Reduction in Maternal Energy Intake during Lactation Decreased Maternal Body Weight and Concentrations of Leptin,Insulin and Adiponectin in Human Milk without Affecting Milk Production,Milk Macronutrient Composition or Infant Growth

Maternal diet has the potential to affect human milk (HM) composition, but very few studies have directly assessed the effect of maternal diets on HM composition. The primary aim of this study was to assess the effect of improving dietary quality in lactating women over 2 weeks on the concentrations of macronutrients and metabolic hormones in HM. The secondary aims were to assess the impact of the dietary intervention on 24 h milk production, maternal body composition and infant growth. Fifteen women completed a 1-week baseline period followed by a 2-week dietary intervention phase targeted towards reducing fat and sugar intake. Maternal anthropometric and body composition and infant growth measurements were performed weekly. Total 24 h milk production was measured before and after the dietary intervention, and HM samples were collected daily. Maternal intakes of energy (−33%), carbohydrate (−22%), sugar (−29%), fat (−54%) and saturated fat (−63%) were significantly reduced during the dietary intervention. HM insulin, leptin and adiponectin concentrations were 10–25% lower at the end of the dietary intervention, but HM concentrations of macronutrients were unaffected. Maternal body weight (−1.8%) and fat mass (−6.3%) were significantly reduced at the end of the dietary intervention, but there were no effects on 24 h milk production or infant growth. These results suggest that reducing maternal energy, carbohydrate, fat and sugar intake over a 2-week period is associated with significant reductions in HM insulin, leptin and adiponectin concentrations. These changes may be secondary to decreases in maternal weight and fat mass. The limited studies to date that have investigated the association between metabolic hormone concentrations in HM and infant growth raise the possibility that the changes in HM composition observed in the current study could impact infant growth and adiposity, but further studies are required to confirm this hypothesis.     

尿毒症血透患者血浆瘦素与胰岛素水平的关系

应用放免法测定尿毒症血透患者及健康人 (各 3 0例 )血浆中瘦素、C肽及胰岛素水平。结果 :血透组血浆瘦素及C肽质量浓度明显高于对照组 (P <0 .0 1 ) ;瘦素质量浓度与体质量指数 (BMI)、C肽及胰岛素呈正相关 (P <0 .0 5 )。提示 :尿毒症维持性血透患者血浆瘦素及C肽质量浓度明显升高 ,瘦素与BMI、C肽及胰岛素水平呈正相关     

Placental leptin correlates with intrauterine fetal growth and development

目的　探讨胎盘肥胖基因及其蛋白表达水平与脐血瘦素和胎儿宫内生长发育的关系。方法　在 4 0例产妇分娩时采集胎盘与脐血 ,采用逆转录聚合酶链反应 (RT PCR)检测胎盘肥胖基因mRNA相对表达水平 ,采用Western Blot检测胎盘肥胖基因蛋白 (瘦素leptin)表达水平 ,采用免疫组化观察胎盘肥胖基因蛋白表达位点 ,采用放射免疫法 (RIA)检测脐血瘦素水平 ,采用Ponderal指数 [PI=10 0×体重 (g) /身长 (cm) 3]估测新生儿营养状态。结果　胎盘组织肥胖基因呈现高效表达 ,在胎盘滋养层细胞浆内肥胖基因蛋白阳性表达。胎盘肥胖基因及其蛋白表达水平与胎儿宫内生长发育状态显著相关 ,13例小于胎龄儿胎盘组织leptin mRNA及其蛋白表达水平显著低于 15例适于胎龄儿 (P =0 .0 0 3和 0 .0 0 8) ,12例大于胎龄儿胎盘组织leptin mRNA及其蛋白表达水平显著高于适于胎龄儿 (P =0 .0 4和 0 .0 2 )。胎盘肥胖基因mRNA及其蛋白表达水平与脐血瘦素水平显著相关 (r =0 .39和0 .4 3,P <0 .0 5) ,与新生儿Ponderal指数 (PI)显著相关 (r=0 .66和 0 .69,P <0 .0 1)。结论　胎盘是脐血瘦素重要来源 ,胎盘瘦素可能对胎儿宫内生长发育有促进作用。     

游离脂肪酸对大鼠骨骼肌细胞瘦素受体基因、蛋白表达及酪氨酸磷酸化的影响

目的　探讨游离脂肪酸是否会对大鼠骨骼肌细胞L eptin受体的基因、蛋白表达及酪氨酸磷酸化产生一定的影响 ,进而导致胰岛素抵抗及葡萄糖代谢的异常 .方法　分离、培养新生 Sprague- Dawley大鼠骨骼肌细胞 ,分别与软脂酸(0 .2 5 m mol· L- 1 )或油酸 (0 .12 5 mmol· L- 1 )孵育 12 ,2 4和36 h,提取蛋白后用 Western印迹法检测 L eptin受体的蛋白水平 .用 RT- PCR检测胰岛细胞内 L eptin受体 RNA含量的变化 .应用免疫沉淀法检测 L eptin受体的酪氨酸磷酸化程度 .结果　软脂酸和油酸孵育后大鼠骨骼肌细胞 L eptin受体的蛋白表达水平在孵育 12和 2 4h后同对照组相比无显著变化 ,在孵育 36 h后同对照组相比显著下调 [软脂酸 (0 .36±0 .0 3)和油酸 (0 .35± 0 .0 4) vs对照 (0 . 39± 0 .0 5 ) ,P<0 .0 5 ];L eptin受体的 RNA水平在孵育 12 h后同对照组相比无显著变化 ,孵育 2 4和 36 h 后显著下调 [2 4h:软脂酸(0 .2 6± 0 .0 3)和油酸 (0 .2 6± 0 .0 4) vs对照 (0 .31± 0 .0 3) ,P<0 .0 5 ;36 h:软脂酸 (0 .2 5± 0 .0 4)和油酸 (0 .2 3± 0 .0 3) vs对照 (0 .2 9± 0 .0 1) ,P<0 .0 5 ];L eptin受体的酪氨酸磷酸化程度在在孵育 12 h后同对照组相比无显著变化 ,孵育 2 4和36 h后显著下调 [2 4h:软脂酸     

人瘦素基因克隆与序列测定

【目的】构建人瘦素基因cDNA克隆 ,并进行序列分析。【方法】用逆转录聚合酶链反应扩增人瘦素基因cDNA ,获得片段 (6 40bp)连接至 pUC19载体 ,并转化大肠杆菌DH5α。以末端终止法进行序列测定。【结果】所克隆的人瘦素cDNA含全长的人瘦素基因编码区 ,仅 2 87位的腺苷酸被鸟苷酸代替 ,导致 96位编码谷氨酰胺的密码子CAA改变为编码精氨酸的CGA ,其意义尚待阐明。【结论】以逆转录聚合酶链反应方法成功地构建了人瘦素基因cDNA克隆。     

妊娠期雌二醇和催乳素与瘦素的关系

目的 研究妊娠期间性激素与瘦素水平之间的关系。方法 在180例不同孕周的妇女中,按孕周分为＜20周组,20－23周组,≥28周组,采用酶联免疫吸附法测定其外周血血清雌二醇（E2）和催乳素（PRL）,放射免疫法测定血清瘦素水平,分析这些激素之间的相互关系。结果 E2和PRL均随妊娠进展而逐步升高（P＜0．0001）,组间均有显著差异（P＜0．05）。各组瘦素水平均高于非妊娠组,但组间差异无显著性。瘦素水平与孕妇体重及体重指数显著相关（P0．01）,与PRL也呈相关（P＜0．05）,而与E2无明显相关。结论 PRL水平与妊娠期瘦素水平升高有一定关系。     

上海地区汉人瘦素受体基因G1n223Arg变异的研究

目的探讨瘦素受体基因Gln223Arg变异与肥胖的关系。方法359例无亲缘关系的上海地区汉人及66例白种人运用PCR-RFLP方法（MspI限制性内切酶）检测瘦素受体基因Gin223Arg变异的基因型。结果中国人中GG、GA及AA基因型频率分别为0.789,0.200及0.011;G及A等位基因频率分别为0.889及0.111,与本研究组中白种人的基因型及等位基因频率分布有显著差异（P=2.98×10-16,3.46×10-18）。在中国人正常体重组与超重组间该基因变异的基因型及等位基因频率分布无显著差异（P=0.369,0.344）。结论瘦素受体基因Gln223Arg变异,在中国人肥胖的发病中可能无重要作用。     

Interactions between the stimulated hypothalamic-pituitary-adrenal axis and leptin in humans

Leptin, produced by adipocytes, has homeostatic effects on body fat mass through inhibition of appetite and stimulation of the sympathetic nervous system. Several studies have reported that high-dose exogenous glucocorticoids increase circulating leptin concentrations in humans. Conversely, leptin has inhibitory effects on the hypothalamic-pituitary-adrenal (HPA) axis, both at the hypothalamic and adrenal levels. We hypothesized that acute hypercortisolism, in the physiological range, may not alter leptin secretion. Four stimuli of the HPA axis were administered to eight healthy male volunteers in a placebo-controlled study. On separate afternoons, in a randomised order, fasting subjects received i.v. injections of saline, naloxone (125 microg/kg); vasopressin (0.0143 IU/kg); naloxone and vasopressin in combination; or insulin (0.15 U/kg; a dose sufficient to induce hypoglycaemia). Plasma concentrations of adrenocorticotrophic hormone (ACTH), cortisol and leptin were measured before and for 120 min after the injection. The cortisol secretory response was greatest after insulin-hypoglycaemia, this response was significantly greater than that following naloxone, naloxone/vasopressin, or vasopressin alone. Despite the cortisol release, leptin concentrations were not increased after any stimulus. Insulin-hypoglycaemia was associated with a decrease in leptin concentration at 60 and 90 min, while naloxone did not alter leptin concentrations. However, basal leptin concentrations were positively correlated with integrated ACTH and cortisol responses to naloxone, but did not correlate with ACTH or cortisol responses to the other stimuli. Thus acute elevations of plasma cortisol, in the physiological range, do not appear to influence plasma leptin concentrations. The fall in plasma leptin concentration after insulin-induced hypoglycaemia may reflect catecholamine secretion after this stimulus.     

肥胖基因蛋白的研究进展

肥胖基因蛋白 (Leptin简称Lep)是由肥胖基因 (OB基因 )编码并由脂肪细胞分泌的一种蛋白质 ,它是脂肪细胞传递大脑有关脂肪组织储存能量情况的信号 ,能减少能量摄取 ,增加能量消耗 ,抑制脂肪合成 ,从而达到减肥目的。另外 ,该药耐受性好 ,无系统或局部反应 ,无明显不良反应     

氯氮平与利培酮对精神分裂症患者血清催乳素的影响

目的 :探讨氯氮平与利培酮对血清催乳素的影响及催乳素与药物疗效、体重、胰岛素抵抗之间的相互关系。方法 :64例停药 1月以上的精神分裂症患者分别服用氯氮平 (n =3 3 )与利培酮 (n =3 1) ,治疗前及治疗后 8周分别测定其空腹血清催乳素、瘦素、胰岛素、血糖水平 ,测身高与体重 ,以体重BMI(BMI =体重 身高2 (kg m2 ) )评定体脂情况 ,以胰岛素抵抗指数 (HOMA -InsulinResistance,HOMA -IR =空腹胰岛素×空腹血糖 )评定胰岛素抵抗 ,以BPRS减分率评定药物疗效。结果 :治疗 8周后利培酮组血清催乳素明显增加 (治疗前vs治疗后 :(651 2 8± 42 9 0 4)mIU Lvs(163 7 60± 10 60 3 5)mIU L ,P =0 0 0 0 ) ,而氯氮平组催乳素浓度无明显改变 (治疗前vs治疗后 :(43 0 57± 43 1 52 )mIU Lvs (3 72 11± 194 57)mIU L ,P =0 687)。多因素逐步回归显示催乳素与性别及不同药物有关。结论 :利培酮能增加血清催乳素水平 ,氯氮平对催乳素基本无影响 ,催乳素与药物疗效、体重、瘦素及胰岛素抵抗等无直接联系