Resistin基因过表达对大鼠胰岛β细胞株 RINm5F基础胰岛素分泌的影响

目的 探讨Resistin基因过表达对大鼠胰岛β细胞株 RINm5F基础胰岛素分泌的影响.方法 体外培养大鼠胰岛β细胞株 RINm5F,采用PCR法扩增大鼠Resistin基因全编码区cDNA片段,BamH和Xho双酶切后插入pcDNA3.1B 表达载体,经测序验证正确后,采用脂质体转染pcDNA3.1-Resistin真核表达质粒入RINm5F细胞,筛选稳定表达株,并采用RT-PCR验证过表达Resistin的效率.在RINm5F细胞密度达到80%,缓冲液洗3遍,继续于缓冲液中生长2 h,收集上清液,采用ELISA法检测细胞培养上清中的胰岛素水平.同时Trizol 一步法提取RINm5F细胞总RNA,采用RT-PCR法检测葡萄糖转运子2(Glut2)mRNA水平,并用紫外吸收剂凝胶密度扫描仪分析条带吸光度值.采用SPSS 11.0软件进行统计学分析.结果 观察过表达Resistin的RINm5F中Resistin mRNA表达,发现过表达Resistin的细胞株中Resistin mRNA水平为对照组的2.46倍(P<0.001).过表达Resistin的RINm5F细胞的基础胰岛素分泌低于转染空载质粒的细胞,较对照组下降约32%(P<0.001).过表达Resistin的RINm5F细胞中Glut2表达明显低于转染空载质粒的细胞,较对照组下降约38%(P<0.05).结论 Resistin基因过表达显著下调胰岛庀赴鸕INm5F的基础胰岛素分泌,其机制可能与Glut2有关.     

Resistin结合多肽对胰岛β细胞株RINm5F分泌功能的影响

目的 先前研究已显示resistin结合多肽(RBP)能拮抗resistin对脂肪细胞脂质代谢和内分泌功能的调节作用.本研究试图阐明RBP对胰岛β细胞株RINm5F分泌功能的影响.方法 以不同水平RBP(10-10,10-11,1012mol/L)与RINm5F共培养30min、60min、2h后取上清,ELISA法测其胰岛素,RT-PCR法检测细胞中葡萄糖转运子2(GLUT2)mRNA表达水平,Western blotting法检测细胞中GLUT2的蛋白水平,并采用FURA-3/AM钙荧光染色法检测胰岛素分泌的重要启动因素:细胞内钙水平.结果 RBP在10-12mol/L时干预2h,不影响胰岛β细胞株RINm5F的细胞活性.但能显著刺激胰岛素分泌,RBP为10-12mol/L时干预2h,细胞内钙明显增多.在Resistin刺激下,GLUT2 mRNA水平和蛋白水平均显著上调.结论 RBP能促进RINm5F细胞株胰岛素的分泌,其可能机制是RBP上调了GLUT2的表达,进而增加了细胞内钙的水平,最终导致胰岛素分泌增加.     

腺病毒介导的白介素10基因转导对鼠胰岛β细胞的保护作用

目的观察腺病毒介导的白介素10(IL-10)基因转导对体外及体内胰岛β细胞的保护作用。方法用携带有IL-10基因的重组腺病毒载体感染RINm5F细胞、昆明小鼠及链脲佐菌素(STZ)诱导的1型糖尿病小鼠,ELISA检测IL-10基因表达、胰岛素水平,病理切片及免疫组化观察胰岛炎积分。结果 RINm5F细胞中检测到IL-10基因及蛋白的有效表达,含IL-10的重组腺病毒(Ad-IL-10)可抑制STZ致细胞凋亡作用。昆明小鼠腹腔注射Ad-IL-10后,再经STZ诱发为1型糖尿病,Ad-IL-10组胰岛炎积分明显降低。经STZ诱导的早期1型糖尿病小鼠,Ad-IL-10组与其他组相比平均血糖水平差别无统计学意义,小鼠胰岛炎症浸润程度与糖尿病对照组差别无统计学意义。结论腺病毒介导的IL-10可在胰岛RINm5F细胞有效表达,并且具有抗凋亡的能力。IL-10基因能够保护胰岛β细胞功能,促进胰岛素分泌,减少小鼠的胰岛炎和糖尿病的发生。IL-10基因对于已发生1型糖尿病早期的昆明小鼠无显著的治疗作用。     

三羟异黄酮对雌二醇和双酚A促神经母细胞瘤细胞增殖的抑制作用

目的 观察大豆异黄酮类物质4',5,7,-三羟异黄酮(genistein,GEN)对17β-雌二醇(E2)和双酚A(BPA)诱导的神经母细胞瘤细胞增殖作用的影响.方法 SK-N-SH细胞经常规培养扩增后分为6组:组1,RPMI1640无酚红培养液加无水乙醇(对照组);组2,加GEN(12.5 μmol/L);组3,加E2(2μmol/L);组4,同时加E2和GEN;组5,加BPA(8 μmol/L);组6,同时加BPA和GEN.分别在24h、48h和72h进行光吸收度(A值)检测,72 h时用流式细胞仪检测细胞周期及凋亡亚二倍体峰;末端脱氧核糖核酸酶介导的dUTP末端标记(TUNEL)法检测细胞凋亡以及Westem blot检测磷酸化Akt和总Akt蛋白表达.结果 48 h和72 h时,组3、5与组1比较,细胞.A值有增加(P<0.01).48h和72h时组4与组3比较,组6与组5比较,细胞A值却降低(P<0.01).48 h时,组4的A值较组3降低10%,组6较组5降低13%(P<0.01);72h时.组4较组3的A值下降17%,组6较组5的A值下降22%(P<0.01).72 h时,组4的G2/M期细胞百分比是组3的1.78倍,组6是组5的1.49倍(P<0.01).72h时.各组磷酸化Akt表达有所不同,GEN干预组的磷酸化Akt光密度值较未干预组有下降.其中,组2的磷酸化Akt表达较对照组下降近15%;组4的磷酸化Akt表达分别较组3下降约11%;组6的磷酸化Akt表达较组5也有下降(均P<0.01);各组的总Akt蛋白表达未见明显差异.同样,各组的细胞凋亡未见统计学差异.结论 4',5,7,-三羟异黄酮可抑制17β-雌二醇和双酚A促神经母细胞瘤细胞体外增殖的作用,该作用可能与G2/M期细胞周期阻滞及PI3K/Akt信号转导通路异常有关.     

香菇多糖对白介素-1β诱导人胚肺成纤维细胞表型转化的影响

目的：研究白介素-1β（IL-1β）对人胚肺成纤维细胞(FB)向肺肌成纤维细胞转化的影响及香菇多糖（LNT）的作用。方法：体外培养人胚肺FB,用不同浓度IL-1β和LNT作用于细胞后,采用CCK-8法检测细胞的增殖情况,免疫细胞化学染色检测α-平滑肌肌动蛋白（α-SMA）,RT-PCR检测纤维连接蛋白（FN）、Ⅰ型胶原蛋白（ColⅠ）和α-SAM mRNA的相对表达量。结果：①IL-1β组细胞增殖的吸光度、α-SMA蛋白及FN、ColⅠ和α-SAM mRNA表达均高于对照组（P<0.01）,且随着IL-1β浓度的增加,表达逐渐增高。②LNT呈浓度依赖性抑制IL-1β诱导的细胞增殖及α-SMA蛋白、FN、ColⅠ和α-SAM mRNA表达（P<0.01）。结论：LNT可抑制IL-1β诱导人胚肺FB增殖和肌成纤维细胞转化及细胞外基质积聚。     

低出生体重新生大鼠胰岛素与K+ATP通道表达的相关性研究

目的明确低出生体重(low birth weight,LBW)新生大鼠胰腺K ATP通道表达和胰岛素表达的相关性。方法采用孕鼠全程饥饿法建立LBW新生大鼠模型,并设立对照组。于生后第一天取血和胰腺,测定血糖和胰岛素水平;应用免疫组化法检测胰岛β细胞量和胰岛素分泌,用半定量RT-PCR法检测K ATP通道和胰岛素表达量。结果LBW组血胰岛素水平、胰腺重量和胰岛素分泌指数均低于对照组,LBW组胰岛素抵抗指数高于对照组(P均<0.05)。LBW组胰岛中胰岛素的积分吸光度以及胰岛素、K ATP通道mRNA表达量均低于对照组(P均<0.05)。LBW组的胰岛素mRNA表达量与KATP通道mRNA表达量相关(r=0.934,P=0.007)。结论低出生体重新生大鼠生后第一天即存在胰岛素分泌缺陷和胰岛素抵抗,胰岛β细胞数量的减少,胰岛素表达减少。其胰岛素分泌缺陷可能与β细胞K ATP通道表达减少有关。     

ShRNA靶向沉默HOXA10基因对U937细胞增殖和凋亡的影响

目的：探讨慢病毒载体介导短发夹RNA （shRNA,siRNA前体）靶向沉默HOXA10基因对U937细胞增殖、凋亡和形态的影响。方法：设计并构建4条针对HOXA10基因的shRNA质粒表达载体,并构建HOXA10基因的过表达质粒,将4条干扰质粒分别和过表达质粒共转染293T细胞,用Western blot 检测出敲减效果最好的1条质粒并包装成慢病毒（lenti-shHOXA10）;将U937细胞分为干扰组（lenti-shHOXA10）、阴性对照组（lenti-NC）和未处理组,通过流式细胞仪测定慢病毒对U937细胞的感染效率并用real-time PCR、Western blot方法测定对HOXA10基因的沉默作用;瑞氏染色观察3组细胞形态上的变化;MTT法检测细胞增殖抑制率;流式细胞术检测3组细胞凋亡率。结果：成功构建了有效沉默HOXA10基因的慢病毒-shRNA载体。干扰组HOXA10 mRNA的沉默效率为(92.3±1.3)%,蛋白表达水平下降91.1％,干扰组细胞抑制率为（43.9±0.7）%,与阴性对照组、未处理组相比差异有统计学意义（P<0.05）;瑞氏染色显示干扰组细胞核质比减小、核分裂相少见;干扰组细胞凋亡率为（27.1±1.4）%,显著高于阴性对照组的（19.4±1.9）%和未处理组的（5.5±1.3）%（P<0.05）。结论：慢病毒载体介导的shRNA可稳定地降低HOXA10基因的表达水平,有效抑制U937细胞增殖和促进其凋亡,HOXA10基因有望成为白血病基因治疗的新靶点。     

三氧化二砷通过毛细血管扩张性共济失调突变和RAD3相关激酶通路上调KG1a细胞UL16结合蛋白1的表达

目的观察三氧化二砷(ATO)对急性髓系白血病细胞KG1a细胞表面NKG2D配体UL16结合蛋白1(ULBP1)表达的影响,探讨其调节ULBP1表达的分子机制。方法常规体外培养KG1a细胞,采用细胞增殖/毒性检测试剂(CCK8)检测不同浓度ATO对KG1a细胞的增殖抑制率;应用实时荧光定量反转录(RT)-PCR方法检测KG1a细胞ULBP1 mRNA表达的影响;流式细胞术检测ATO对KG1a细胞表面ULBP1蛋白表达的影响。加入毛细血管扩张性共济失调突变和RAD3相关激酶(ATM/ATR)抑制剂咖啡因,观察其是否影响ATO对KG1a细胞ULBP1 mRNA及蛋白的表达。采用Western blot法观察ATO对KG1a细胞中CHK1、CHK2蛋白及其磷酸化表达的影响。结果不同浓度(1、2、3、4、5μmol/L)ATO均可抑制KG1a细胞的增殖,呈浓度依赖性,其对KG1a细胞的半数抑制浓度(IC50值)为2.7μmol/L。荧光定量RT-PCR法检测结果示ATO可使KG1a细胞ULBP1 mRNA的相对表达水平升高,ATO在浓度分别为1、2、3、4、5μmol/L时,与未加药组比较,ULBP1 mRNA相对表达水平分别升高至(1.86±0.30)倍、(3.02±0.71)倍、(3.16±0.75)倍、(4.80±0.70)倍、(3.70±0.89)倍,差异均有统计学意义(均P<0.05);与未加药组相比,当ATO浓度分别为1、2、3、4、5μmol/L时,ULBP1蛋白相对表达水平均显著升高,差异均有统计学意义(均P<0.05)。咖啡因预先处理KG1a细胞2 h再联合ATO共同孵育KG1a细胞24 h,ULBP1 mRNA和蛋白表达水平均显著降低。在咖啡因浓度为8 mmol/L时,ULBP1 mRNA相对表达水平由不用咖啡因处理组的(9.55±0.38)倍降为(6.36±0.93)倍,差异有统计学意义(P<0.05);流式细胞术检测结果发现,当咖啡因浓度分别为2、4、8 mmol/L时,ULBP1蛋白相对表达水平由不用咖啡因处理组的(3.50±0.08)倍分别降为(2.17±0.07)倍、(2.02±0.06)倍、(1.75±0.06)倍,差异均有统计学意义(均P<0.05)。CHK1和CHK2蛋白相对表达水平均随ATO浓度的升高而降低,而CHK1和CHK2磷酸化蛋白的相对表达水平均随ATO浓度的升高而升高。结论ATO诱导上调KG1a细胞ULBP1 mRNA及蛋白的表达,ATM/ATR-CHK1/CHK2通路可能参与这一过程。     

同源盒基因HOXA9在儿童急性白血病中的表达及其临床意义

目的：研究同源盒基因HOXA9在儿童急性白血病（AL）患儿骨髓单个核细胞中的表达,并探讨其临床意义。方法：采用RT-PCR方法检测46例不同时期AL患儿HOXA9 mRNA的表达水平,以15例特发性血小板减少性紫癜（ITP）患儿作为对照。结果：46例AL患儿（52份骨髓标本）HOXA9基因阳性表达率为63%,其中急性髓细胞白血病(AML)组阳性表达率（86%）明显高于急性淋巴细胞白血病（ALL）组（35%）及对照组（13%）（P<0.05）; AML组HOXA9 mRNA表达水平明显高于ALL组及对照组（P<0.05）。HOXA9在各型儿童AML中表达不同,mRNA相对表达水平依次为：M5型＞M4型＞M1和（或）M2型,而在M3型中未检测到表达。HOXA9在AML患儿高危组中的阳性表达水平较高。AML患儿初治组HOXA9基因阳性表达率及mRNA水平明显高于缓解组和对照组（P<0.05）,而缓解组与对照组比较差异无统计学意义;未缓解组HOXA9基因表达显著高于缓解组和对照组（P<0.05）。结论：HOXA9基因高表达与AL的发生相关;AML患儿HOXA9基因表达水平明显高于ALL患儿。HOXA9基因高表达者与白血病危险程度有关,且提示预后不良。因此,HOXA9基因有望成为儿童AL诊断、治疗及判断预后的一个靶点。     

苦参碱对人横纹肌肉瘤RD细胞增殖和凋亡的影响

目的：探讨苦参碱（matrine, Mat）对体外人横纹肌肉瘤RD细胞增殖和凋亡的影响,以及Mat诱导RD细胞凋亡的相关机制。方法：采用MTT比色法检测终浓度为0.5、1.0、1.5和2.0 mg/mL Mat对RD细胞的增殖抑制率;流式细胞术检测上述4种不同浓度Mat对RD细胞的凋亡作用;RT-PCR法检测终浓度为0.5、1.0和1.5 mg/mL Mat对RD细胞Cyclin D1及Survivin mRNA表达的影响。结果：各浓度实验组RD细胞的增殖抑制率和凋亡率均高于未经Mat处理的对照组（均P<0.01）,且随着药物浓度增加,细胞增殖抑制率逐渐增高,呈剂量依赖性。RT-PCR检测Cyclin D1 及Survivin mRNA在各组RD细胞中均有表达,两者的表达水平在各浓度处理组中与对照组相比均有明显下降（P＜0.01）。其中Cyclin D1在各浓度组间比较差异均有统计学意义（P＜0.05）,而Survivin仅在0.5 mg/mL 和1.5 mg/mL组间差异有统计学意义（P＜0.05）。结论：Mat能明显抑制RD细胞的增殖,并诱导其凋亡;其抗肿瘤机制可能与下调Survivin和Cyclin D1 mRNA的表达有关。     

抵抗素及其结合多肽对大鼠骨骼肌细胞糖摄取功能的影响

目的探讨抵抗素及其结合多肽(RBP)对大鼠骨骼肌细胞糖摄取功能的影响。方法体外培养的大鼠骨骼肌细胞(L6)随机分为对照组,抵抗素(10 nmol/L)组,RBP(1 nmol/L)组、抵抗素(10 nmol/L) RBP(1 nmol/L)组,培养0.5 h后,液闪计数法(LSC)观察L6细胞糖摄取功能的变化,RT-PCR、Western blot法检测葡萄糖转运载体(GLUT)4基因的表达及转位变化。结果与对照组相比,抵抗素组糖摄取功能下降,RBP组及抵抗素 RBP组糖摄取功能无明显变化(P<0.05);与抵抗素组相比,抵抗素 RBP组糖摄取功能明显上调(P<0.05)。4组L6细胞的GLUT4基因的蛋白表达及转位均无明显变化(P>0.05)。结论抵抗素能抑制骨骼肌细胞的糖摄取;但对正常骨骼肌细胞糖摄取功能无明显影响;RBP但能有效拮抗抵抗素抑制骨骼肌细胞糖摄取的作用。     

肥胖症儿童血清抵抗素水平与胰岛素抵抗关系的研究

目的探讨肥胖症儿童血清抵抗素水平与高胰岛素血症和(或)胰岛素抵抗的关系。方法采用酶联免疫法测定34例肥胖儿童,31例正常对照的血清抵抗素水平。分析血清抵抗素与体重指数、体脂百分比、腰臀比及空腹血糖、空腹胰岛素水平、胰岛素抵抗指数、胰岛β细胞功能指数的相关关系。结果(1)肥胖组及对照组抵抗素浓度(对数转换值3.1±0.5)高于对照组(对数转换值2.7±0.8)(P<0.05)。(2)抵抗素与性别、年龄、收缩压、舒张压无相关关系;与体重指数、体脂百分比、腰臀比呈正相关(相关系数分别为r=0.299、0.304、0.322,P<0.01);与空腹血糖及空腹胰岛素水平呈正相关(相关系数为r=0.299和r=0.303,P<0.05);与胰岛素抵抗指数呈正相关(r=0.324,P<0.01),与胰岛β细胞功能指数无相关关系。(3)多元逐步回归分析表明,胰岛素抵抗指数为影响抵抗素最为显著的因素(R2=0.105);标准化偏回归系数0.279(P<0.01)。结论肥胖症儿童血清抵抗素水平较正常儿童增高,并与肥胖程度,脂肪分布密切相关。抵抗素可能与肥胖症儿童发生高胰岛素血症和(或)胰岛素抵抗有关。     

Concentrations of adipokines in children before and after hematopoietic stem cell transplantation

Adipokines have multiple effects, including regulation of glucose metabolism, cell proliferation, inflammation, and angiogenesis. The aim of the study was to determine plasma concentrations of adiponectin, apelin, leptin, and resistin as well as soluble leptin receptor in pediatric hematopoietic stem cell transplantation (HSCT). The expression of genes encoding the studied peptides was measured using microarray technique. Plasma concentrations of tested peptides were measured before and after oral glucose tolerance test in children treated with HSCT (n = 38) and in healthy controls (n = 26). The peptides were measured before HSCT (pre-HSCT group; n = 38) and after a median of 6 months after HSCT (post-HSCT group; n = 27 of 38 children treated with HSCT). In addition, measurements of fasting plasma glucose, insulin, lipids, and high-sensitivity C-reactive protein (hsCRP) were performed. In both HSCT groups, atherogenic lipid profile, low-grade systemic inflammation was observed. Leptin, adiponectin, and resistin also appear to be good markers of disease burden and low-grade systemic inflammation. Adipokines may be good markers of disease burden and may influence metabolic complications of HSCT. Future studies on larger groups of patients will explain if changes of the concentrations of leptin, adiponectin, and apelin observed in our study and confirmed by expression levels influence engraftment and reconstitution of cell lines.     

Resistin in preterm and term newborns: relation to anthropometry, leptin, and insulin

This study aimed to investigate 1) the plasma resistin concentration at birth, 2) the relationship of resistin with leptin and insulin, and 3) the association of resistin with anthropometric indexes in newborn infants. Blood samples for hormonal assay were obtained from preterm and term newborns within the first 2 h of life and before milk feeding or energy intake. Although these infants required blood sampling for clinical reasons, all were proved to be noninfected. Plasma resistin was significantly higher in term than in preterm infants. It was also significantly correlated with serum leptin, and both hormones were significantly associated with gestational age and anthropometric indexes. Infants who were born vaginally were found to have significantly higher plasma resistin levels compared with those who were born by cesarean section. In the multivariate forward stepwise regression models, resistin was found to be significantly associated with the mode of delivery and gestational age or birth weight. The association among resistin, leptin, and anthropometric indexes suggested that both hormones might be gestation related. A high circulating resistin level at term gestation could be advantageous to the infant by promoting hepatic glucose production and preventing hypoglycemia after birth. Infants who were born vaginally had significantly higher plasma resistin levels, suggesting that this hormone might also be associated with stress or inflammation induced by the birth process.     

Management Challenges in a Child with Hyperinsulinemic Hypoglycemia

Malignant insulinoma is very rare in children. Herein, we present a case of a child with malignant insulinoma along with islet cell hyperplasia. She initially presented with features of hyperinsulinemic hypoglycemia at 18 mo of age. Magnetic resonance imaging (MRI) of the abdomen showed a mass at the junction of the head and body of the pancreas. The tumor was enucleated. Five months later symptoms of hypoglycemia recurred. A subtotal pancreatectomy was performed. She continued to have hypoglycemia, although less frequently. She was put on increasing doses of diazoxide. Seven months later, MRI of the abdomen and a PET scan revealed metastatic deposits in the liver, which were confirmed by histopathology and immunostaining. To the best of our knowledge, this is the youngest child with metastatic insulinoma reported so far.     

IGF binding protein-3 treatment alters intestinal cell proliferation but not body weight of adult cystic fibrosis transmembrane conductance regulator deficient mice

The intestinal phenotype of cystic fibrosis (CF) transmembrane conductance regulator deficient mice includes altered cell homeostasis and a distended crypt-villus axis, which, in previous work, was inversely proportional to body weight. To investigate this correlation, herein, we treated CF mice with IGF binding protein-3 (IGFBP-3), a protein which, as it has potent effects on cell proliferation and apoptosis, we hypothesized would alter the intestinal cell homeostasis, and assessed body weight. Six-week-old C57BL/6JxBALB F2 CF and WT mice received recombinant human IGFBP-3 (rhIGFBP-3, 20 mg/kg) or vehicle treatment, and weight gain, serum protein levels, and intestinal histology were assessed. Administration of rhIGFBP-3 to CF mice significantly increased the number of Igfbp-3 positive cells in the intestine and partially reversed the hyperproliferative phenotype of intestinal crypts and muscularis externa, while not affecting apoptosis. Serum Igfbp-3 levels were increased, and Igf-I, albumin, and triglycerides measures were decreased in CF compared with WT mice. rhIGFBP-3 treatment significantly increased serum albumin and triglycerides but did not affect weight gain in CF mice. We have identified rhIGFBP-3 treatment to reduce intestinal cell proliferation, resulting in decreases in crypt depth and muscularis externa thickness in CF mice.     

转神经生长因子基因诱导神经母细胞瘤分化的研究

目的观察转染神经生长因子（nerve growth factor，NGF）基因诱导神经母细胞瘤（neuroblastoma，NB）细胞系的分化，探讨NGF在NB细胞分化中的作用。方法取本院住院NB患儿新鲜手术标本，进行原代细胞培养并分离纯化，建立细胞系，作为细胞模型。通过脂质体法介导含有NGF基因的载体质粒转染NB细胞。倒置相差显微镜观察转染前后细胞的形态学变化；MTT法及有丝分裂指数测定细胞增殖的改变。结果转染后的NB细胞表达较高水平的NGF，细胞增殖受到抑制并发生形态学改变。结论所建立的NB为可诱导型，即N型；转染NGF基因的NB细胞表达较高水平的NGF；转染NGF基因的NB细胞系表现为增殖抑制和分化。     

Resistin and leptin in breast milk and infants in early life

Background

The role of adipokines in early life is considered an emerging topic issue in nutritional researches.

Aims

To evaluate serum resistin and leptin concentrations and their relations in infants and in breast milk.

Study design

We enrolled 41 term, AGA, healthy infants, of which 23 exclusively breast-fed (BF) and 18 formula-fed (FF), aged less than 6 months. Breast milk (BM) samples were collected from 23 breastfeeding mothers of the infants enrolled. Resistin concentration in serum and BM was determined by ELISA test (Human-Resistin-ELISA, Mediagnost, Reutlingen, Germany). Leptin concentration was determined by Radioimmunoassay method (LEP-R40, Mediagnost, Reutlingen, Germany). Infants weight, length and body mass index were measured. We used Mann–Whitney test. Spearman correlation was applied. Statistical significance was set at p < 0.05. Data are reported as median and interquartile range (IR).

Results

Infants serum resistin concentration was 9.30 (5.02) ng/ml. Breast milk resistin concentration (n = 23) was 0.18 (0.44) ng/ml. Leptin concentration was 3.04 (3.68) ng/ml in infants serum and in BM was 2.34 (5.73) ng/ml. Serum resistin concentrations in BF infants correlated positively with BM resistin (r = 0.636, p = 0.035). We have shown a positive correlation between resistin and leptin in total group of infants (r = 0.44, p = 0.05), confirmed in breastfed subjects (r = 0.65, p = 0.02). No correlations were found between serum hormones and anthropometric parameters of infants.

Conclusion

Our findings show interestingly a positive correlation between resistin concentrations in BF infants serum and in BM and between resistin and leptin in infants.