瘦素与骨关节炎

瘦素是一种由肥胖基因编码的一种分泌型蛋白质,分子质量约为16 kDa,主要由白色脂肪组织产生.它具有细胞因子和激素的双重功能,起着调节能量代谢、炎症反应、免疫反应、神经内分泌及血管生成的作用等.本文就瘦素在骨关节炎中作用的研究现状及争论作一综述.     

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。     

瘦素与脂肪生成

瘦素是一种由肥胖基因编码、主要由脂肪组织合成和分泌的蛋白质,通过与其受体结合而发挥多种生物学效应.许多研究发现瘦素能减少脂肪蓄积,但其发挥作用的机制还不是很清楚.本文就瘦素对脂肪生成的作用,尤其是瘦素对前脂肪细胞增殖与分化的影响进行综述.     

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.     

瘦素在乳腺癌发病中的作用

瘦素是一种由肥胖基因(ob基因)编码表达的小分子蛋白,在调控机体的摄食行为和脂肪代谢方面具有重要作用.近来大量研究发现瘦素在体外可促进乳腺细胞转化、癌细胞增生并促进血管生成.这表明瘦素在乳腺癌的发生发展中可能起重要作用,但具体机制尚未阐明.本文主要从体外实验、动物试验和乳腺癌病理组织研究3方面对瘦素在乳腺癌发病中的作用的近年相关研究进展进行综述.     

瘦素在乳腺癌发病中的作用

瘦素是一种由肥胖基因(ob基因)编码表达的小分子蛋白,在调控机体的摄食行为和脂肪代谢方面具有重要作用.近来大量研究发现瘦素在体外可促进乳腺细胞转化、癌细胞增生并促进血管生成.这表明瘦素在乳腺癌的发生发展中可能起重要作用,但具体机制尚未阐明.本文主要从体外实验、动物试验和乳腺癌病理组织研究3方面对瘦素在乳腺癌发病中的作用的近年相关研究进展进行综述.     

瘦素在乳腺癌发病中的作用

瘦素是一种由肥胖基因(ob基因)编码表达的小分子蛋白,在调控机体的摄食行为和脂肪代谢方面具有重要作用.近来大量研究发现瘦素在体外可促进乳腺细胞转化、癌细胞增生并促进血管生成.这表明瘦素在乳腺癌的发生发展中可能起重要作用,但具体机制尚未阐明.本文主要从体外实验、动物试验和乳腺癌病理组织研究3方面对瘦素在乳腺癌发病中的作用的近年相关研究进展进行综述.     

瘦素神经保护作用的研究进展

瘦素（Leptin）是于1994年发现的一种主要由脂肪组织分泌并释放入血的多肽类激素,可通过中枢神经系统调节体重和能量平衡。随着瘦素及其受体在中枢神经系统和外周组织表达谱的不断完善,瘦素在神经内分泌、血管新生、生殖、免疫调节和创伤修复等方面的作用也逐渐被人们所认知。近年来,瘦素的神经保护作用受到研究者们的重视,越来越多的证据表明瘦素能够促进脑发育和成熟,并且在脑损伤和退行性病变过程中能够对神经元细胞发挥抗凋亡和保护作用,展示了在神经修复领域较好的应用前景。     

痩素与绝经后骨代谢的研究进展

绝经后骨质疏松症是由于绝经所导致的骨量减少及骨组织结构变化,使骨脆性增加易于骨折,以及由骨折引起的一系列严重威胁女性健康的并发症。如何找到一种安全,有效的抗骨质疏松症药物,是目前研究的热点。瘦素（leptin)是由肥胖基因编码的一种多肽,主要由脂肪组织分泌,通过瘦素受体（leptin receptor,ObR)发挥其生物学效应。近年来研究发现瘦素除调节糖、脂代谢外,对骨代谢也具有多重调节作用。本文从人体研究、动物实验以及体外研究多个角度,就瘦素与绝经后骨代谢的关系进行了分析,以期为绝经后骨质疏松症的治疗提供新思路。     

Leptin and bone metabolism

Leptin is a hormone involved with satiety and energy balance and proposed to be an anti-obesity factor. Much effort has been dedicated to the relationship between leptin and bone. This interest stems from the knowledge that body weight is a major determinant of bone density. It is known that obese persons have stronger bones and lose bone tissue at a slower pace. Therefore, attention has been given to leptin as a mediator of increased osteogenesis. Leptin has been shown to play a role on bone both in vitro and in vivo.The administration of leptin in vitro induced the expression of leptin receptors on stromal cells, the differentiation to osteoblasts and inhibition of differentiation into the adipocyte phenotype. In addition, leptin was able to inhibit osteoclastogenesis of peripheral blood mononuclear cells. Therefore, there is in vitro and experimental evidence that leptin is able both to stimulate osteoblasts and inhibit osteoclast differentiation. This would be in line with the hypothesis that the correlation between obesity and increased BMD is linked to leptin activity. However, experimental results are indicative of a role of CNS in mediating the effect of leptin on bone metabolism. These effects are opposite to the direct effects on bone cells and lead to bone loss. To solve the problem, it has been suggested that obese individuals have a resistance of nervous structures to leptin. In chronic renal failure serum leptin levels are markedly increased. An inverse correlation between histomorphometric parameters of bone turnover and serum leptin levels and between leptin and PTH have been reported.Therefore, the hypothesis has been raised that leptin lowers bone turnover in chronic renal failure. Since leptin has a direct stimulatory effect on bone and an indirect opposite effect via the CNS, it has been suggested that in CRF a resistance of nervous structures to leptin, like in obesity, may be present. By now, coherent findings suggest that the prevailing effect of leptin on bone in ESRD is that of reducing bone turnover.     

Factors associated with serum leptin in patients with chronic kidney disease

BACKGROUND AND AIMS: Serum leptin levels are elevated in patients with kidney failure. Data on the associations of serum leptin and on the relationship of leptin with both kidney function and inflammation, are limited in patients with reduced glomerular filtration rate (GFR). We evaluated the independent associations of serum leptin in patients with reduced GFR. MATERIAL AND METHODS: Serum leptin and C-reactive protein (CRP) were measured in samples from 798 participants of the Modification of Diet in Renal Disease Study. Multivariable analysis was used to evaluate the independent effects of kidney function and CRP on leptin levels. RESULTS: Median (interquartile range) of serum leptin was 9.1 ng/ml (14.0). Female gender, higher percent body fat, higher insulin levels, older age, lower GFR and higher CRP were associated with higher serum leptin levels and explained 51% of the variability in the logarithm of serum leptin levels. After adjusting for the other variables, a 10 ml/min/1.73 m2 lower GFR was associated with 6% higher mean serum leptin levels. Percent body fat and gender, explained 45% of the variability in serum leptin levels. CONCLUSIONS: Level of kidney function and CRP are associated with serum leptin in patients with reduced GFR. However, there is a stronger association between serum leptin and indices of body fat and gender in patients in the earlier stages of chronic kidney disease. 50% of the variability remains unexplained in patients with reduced GFR.     

Glucose-containing peritoneal dialysis fluids regulate leptin secretion from 3T3-L1 adipocytes.

BACKGROUND: A marked elevation of serum leptin is observed soon after the start of peritoneal dialysis (PD), suggesting that leptin production may be stimulated by this treatment. Glucose metabolism is the major factor regulating leptin. The current study was designed to test if glucose-based PD fluids might regulate leptin production in vitro. METHODS: 3T3-L1 adipocytes were exposed to a 50:50 mixture of dialysis solutions and medium M199 containing 10% serum for 相似文献   

Leptin potentiates thermogenic sympathetic responses to hypothermia: a receptor-mediated effect

Leptin contributes to the regulation of thermogenesis. In rodents, sympathetic nerve activity efferent to interscapular brown adipose tissue (IBAT-SNA) is involved. On the basis of the hypotheses that 1) leptin acutely potentiates hypothermia-induced increases in IBAT-SNA; 2) this action of leptin is specific to IBAT-SNA, i.e., it does not occur with renal sympathetic nerve activity (R-SNA); and 3) this effect of leptin depends on intact and functional leptin receptors, we measured IBAT-SNA and R-SNA in anesthetized lean and diet-induced obese Sprague-Dawley and in obese Zucker rats, randomly assigned to low-dose leptin or vehicle. Before the start of leptin or vehicle and 5 min, 90 min, and 180 min after, hypothermia (30 degrees C) was induced. Compared with vehicle, leptin did not significantly alter baseline R-SNA or IBAT-SNA. In lean Sprague-Dawley rats, hypothermia-induced increases in IBAT-SNA were significantly augmented by leptin but not by vehicle. In obese Sprague-Dawley rats, leptin did not potentiate hypothermia-induced increases in IBAT-SNA. In Zucker rats, IBAT-SNA did not increase with hypothermia and leptin was not able to induce sympathoactivation with cooling. Changes in R-SNA during hypothermia were not significantly modified by leptin in either group. Thus, low-dose leptin, although not altering baseline SNA, acutely enhances hypothermia-induced sympathetic outflow to IBAT in lean rats. This effect is specific for thermogenic SNA because leptin does not significantly alter the response of R-SNA to hypothermia. The effect depends on intact and functional leptin receptors because it occurs neither in rats with a leptin receptor defect nor in rats with acquired leptin resistance.     

Duodenal leptin stimulates cholecystokinin secretion: evidence of a positive leptin-cholecystokinin feedback loop

Some of the actions of leptin depend on cholecystokinin (CCK). However, it is unknown whether leptin modulates the release of CCK. Here, we demonstrate in vitro that leptin induces the phosphorylation of extracellular signal-related kinase (ERK)-1/2 proteins and increases CCK release (EC(50) = 0.23 nmol/l) in CCK-secreting STC-1 cells. We showed that rat duodenal juice contains leptin that circulates free and bound to macromolecules, suggesting that leptin has a lumenal action on the intestine. In vivo in the rat, duodenal infusion of leptin increased plasma CCK at levels comparable to those induced by feeding. Moreover, meal-induced increases in plasma CCK were markedly reduced in obese fa/fa rats, whereas the mobilization of the gastric leptin pool was similar in lean and obese Zucker rats. The release of CCK by leptin presumably generates a positive feedback loop. Indeed, the blockade of CCK receptors reversed the meal reduction of the stomach leptin pool and the meal-increased plasma insulin, consistent with the previous concept of an entero-insular axis. Collectively, these data support a novel mode of action of leptin where leptin and CCK may potentiate their own effects by cross-stimulating their secretion. The impairment of this leptin-CCK loop may have pathological implications related to obesity and diabetes.     

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.     

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.     

Free serum leptin but not bound leptin concentrations are elevated in patients with end-stage renal disease.

BACKGROUND: Leptin is a 16-kDa protein that is thought to be a regulator of food intake and body weight. Although total serum leptin levels have been reported to be elevated in obese and normal weight patients with end-stage renal disease (ESRD), it is not known whether serum-free leptin concentrations are also increased in patients with ESRD with no apparent nutritional problems. Furthermore, there are no data on how different dialysis modes (high-flux haemodiafiltration and low-flux dialysis) influence serum leptin subfractions. METHODS: We measured fasting serum free and bound leptin levels in three groups of male subjects: patients on haemodiafiltration with high flux dialysers (n=11), patients on haemodialysis with low-flux dialysers (n=17) and healthy age (61+/-8 years) and BMI (23.8+/-3.1 kg/m(2)) matched control subjects (n=28). Both leptin components were determined before and after a single dialysis session. RESULTS: Body mass indices were correlated with serum free leptin levels in both patients (r=0.69, P<0.001) and controls (r=0.77, P<0.001). Mean (SD) serum free leptin levels were significantly higher in ESRD patients than in control subjects (91+/-33 vs 41+/- 21 pmol/l; P<0.01). Bound leptin levels did not differ in both groups (0.67+/-0.12 vs 0.56+/-0.11 nmol/l, NS). Elevated serum-free leptin levels in ESRD patients could be reduced by haemodiafiltration with high-flux membranes, but not with low-flux haemodialysis membranes.The former led to a reduction of initial serum free leptin values to 76+/-17% (P<0.01), whereas bound leptin remained unaffected. CONCLUSION: Serum-free leptin levels are elevated in ESRD without any apparent effect on body weight. In contrast, serum bound leptin levels remain stable, thus central feedback regulation via the bound form of the hormone may serve as an alternative explanation in the regulation of food intake and energy expenditure in chronic patients on haemodialysis with no apparent nutritional problems.