奶牛Leptin长型受体(OB-Rb)竞争RT-PCR内标物的构建

为了构建奶牛瘦素长型受体(OB-Rb)的定量PCR内标物。应用RT-PCR方法,克隆、测序287bp的OB-Rb片段,应用限制性内切酶BglⅡ插入470bp外源片段,构建了一个重组的竞争模板,为建立竞争性RT-PCR法检测奶牛瘦素长型受体mRNA奠定了基础。

Expression of Leptin Long-form Receptor mRNA in Luteinized Granulosa Cells of Obese Women with Polycystic Ovary Syndrome

To investigate the expression of mRNA of leptin long-form receptor （OB-Rb） in luteinized granulosa ceils of obese women with polycystic ovary syndrome （PCOS）, and to determine the role of leptin in the physiopathology of PCOS, luteinized granulosa cells were collected from the follicle fluid of 10 obese women who met the diagnostic criteria for PCOS and their BMI was equal to or greater than 25 kg/m^2, and at the same time, granulosa cells were collected from 10 normal women undergoing IVF-ET who served as the control group. Some luteinized granulosa cells were taken from normal women for in-vitro culture, into which human leptin of different concentrations was added （0, 10, 100 and 1000 ng/mL）. After stimulation with leptin for 48 h, RT-PCR was employed for the detection of the expression of OB-RLInRNA in the luteinized granulosa cells. Our results showed that the level of OB-RLmRNA in luteinized granulosa cells of obese PCOS women was higher than those in the control （P〈0.05）. In luteinized granulosa cells cultured in vitro and stimulated by human leptin for 48 h, the level of OB-RLmRNA was higher than those without leptin stimulation （P〈0.01）, and when leptin concentration was at 100 ng/mL, and the level of OB-RLmRNA reached a peak, It is concluded that in obese PCOS women, the level of serum leptin is increased, which promotes the expression of OB-RL in luteinized granulosa cells and increases the sensitivity of the granulosa cells to leptin. Leptin may contribute to anovulation in obese women with PCOS.

Clinical significance of the leptin and leptin receptor expressions in prostate tissues

Aim： To evaluate the expression of leptin and leptin receptor in benign prostatic hyperplasia （BPH） and prostate cancer （PCa）, and to investigate whether they are associated with the development and progression of PCa. Methods： hnmunohistochemical staining was performed to examine the expression of leptin and leptin receptor in BPH and PCa. PCa was divided into three groups： localized PCa, locally advanced PCa and metastatic PCa. The positive staining was identified and the percentage of the positive staining was graded. We also assessed the relationship between both the Gleason score and body mass index （BMI） and PCa. Results： The percentage of the leptin expression in PCa was significantly higher than that in BPH （P 〈 0.01）. For the PCa group, the expressed levels of leptin showed a considerable correlation with localized PCa and metastatic PCa （P 〈 0.05）. Leptin receptor, however, did not reveal a definite difference between BPH and PCa. The expression of leptin indicated a significant difference between well-differentiated PCa （Gleason score ≤6） and poorly differentiated PCa （Gleason score 8-10） （P 〈 0.05）. The relation between the leptin expression level in PCa and the BMI was not remarkable （P = 0.447）. Conclusion： Our results suggest that leptin might have a promoting effect on the carcinogenesis and progression of PCa.

Neuropeptide Y and leptin receptor expression in the hypothalamus of rats with chronic immobilization stress

In this study, Sprague-Dawley rats were immobilized to a frame for 3 hours a day for 21 days to establish a model of chronic immobilization stress. The body weight and food intake of rats subjected to chronic immobilization stress were significantly decreased compared with the control group. Dual-labeling immunofluorescence revealed that the expression of leptin receptor and the co-localization coeffient in these leptic receptor neurons in the arcuate nucleus of the hypothalamus were both upregulated, while the number of neuropeptide Y neurons was decreased. Chronic immobilization stress induced high expression of leptin receptor in the arcuate nucleus and suppressed the synthesis and secretion of neuropeptide Y, thereby disrupting the pathways in the arcuate nucleus that regulate feeding behavior, resulting in diminished food intake and reduced body weight.

Effects of Metformin Treatment on Soluble Leptin Receptor Levels in Women with Polycystic Ovary Syndrome

The effects of metformin treatment on soluble leptin receptor (sOB-R) levels in women with polycystic ovary syndrome (PCOS) were investigated.This prospective and open-label study was conducted by the Department of Obstetrics & Gynecology at Union Hospital,Tongji Medical College of Huazhong University of Science and Technology,China.Fifty-five women with PCOS and insulin resistance (IR) were treated with metformin for 6 months.According to body mass index (BMI),the patients were divided into two groups:lean PCOS group (BMI <23 kg/m^2,n=34) and overweight or obese PCOS group (BMI >23 kg/m^2,n=21).Before and after treatment,serum luteinizing hormone (LH),follicle stimulating hormone (FSH),testosterone (T),androstenedione (A),dehydroepiandrosterone sulfate (DHEAS),insulin and sOB-R levels were determined.Thirty-one BMI-matched ovulatory women served as controls.The results showed:(1) The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR),androgen levels and hirsutism scores were higher,and sOB-R levels were lower in PCOS groups than in control group.A subgroup analysis of lean and overweight or obese PCOS patients revealed there was significant difference in sOB-R level between lean PCOS group and overweight or obese PCOS group.There were no significant differences in anthropometric parameters between lean PCOS patients and BMI-matched controls.However,sOB-R level was significantly lower in lean PCOS women than in controls.(2) There was no correlation between sOB-R level and BMI,waist and hip circumference,total testosterone,androstendione,DHEAS,LH or hirsutism scores in PCOS patients,but there was a significant negative correlation between sOB-R and HOMA-IR.(3) After treatment with metformin for 6 months,serum insulin levels decreased,and sOB-R levels increased significantly (P<0.01).It was suggested that considering low sOB-R levels supposedly compensate diminished leptin action,PCOS per se might cause leptin resistance.It is likely that reduction of hyperinsulinemia produced by metformin effectively improves the sOB-R levels in PCOS.

Serum leptin and soluble leptin receptor in non-alcoholic fatty liver disease

AIM: To determine the role of leptin system in non-al- coholic fatty liver disease (NAFLD) development by deli- neating the changes in serum levels of leptin and soluble leptin receptor (sOB-R). METHODS: Blood samples were collected from 30 consecutive patients with liver-biopsy-proven NAFLD and 30 patients with cholecystolithiasis (stationary phase) as controls. Serum leptin levels were determined by radio- immunoassay and concentration of sOB-R was measured by ELISA. Body mass index (BMI) was calculated for all subjects, and serum insulin, C-peptide, and lipoprotein levels were also detected. RESULTS: Mean serum leptin level and BMI in the NAFLD group were significantly higher than in the con- trols (both P < 0.001), but mean sOB-R level was lower in the NAFLD group when compared to the controls. Both men and women in the NAFLD group had higher mean serum leptin levels and lower sOB-R levels than did the men and women in the control group (all P < 0.001). The- re was a significant negative correlation between serum leptin and sOB-R levels (r = -0.725, P < 0.001). Multiva- riate analysis showed that the percentage of hepatocyte steatosis, sex, BMI, and homeostasis model assessment of insulin resistance (HOMA IR) were independently rela- ted to serum leptin levels. CONCLUSION: Elevated serum leptin seems to be afeature of steatosis, and serum leptin seems to increase as hepatocyte steatosis develops. An enhanced release of leptin is accompanied by an decrease in sOB-R con- centration, which suggests higher resistance of periphe- ral tissues towards the action of leptin.

Association analyses of single nucleotide polymorphisms in the <i>leptin</i>and <i>leptin receptor</i>genes on milk and morphological traits in Holstein cows

To date, only a few SNP in the leptin receptor gene have been detected and analyzed while the leptin gene has been extensively characterized and several polymorphisms were detected and associated to functional and productive traits in cattle. In this work, for the first time, the bovine leptin receptor gene was fully characterized by sequencing the whole coding region and part of the 5’ flanking region. A group of 95 Holstein cows was genotyped in order to search for SNP at both the LEPR and LEP genes, and to associate them with milk and morphological traits. Nine novel SNP in the leptin receptor gene and one novel SNP in the leptin gene were detected. Four SNP of the leptin receptor gene and one SNP of leptin gene showed a significant effect on one or more analyzed traits, and, in all cases, the greatest effect was observed on fat content. This study provided knowledge of the existence of further polymorphisms in the leptin receptor and leptin genes that have an influence on some important economic traits.

Possible involvement of leptin and leptin receptor in developing gastric adenocarcinoma

AIM: To investigate the expression of leptin and leptin receptor (ob-R) in intestinal-type gastric cancer and precancerous lesions, and to explore the possible mechanism and role of the leptin system in developing intestinal-type gastric adenocarcinoma.METHODS: Immunohistochemistry was performed to examine the expression of leptin and leptin receptor in archival samples of gastric adenocarcinoma and preneoplastic lesions, including intestinal metaplasia and mild to severe gastric epithelial dysplasia. Positive staining was identified and percentage of positive staining was graded.RESULTS: Dual expression of leptin and leptin receptor were detected in 80% (16/20) intestinal metaplasia,86.3% (25/30) mild gastric epithelial dysplasia, 86.7%(26/30) moderate gastric epithelial dysplasia, 93.3%(28/30) severe gastric epithelial dysplasia, 91.3% (55/60)intestinal-type gastric adenocarcinoma and 30.0% (9/30)difffuse-type gastric carcinoma. The percentage of dual expression of leptin and leptin receptor in intestinal-type gastric adenocarcinoma was significantly higher than that in diffuse-type gastric adenocarcinoma (x2 = 37.022,P＜0.01).CONCLUSION: Our results indicate the presence of an autocrine loop of leptin system in the development of intestinal-type gastric adenocarcinoma.

Differential Expression of Leptin and Leptin Receptor mRNA in Obese and Non-Obese Women across the Menstrual Cycle Title

OBJECTIVE: The aim of this study was to investigate the messenger ribonucleic acid expression of leptin (L-mRNA) and the leptin receptor (OB-RmRNA) in subcutaneous fat tissue and to determine their relationship with leptin and testosterone and steroid serum levels over the course of the menstrual cycle (MC), in obese (OBW) and non-obese women (NOW). DESIGN: Observational study investigating mRNA transcript expression of leptin and the leptin receptor from human subcutaneous fat specimens, as well as leptin serum levels, both in relation to the testosterone and sex hormones during the MC in obese and non-obese women. METHODS: Nineteen women, thirteen with a body mass index (BMI) > 25 Kg/m2 and 6 with BMI 2 were included. RT-PCR was used to detect L-mRNA transcripts of leptin and its receptor in samples from 28 fat biopsies taken from seven volunteers (20 from OW and 8 from NOW). The serum concentrations of leptin and steroid hormones were measured throughout the MC using radioinmuno analysis. RESULTS: The percentages of women expressing leptin L-mRNA during the phases of the MC were: early follicular (EF), 14.3%;late follicular (LF), 28.6%;early luteal (EL), 14.3%;and late luteal (LL), 42.9%. The percentages of OB-RmRNA were: EF, 71.4%;LF, 14.3%;EL, 28.6%;and LL, 71.4%. Leptin serum levels were directly related to BMI (p < 0.001), and testosterone (p < 0.001) and indirectly to SHBG (p < 0.001). CONCLUSION: The L-mRNA expression and its receptor in subcutaneous human tissue are regulated throughout the MC in a periodic manner. The physiological role of testosterone in regulation of expression L-mRNA and OB-RmRNA during the secretory phase of the MC in obese women requires further investigation.

Expression of Long Form Leptin Receptor mRNA in Pituitary of Pigs around Puberty

[ Objective] To study the expression of long form leptin receptor （Ob.Rb） mRNA in pituitary of pigs around puberty and explore the rela- tionship between Ob-Rb mRNA and porcine development around pituitary. [Method] Three Sujiang pigs were randomly selected at the age of 120 d, puberty and 180 d, respectively. A pair of primers was designed according to the Ob-Rb sequence published in the GenBank. Total RNAs were extracted from pituitary. The expression of Ob-Rb mRNA was detected by the real-time quantitative RT-PCR. [ Result] The Ob-Rb mRNA was de- tected in pituitaries of pigs at the age of 120 d, puberty and 180 d, respectively. The expression level of Ob-Rb mRNA was lowest at puberty. It was significantly different from that in the 120-day-old pigs and not significantly different from that in the 180-day-old pigs. [ Conclusion] The low expres- sion level of Ob-Rb mRNA is conductive to the arrival of puberty.

Breeding of Leptin Receptor Gene Knockout Mice and Genotype Identification of the Offspring

The leptin（ LP） receptor gene heterozygous mice were mated in four ways. Genomic DNA was extracted from offspring tails and analyzed by PCR. The result showed that the ratios of the offspring genotypes fit the Mendel＇s laws. The male and female LP^（-/-）mice（ DB / DB mice） were infertile. LP^（-/-）mice could be effectively bred by mating of male and female LP^（＋/-）mice. PCR methods could identify LP^（-/-）mice precisely.

miR-155/瘦素受体/AMPK轴在结核菌素诱导破骨细胞形成中的作用及机制

背景:破骨细胞异常活化在脊柱结核骨质破坏中起重要作用。在骨质疏松发病过程中,敲低miR-155通过增加瘦素受体的表达来激活磷酸腺苷依赖的蛋白激酶(AMP-dependent protein kinase,AMPK),进而抑制破骨细胞分化及骨吸收。但miR-155/瘦素受体/AMPK轴在脊柱结核骨质破坏中的作用尚不清楚。目的:研究miR-155/瘦素受体/AMPK轴在结核菌素诱导破骨细胞形成中的作用及机制。方法:培养单核巨噬细胞RAW264.7细胞,用不同浓度(1.0,2.5,5.0,10.0 IU/mL)结核菌素处理,转染阴性对照序列或miR-155抑制物、阴性对照siRNA序列或瘦素受体siRNA序列。采用抗酒石酸酸性磷酸酶染色检测破骨细胞数量,荧光定量PCR检测miR-155 mRNA表达,Western blot检测瘦素受体、p-AMPK蛋白表达,双荧光素酶报告基因验证miR-155靶向瘦素受体。结果与结论:①与对照组比较,2.5,5.0,10.0 IU/mL结核菌素组破骨细胞数量、miR-155 mRNA表达水平明显增加,瘦素受体、p-AMPK蛋白表达水平明显降低(P<0.05);②与阴性对照+5.0 IU/mL结核菌素组比较,miR-155抑制物+5.0 IU/mL结核菌素组破骨细胞数量、miR-155 mRNA表达水平明显降低,瘦素受体、p-AMPK蛋白表达水平明显增加(P<0.05);③与阴性对照组比较,miR-155抑制物组瘦素受体野生型双荧光素酶报告基因的荧光活力增加,miR-155模拟物组瘦素受体野生型双荧光素酶报告基因的荧光活力降低(P<0.05);④与阴性对照siRNA+miR-155抑制物+5.0 IU/mL结核菌素组比较,瘦素受体siRNA+miR-155抑制物+5.0 IU/mL结核菌素组miR-155 mRNA表达水平无明显变化(P>0.05),破骨细胞数量明显增加,瘦素受体、p-AMPK蛋白表达水平明显降低(P<0.05);⑤结果表明,结核菌素通过增加miR-155表达抑制下游瘦素受体表达及AMPK激活,进而诱导破骨细胞形成。

The effect ofthe leptin and its receptorexpression in CRF rat by the Reinforcing Kidney and Exhausting ToxinMixture

Objective:To investigate the adjusting malnutrition mechanism by the Reinforcing Kidney and Exhausting Toxic Mixture(REM)on the chronic renal failure (CRF) rat.Methods:60 wistar rats weved ivided into 3 groups randomly :the normal controc group(group Ⅰ),CRF group(group Ⅱ),and CRF rat perfusingwithREM group(group Ⅲ). Taking theirfat,kidneytissuefor detecting the protein expression of the leptin,leptin receptor(Ob-R) by the means ofimmunohistochemistry.Result:Comparing with control group, the leptinprotein express intensely in CRF rat ; In kidney tissue,the ob-R express weakly. After perfusing the REM ,comparing with CRF groupthe renal ob-R express strongly than CRF group. Conclusion: Maybe the REM could do a little better with the malnutritionof CRFratsby adjusttingthe activity of ob-R in kidney.

高脂膳食诱导肥胖并影响脂肪组织MCHR1和OB-Rb的表达

目的:比较不同方式高脂饮食对大鼠脂肪组织黑色素聚集激素受体1(melanin concentrating hor-mone receptor 1,MCHR1)和瘦素受体(OB-Rb)表达的影响。方法:断乳大鼠分成3组:正常膳食组(NC组,13%热卡来自脂肪),与正常膳食组等热量的高脂膳食组(PHF组,47%热卡来自脂肪)及自由摄入高脂膳食组(HF组,47%热卡来自脂肪)。喂养8周后,称量大鼠体质量,检测血清中的黑色素聚集激素(melanin con-centrating hormone,MCH)和瘦素(leptin)浓度。运用实时定量PCR检测脂肪组织的MCHR1和OB-Rb mRNA水平。结果:HF组和PHF组体质量显著高于NC组(P<0.01),血清中MCH和leptin浓度较NC组有明显增高(MCH,P<0.01;leptin,P<0.05)。同对照组相比,HF组和PHF组脂肪组织中的MCHR1 mRNA水平显著升高(P<0.05),而OB-Rb mRNA却显著降低(HF组,P<0.01;PHF组,P<0.05)。HF组和PHF组的体质量、血清学指标及实时定量PCR结果差异无统计学意义(P>0.05)。结论:等热量和高热量高脂膳食都能诱导大鼠肥胖和代谢异常;高脂膳食所诱导的机体肥胖及代谢紊乱与脂肪组织中MCHR1 mRNA上调和OB-RbmRNA下调有关。

蓝塘猪和长白猪leptin和leptin受体基因表达的变化

用实时荧光定量PCR方法研究了蓝塘猪和长白猪1、27、90、150和180日龄阶段脂肪组织中leptin基因mRNA和下丘脑中leptin受体基因mRNA的变化,并对2个品种不同生长阶段血液中leptin含量的变化规律进行了探讨。结果表明:(1)蓝塘猪180日龄时皮下脂肪中leptin基因表达量显著高于其它各阶段,而与长白猪相比,蓝塘猪除1日龄低于长白猪外,其它各个阶段均高于长白猪,180日龄两者差异极显著;长白猪各阶段间差异不显著;(2)蓝塘猪180日龄时下丘脑中leptin受体基因的表达量显著高于其它各阶段,长白猪180日龄时最高,且显著高于1日龄和27日龄,蓝塘猪与长白猪1日龄时差异显著;(3)蓝塘猪血清中leptin浓度各阶段均高于长白猪,两品种均是150日龄时最高,蓝塘猪150日龄显著高于27日龄和180日龄,长白猪各阶段差异不显著。

leptin及其受体的研究进展

leptin是肥胖基因 (obesegene ,OB基因 )的蛋白产物 ,具有广泛的生物学功能。据现有研究发现 ,leptin具有参与调节摄食、能量代谢、激素分泌、生长、生殖和免疫等过程的功能。leptin通过其受体发挥调节作用。笔者综述了leptin的受体、生物学功能、调控动物体重的作用机理及leptin抵抗。

瘦素及其功能性受体OB-Rb在非小细胞肺癌表达的临床病理研究

目的:研究瘦素和瘦素功能性受体OB-Rb在非小细胞肺癌(non-small cell lung cancer,NSCLC)中的表达,并探讨瘦素和OB-Rb在NSCLC发生、发展过程中的意义。方法:采用RT-PCR和免疫组织化学方法,检测38例NSCLC肿瘤组织及其癌旁组织中瘦素和瘦素受体OB-Rb的mRNA和蛋白表达情况,同时将其蛋白表达水平与NSCLC的临床病理参数进行相关性分析。结果:瘦素与OB-Rb的mRNA在肺癌组织表达水平显著高于癌旁组织(P=0.000)。瘦素蛋白在肺癌组织和癌旁组织的阳性表达率分别为71.1%和26.3%(P<0.005),OB-Rb蛋白在肺癌组织和癌旁组织的阳性表达率分别为63.2%和31.6%(P<0.010);瘦素和OB-Rb蛋白与NSCLC细胞类型、分化程度、TNM分期及淋巴结转移无明显相关性(P>0.05),瘦素与OB-Rb蛋白在NSCLC中的表达也无显著关联(P>0.05)。结论:瘦素和OB-Rb在肺癌组织表达上调,瘦素可能是NSCLC发生、发展过程中的一种促肿瘤生长因子。瘦素和OB-Rb在NSCLC的促癌作用没有直接的协同效应,可能是通过各自不同的机制参与NSCLC的病程。

长型Leptin(瘦素)受体mRNA在大鼠消化道中的表达

本试验以 5只 SD雌性大鼠为研究对象 ,采用原位杂交技术研究了大鼠消化道长型 Leptin (瘦素 )受体 m RNA的表达及其分布。结果表明 ,长型 Leptin受体 m RNA在大鼠胃和十二指肠的粘膜及粘膜下层组织中广泛表达 ,从而证明了在大鼠消化道存在长型

不同阶段运动干预对2型糖尿病大鼠骨骼肌leptin及其受体蛋白表达的影响

目的：1）探讨2型糖尿病糖脂代谢紊乱的机制;2）观察在2型糖尿病发生发展的不同阶段施加长期有氧运动干预改善糖脂代谢紊乱的效果及作用的机制.旨在为揭示不同运动干预在改善2型糖尿病大鼠瘦素抵抗中的作用及其作用机制提供实验依据.方法：将55只刚断乳雄性大鼠随机分为两组组,正常对照组（CON,11只）,高脂高糖组（HLG,44只）,其中正常饮食对照组用普通饲料,HLG组给与高脂高糖饮食喂养六周后.体重超过正常组25％,为肥胖模成功,再给与腹腔注射小剂量（35 mg/kg）的链脲佐菌素（STZ）,造2型糖尿病模型,将造模成功鼠按血糖水平随机分成糖尿病对照组（DC,8只）,糖尿病运动1组（DE1,8只）,糖尿病运动2组（DE2,8只）和糖尿病运动3组（DE3,8只）,分别在1～6周,7～12周和1～12周进行游泳训练,实验结束后测定血糖、胰岛素、瘦素、骨骼肌中TG、FFA含量和瘦素及其素受体的蛋白表达等指标.结果：DC组体重、腹腔脂肪、血清胰岛素、葡萄糖、瘦素和胰岛素的耐受性均显著高于CON组;而DE1-3组体重、腹腔脂肪、血清胰岛素、葡萄糖和瘦素均均出现不同程度的下降,以DE3组下降效果明显.肌肉中TG,FFA含量DC组明显高于CON组;DE1-3与DV组相比均有均下降趋势,只有DE3组有统计学差异;且DE3组的TG含量也显著低于DE2组.DC组骨骼肌中瘦素含量显著升高（P＜0.01）,但瘦素受体含量明显降低（P＜0.05）;DE1-3组与DC组相比,瘦素水平有下降的趋势,相反他们的瘦素受体含量都有升高的趋势,其中DE3组的变化有统计学意义.结论：1）高脂膳食结合小剂量的STZ诱导的2型糖尿病大鼠骨骼肌瘦素抵抗,降低了其对骨骼肌脂代谢的调节作用,导致骨骼肌脂质的过度沉积,引发了整体水平瘦素抵抗和胰岛素抵抗.2）在糖尿病发生、发展的不同阶段施加有氧训练可不同程度改善骨骼肌瘦素抵抗,改善了机体的糖脂代谢,缓解了胰岛素抵抗和瘦素抵抗,在糖尿病发生发展的全过程施加运动干预的效果更好.

结直肠癌组织leptin受体的表达及临床意义

背景与目的:结直肠癌发病比例逐年增高,公认同饮食、能量消耗等均有关联;肥胖基因(Ob基因)的表达产物leptin蛋白(瘦素)在调节能量支出、代谢、激素分泌、生殖和免疫等领域有较多的研究,但在结直肠组织中是否存在leptin受体蛋白说法不一。本研究了解leptin受体在人结直肠和结直肠癌细胞中的存在,探讨leptin受体的表达与肿瘤分期、分化、年龄和体重指数之间的关系。方法:免疫组织化学方法检测固定标本的leptin受体,ELISA方法测定新鲜组织匀浆上清液中leptin受体。分别比较不同体重、TNM分期、年龄和性别的检测结果。结果:leptin受体在结直肠癌组织和正常结直肠组织中均有表达,癌肿组织的阳性率(48%)高于交界处的(30%),交界处的又高于正常结直肠组织(28%)。Ⅲ/Ⅳ期病例肿瘤组织匀浆上清液中leptin受体的表达为1613±570,高于Ⅰ/Ⅱ期的表达1245±472(P<0.01)。但leptin受体的表达与结直肠癌组织分化、患者的年龄和体重指数之间未见相关。结论:结直肠癌组织及正常结直肠组织上均存在leptin受体,癌组织中有更高的检出率,且高分期的病例较低分期的病例有更高的leptin受体蛋白表达。同性别、年龄、肿瘤部位和体重指数无相关性。