化为成熟脂肪细胞并随机分为四组:正常对照组、低浓度组、中浓度组和高浓度组,分别培养于含瘦素浓度为0ng/ml、10ng/ml、100ng/ml、1000ng/ml的培养液a中。培养4h后收集培养液检测游离脂肪酸和甘油浓度,取脂肪细胞经油红O染色后图像分析计算脂肪颗粒的积分光密度。结果:与对照组相比,低浓度组培养液中游离脂肪酸和甘油浓度分别增加87%(P<0.01)和5%(P<0.01),脂肪颗粒积分光密度减少12%(P<0.01);中浓度组培养液中游离脂肪酸和甘油浓度分别增加181%(P<0.01)和8%(P<0.01),脂肪颗粒光密度减少21%(P<0.01);高浓度组培养液中游离脂肪酸和甘油的浓度分别增加312%(P<0.01)和17%(P<0.01),脂肪颗粒的积分光密度减少35%(P<0.01)。游离脂肪酸和甘油浓度与瘦素浓度呈正相关,脂肪颗粒积分光密度与瘦素浓度呈负相关。结论:瘦素瞬时作用脂肪细胞,可促进脂肪分解代谢、减少脂肪蓄积;且随着瘦素浓度增加,作用更强,呈剂量依赖性。瘦素对脂肪细胞存在自分泌调节作用,可能在肥胖发病机制中起重要作用。     

Leptin in chronic kidney disease: a link between hematopoiesis,bone metabolism,and nutrition

Anemia, dyslipidemia, malnutrition, together with mineral and bone disorders are common complications in patients with chronic kidney disease (CKD). All are associated with increased risk of mortality. Leptin is a small peptide hormone that is mainly but not exclusively produced in adipose tissue. It is also secreted by normal human osteoblasts, subchondral osteoblasts, placental syncytiotrophoblasts, and the gastric epithelium. Leptin binds to its receptors in the hypothalamus to regulate bone metabolism and food intake. Leptin also has several other important metabolic effects on peripheral tissues, including the liver, skeletal muscle, and bone marrow. Leptin is cleared principally by the kidney. Not surprisingly, serum leptin appears to increase concurrently with declines in the glomerular filtration rate in patients with CKD. A growing body of evidence suggests that leptin might be closely related to hematopoiesis, nutrition, and bone metabolism in CKD patients. Results are conflicting regarding leptin in patients with CKD, in whom both beneficial and detrimental effects on uremia outcome are found. This review elucidates the discovery of leptin and its receptors, changes in serum or plasma leptin levels, the functions of leptin, relationships between leptin and the complications mentioned above, and pharmaceutical interventions in serum leptin levels in patients with CKD.     

Leptin, obesity and cardiovascular disease

PURPOSE OF REVIEW: Obesity is a risk factor for cardiovascular diseases. Leptin levels are increased in obesity and leptin exhibits cardiovascular actions that may contribute to increased cardiovascular risk. We review the sympathetic, renal and vascular actions of leptin and their relevance to cardiovascular disease. RECENT FINDINGS: Leptin possesses cardio-renal actions potentially contributing to obesity-related hypertension including generalized sympathoactivation. However, given that leptin resistance occurs in obesity, it has been difficult to link hyperleptinemia with hypertension. One possibility is that leptin resistance is confined to the metabolic effects of leptin, with preservation of its sympathoexcitatory actions. Other mechanisms may contribute to the pressor effects of leptin. For instance, angiotensin II induces leptin generation. Leptin also potentiates the pressor effect of insulin. Therefore, interactions between angiotensin II and insulin with leptin could have deleterious cardiovascular effects in obesity. Additionally, leptin appears to stimulate vascular inflammation, oxidative stress and hypertophy. These actions may contribute to the pathogenesis of hypertension, atherosclerosis, and left ventricular hypertrophy. SUMMARY: The potential actions of leptin in the pathophysiology of cardiovascular complications of obesity are diverse, despite evidence of leptin resistance to its metabolic actions. However, most information about cardiovascular actions of leptin derives from in-vitro and animal studies. Future research in humans is widely awaited.     

Review of the role of leptin in the regulation of male reproductive function

Since discovered in 1994, leptin has been thought to be a pleiotropic hormone that regulates food intake, controls energy balance in the body and influences multiple tissues in the body. Leptin plays an important mediating role in the regulation of neuroendocrine and can transmit the nutritional status signals to the reproductive‐related central nervous system. Many studies have shown that leptin may play an important role in the control of reproductive function. Leptin can act on all levels of the hypothalamus–pituitary–gonadal (HPG) axis and may have local effects on the function of testis and spermatogenesis. Leptin is critical for puberty initiation and can also modulate testosterone synthesis by downregulating cAMP‐dependent activation of steroidogenic genes expressions. Leptin is found to be higher in infertile men than in normal subjects. Yet, the exact role of leptin in the regulation of male reproductive function remains incomplete. The purpose of this review was to summarise the recent research about the biological effects of leptin on male reproductive system. In‐depth study of leptin in reproductive system will help to reveal the pathogenesis of infertility and provide new treatment ideas for human assisted reproductive technology.     

Role of Leptin in Farm Animals: a Review

The discovery of hormone leptin has led to better understanding of the energy balance control. In addition to its effects on food intake and energy expenditure, leptin has now been implicated as a mediator of diverse physiological functions. Recently, leptin has been cloned in several domestic species. The sequence similarity suggests a common function or mechanism of this peptide hormone across species. Leptin receptors are expressed in most of tissues, which is consistent with the multiplicity of leptin functions. The main goal of this review was to summarize knowledge about effect of leptin on physiology of farm animals. Experiments point to a stimulatory action of leptin on growth hormone (GH) secretion, normal growth and development of the brain. Surprisingly, leptin is synthesized at a high rate in placenta and may function as a growth factor for fetus, signalling the nutritional status from the mother to her offspring. Maturation of reproductive system can be stimulated by leptin administration. Morphological and hormonal changes, consistent with a major role of leptin in the reproductive system, have also been described, including the stimulation of the release of luteinizing hormone (LH), follicle‐stimulating hormone (FSH) and prolactin. Leptin has a substantial effect on food intake and feeding behaviour in animals. Administration of leptin reduces food intake. Its level decrease within hours after initiation of fasting. Leptin also serves as a mediator of the adaption to fasting, and this role may be the primary function for which was the molecule evolved.     

瘦素介导的细胞内信号途径在创面愈合中的作用

目的综述瘦素(Leptin)介导的细胞内信号途径及其对创面愈合作用的研究进展。方法广泛查阅近年文献,对Leptin理化性质、受体作用机制、受体相关的细胞内信号途径及其在皮肤和黏膜创面愈合中的作用进行综述。结果Leptin是一种由ob基因表达、相对分子质量为16×103的蛋白激素,通过结合其特异性受体,活化Janus激酶/信号传导及转录活化子途径、丝裂原活化的蛋白激酶通路和磷脂酰肌醇-3-激酶通路等主要信号途径,参与机体能量代谢、体重平衡、创伤愈合等多种功能的调控。Leptin受体广泛存在于机体各种组织,提示Leptin功能的多向性。皮肤创伤后局部Leptin表达增多,能促进角化细胞增殖、上皮形成、成纤维细胞增殖和胶原合成,起到加速创伤修复的作用。黏膜损伤或黏膜细菌感染后Leptin表达也显著增高,可通过调节黏膜腺体分泌、改善黏膜血流量以及与内皮素1协同作用来促进黏膜损伤的修复。结论Leptin能够通过活化其受体相关的细胞内信号途径促进创面愈合。     

瘦素受体在睾丸的表达分布及其功能

瘦素是肥胖基因的蛋白产物,参与了机体体重和能量调节、免疫调节、血管生成、炎症反应和青春期启动及生殖调节等一系列重要生理活动。瘦素发挥的不同作用与其受体(Ob-R)表达分布的时空特征相关,瘦素在睾丸内发挥着多种重要的生物学作用。本文通过综述Ob-R在大、小鼠及人类睾丸的不同细胞和不同发育阶段以及生理和病理状态下的表达和分布情况,结合已有的体外实验结果,探讨了Ob-R与睾丸功能的关系,希望能为进一步研究人类睾丸的生理发育及男性不育的病理生理机制开拓思路。     

Leptin treatment induces loss of bone marrow adipocytes and increases bone formation in leptin-deficient ob/ob mice.

Normal mice and leptin-deficient ob/ob mice were treated with leptin to study effects on osteogenesis and adipogenesis in bone marrow. Leptin treatment significantly decreased bone marrow adipocyte size and number in ob/ob mice while increasing bone formation, BMC, and BMD. The results suggest that, in leptin-sensitive animals, the reduction in marrow adipocytes has positive effects on bone formation. INTRODUCTION: Adipocytes, osteoblasts, and osteoclasts have leptin receptors, and leptin can also affect bone metabolism indirectly through its receptors in the hypothalamus. We examined the effects of leptin treatment on bone formation, BMD, and marrow adipocyte population in normal mice and leptin-deficient ob/ob mice. MATERIALS AND METHODS: At the age of 15 weeks, mice were implanted with Alzet osmotic pumps for subcutaneous delivery of treatment solutions (saline, 2.5 microg leptin/day, or 10 microg leptin/day) for 14 days at a delivery rate of 0.25 microl/h. Bone formation was assessed using fluorochrome labels, cell populations were quantified using histomorphometry, and bone densitometry was measured using DXA. We also used a Luminex Beadlyte assay system to quantify cell survival markers in bone marrow samples. RESULTS AND CONCLUSIONS: Results indicate that both doses of leptin decreased the number of marrow adipocytes in ob/ob mice by >20% (p < 0.05) compared with PBS-treated ob/ob mice. The decrease in adipocyte number with leptin treatment is accompanied by an increase in concentration of the apoptosis marker caspase-3 in bone marrow adipocytes and hematopoietic cells. Both leptin doses also significantly (p < 0.05) increased the percentage of fluorochrome-labeled tibial endosteal surface by >30% compared with PBS-treated ob/ob mice. Leptin treatment increased whole body BMC by >30% in the ob/ob mice receiving the highest leptin dose. Leptin treatment provided no increase in bone formation, BMC, or BMD in normal, leptin-replete mice.     

Role of selective leptin resistance in diet-induced obesity hypertension

Leptin is an adipocyte-derived hormone that plays a key role in the regulation of body weight through its actions on appetite and metabolism. Leptin also increases sympathetic nerve activity (SNA) and blood pressure. We tested the hypothesis that diet-induced obesity is associated with resistance to the metabolic actions of leptin but preservation of its renal SNA and arterial pressure effects, leading to hypertension. Mice were fed a high-fat diet for 10 weeks to induce moderate obesity. The decrease in food intake and body weight induced by intraperitoneal or intracerebroventricular leptin was significantly attenuated in the obese mice. Regional SNA responses to leptin were differentially altered in diet-induced obese mice. Renal SNA response to leptin was preserved, whereas lumbar and brown adipose tissue SNA responses were attenuated in obese mice. Radiotelemetric arterial pressure was approximately 10 mmHg higher in obese mice. Furthermore, the increase in arterial pressure in response to long-term (12 days) leptin treatment was preserved in obese mice. Thus, mice with diet-induced obesity exhibit circulating hyperleptinemia and resistance to the metabolic actions of leptin. However, there is preservation of the renal sympathetic and arterial pressure responses to leptin, which represent a potential mechanism for the adverse cardiovascular consequences of obesity.     

Leptin in end stage renal disease (ESRD): a link between fat mass, bone and the cardiovascular system

Adipose tissue is now considered an important system operating strictly in concert with other systems. The adipocyte is the main producer of two pleiotropic compounds, leptin and adiponectin, modulating inflammation and having multiple effects in disparate organs including the cardiovascular and the central nervous system. Leptin has disparate influences on various physiologic and organ systems including glucose homeostasis, hematopoiesis and the reproductive and cardiovascular systems and is a crucial hormone for the regulation of food intake and body weight. Peripherally, leptin modulates insulin sensitivity and high leptin triggers insulin resistance and vice versa. Obesity, a situation where circulating leptin attains very high levels is accompanied by increased bone mass, a phenomenon which may depend on direct stimulation of osteoblasts by leptin. However in animal models the stimulating effect of leptin on the osteoblast is counterbalanced by a strong inhibitor effect on bone formation in the central nervous system. Two recent studies reported an inverse link between leptin, bone mass and PTH in dialysis patients suggesting that leptin may be implicated in low bone turnover in these patients, likely by a mechanism involving the central nervous system. Leptin induces vascular calcifications in vitro. In uremic man leptin is unrelated to valvular calcifications but predicts incident cardiovascular events in overweight and obese dialysis patients. Leptin seems to be a relevant player in the emerging connection between bone and cardiovascular alterations in patients with end stage renal disease.     

Effect of leptin on motility, capacitation and acrosome reaction of human spermatozoa

Leptin is a polypeptide hormone with important roles in reproduction. It has been detected in human seminal plasma as well as on human ejaculated spermatozoa. This study aimed at studying the possible role of leptin in regulating human sperm functions. Immunofluorescent staining was used to study the expression of leptin and its receptor. The correlation between the concentration of leptin and soluble leptin receptor (ObRs) in seminal plasma as measured by enzyme-linked immunosorbant assay and sperm motility parameters measured by computer-assisted sperm analyais (CASA) was determined. The effects of recombinant leptin on human sperm motility, capacitation and acrosome reaction as measured by chlortetracycline staing were also studied. Leptin immunoreactivity was demonstrated at the equatorial and neck regions of human spermatozoa, whereas that of ObRs was shown up on the tail. After Percoll separation, spermatozoa with high density had more intense leptin immunoreactivity compared with those with low density. No significant correlation was found between seminal plasma concentration of leptin/ObRs and sperm motility parameters. After incubation with recombinant human leptin for either 3 h or overnight, there was no change in all the CASA motility parameters determined and percentages of capacitated and acrosome-reacted spermatozoa. We concluded that leptin does not have a significant effect on motility and capacitation/acrosome reaction in human ejaculated mature spermatozoa. Its role in male reproduction is yet to be determined.