重组GnRH主动免疫公猪的效果及对垂体GnRH受体、FSHβ和LHβ基因表达的影响

目的:探讨重组GnRH六聚体-麦芽糖结合蛋白(MBP-GnRH-6)主动免疫的去势效果和对垂体GnRH受体、FSHβ和LHβ mRNA的影响.方法:7头公猪在9周龄时用重组GnRH主动免疫,放免法测血清睾酮浓度,ELISA法测抗体效价,实时荧光定量PCR分析垂体中GnRH受体、FSHβ和LHβ mRNA的变化.结果:重组MBP-GnRH-6主动免疫公猪后,血清GnRH抗体效价显著上升,且降低了外周血清睾酮浓度(P＜0.05),睾丸重量也明显下降((P＜0.01),组织切片显示,曲细精管仅有少数退化的精原细胞.免疫组公猪垂体中FSHβ mRNA和LHβ mRNA显著下降(P＜0.05),GnRH受体mRNA与阉割公猪相比差异显著(P＜0.05),但是与未阉割公猪相比差异不显著(P＞0.05).结论:公猪接种重组MBP-GnRH-6能诱发免疫反应,中和内源GnRH的生物活性,降低了垂体GnRH受体、FSHβ和LHβ基因表达,且抑制睾酮的合成,从而导致性器官发育受阻.     

重组人生长激素对烧伤病人代谢的影响及临床应用

生长激素（growth hormone，GH）是由垂体前叶嗜酸粒细胞分泌的含191个氨基酸非糖基化蛋白，它的主要生理功能是促进生长，促进蛋白合成，减少蛋白质的消耗，同时使脂肪组织氧化率提高，替代蛋白质氧化。临床用于治疗生长激素缺乏性侏儒症，近年来生长激素应用范围逐渐增加，逐渐应用于Turner综合征，慢性肾功能衰竭、大手术后、不育症，烧伤治疗等。重组人生长激素（rhGH）应用于烧伤病人之后，可以加快创面愈合的速度，有助于逆转烧伤后超高代谢，改善氮平衡。国内外的很多学者都对重组人生长激素应用于烧伤病人治疗的作用机制、给药时机、剂量和不良反应等作了广泛的研究，现综述如下。[第一段]     

雌二醇对大鼠凳下腺GnRH,GH生成的影响

目的 研究雌二醇（estradiol17β,E2)对颌下腺促性腺激素释放激素（gonadotropin relesaing hormoe GnRH)和生长激素（growth factor,GH)生成的影响。方法 采用免疫组织化学的ABC法。结果 雌二醇促进颌下腺GnRH的生成而对GH的产生有抑制作用。结论 雌二醇可能对颌下腺GnRH和GH的合成起重要的调节作用。     

生长激素释放激素和胰高血糖素对成人及生长激素缺乏患者生长激素分泌的影响

本文报告正常成人和成年生长激素缺乏(GHD)患者血清生长激素(GH)对GH释放激素(GHRH)和胰高血糖素(G1u)的反应。肌注G1u后血糖失升高后降低,血糖下降是兴奋GH分泌的因素。联合注射G1u/GHRH后的血清GH峰值部GH反应曲线下面积等于单独注射G1u和GHRH的和。二例对GHRH有GH分泌反应的GHD患者,对单独注射G1u无GH分泌反应。他们的GH分泌对联合注射G1u/GHRH与单独注射GHRH的反应相同。作者认为注射G1u引起的血糖下降可能是通过抑制下丘脑释放生长抑素从而引起GH的分泌。     

聚乙二醇化重组人生长激素对离体豚鼠乳头肌细胞动作电位的影响

目的 探讨聚乙二醇化重组人生长激素(PEG-rhGH)对离体豚鼠乳头肌细胞动作电位的影响,并以重组人生长激素(rhGH)为阳性对照物比较二者的体外生物活性.方法 健康雄性DHP豚鼠12只,随机分为2组,PEG-rhGH干预组和rhGH干预组,每组6只.采用累计给药法和给药前后自身对照方法,分别观察不同质量浓度(1、5、...     

两种不同剂型基因重组人生长激素治疗生长激素缺乏性矮小的临床研究

目的观察基因重组人生长激素（rhGH）水剂与粉剂治疗生长激素缺乏性矮小的效果。方法将36例生长激素缺乏性矮小儿童随机分为A、B两组,分别采用rhGH水剂与粉剂治疗6个月,比较其治疗前后的年生长速率和青春期发育情况,及不良反应的发生率。结果经rhGH治疗,A、B两组生长激素缺乏性矮小儿童的年生长速率均明显的提高,身高年龄的增长明显快于生活年龄和骨龄的增长,A、B两组组间比较无统计学差异（P〉0.05）,没有明显青春期加速的现象。A、B两组胰岛素样生长因子-1（IGF-1）及其结合蛋白-3（IGFBP-3）含量,与治疗前相比差异有显著性（P〈0.01）;但两组组间比较无统计学差异（P〉0.05）。结论两种剂型rhGH均可显著改善生长激素缺乏性矮小儿童的身高,且青春期、骨龄均不提前。但粉剂治疗费用低于水剂,更易临床推广。     

重组人生长激素对内毒素血症大鼠的治疗作用

目的 :观察重组人生长激素 (rhGH)对大鼠内毒素血症的治疗效果。方法 :76只SD大鼠随机分为正常对照组、内毒素血症组 (仅腹腔注射鸵鸟株大肠杆菌 (1 5ml/kg ,1× 1 0 10 cfu/L)及治疗组 (腹腔注射鸵鸟株大肠杆菌后行rhGH肌肉注射 (2 2 5IU/kg/d)。内毒素血症组及治疗组又依观察时点再分为 1天、3天两个亚组。采用放射免疫分析方法测定血浆肿瘤坏死因子 α(TNF α)浓度并观测大鼠血压的变化。结果 :与正常对照组相比 ,无论是内毒素血症组还是治疗组 ,1天时其大鼠血浆TNF α浓度均明显升高 (P <0 .0 5 ) ;虽然两组大鼠血压都降低 (P <0 .0 5 ) ,但治疗组大鼠血压降低幅度明显小于内毒素血症组 (P <0 .0 0 1 )。 3天时 ,内毒素血症组大鼠血浆TNF α浓度降至正常对照水平 ,而治疗组大鼠血浆TNF α浓度却明显低于正常对照组 (P <0 .0 0 1 )及内毒素血症组 3天水平 (P <0 .0 5 )。结论 :rhGH能明显减轻内毒素血症大鼠血压的下降 ,对内毒素血症大鼠具有较理想的治疗效果 ;rhGH减轻血压下降的机制可能与其能抑制TNF的释放等有关     

GnRH激动剂主动免疫对GnRHR在腺垂体与子宫表达及分布的作用研究

目的探讨GnRH激动剂主动免疫对绵羊腺垂体与子宫GnRHR表达及分布的影响,为深入研究GnRH-A调节生殖功能的机理及合理应用提供依据。方法 28只5～6月龄健康母绵羊(Ovis aries)随机分为4组(n=7),实验Ⅰ组(EG-Ⅰ)、实验Ⅱ组(EG-Ⅱ)和实验Ⅲ组(EG-Ⅲ)于0 d和14 d分别皮下注射阿拉瑞林抗原200μg、300μg和400μg(0 d和14 d各1次);对照组(CG)皮下注射2.0 ml药物的溶媒(0 d和14 d各1次)。各组于70 d无菌切取腺垂体和子宫。提取腺垂体总RNA,实时荧光定量PCR(FQ-PCR)检测GnRHR mRNA表达的变化,Western blotting分析子宫GnRHR蛋白表达,免疫组织化学SP法染色检测GnRHR表达的变化。结果 EG-Ⅰ、EG-Ⅱ和EG-Ⅲ腺垂体GnRHR mRNA表达量均低于对照组,以EG-Ⅲ最小(P<0.01)。与CG相比,EG-Ⅰ、EG-Ⅱ和EG-Ⅲ子宫GnRHR蛋白表达水平分别减少3.46%、4.90%和24.78%(P<0.05)。子宫组织中有GnRHR分布主要见于子宫内膜细胞和子宫腺上皮细胞的胞质和胞核,EG-Ⅲ灰度值显著低于CG(P<0.05)。结论 GnRH激动剂主动免疫可以剂量依赖性地抑制垂体GnRHR mRNA和子宫组织中GnRHR蛋白的表达。GnRHR主要分布在子宫内膜上皮细胞和腺上皮细胞的胞核和胞质,GnRHR激动剂免疫对子宫中GnRHR的分布具有抑制作用。     

大鼠胃壁细胞GnRH受体的定位及GnRH类似物对壁细胞内钙的影响

目的　观察促性腺激素释放激素 (gonadotropin releasinghormone,GnRH)受体在培养的大鼠胃粘膜壁细胞中的定位 ,并探讨GnRH类似物阿拉瑞林 (alarelin)对壁细胞内游离钙动员的机制。　方法　采用免疫组织化学和原位杂交技术 ;应用Ca2 + 指示剂Fluo 3 AM作为细胞内钙离子的荧光探针 ,对负载培养的胃壁细胞 ,应用激光共聚焦显微镜技术检测单个细胞内钙荧光强度的变化。　结果　大鼠胃壁细胞呈GnRH受体免疫反应阳性 ,阳性物质位于细胞质 ,细胞核为阴性 ;同样壁细胞内可检测到GnRH受体mRNA杂交信号 ,阳性物质位于细胞质 ,细胞核为阴性 ;胞内Ca2 + 浓度变化为 :1 在Hank液中 ,GnRH类似物浓度为 10 - 8、10 - 7、10 - 6 mol L时 ,胃壁细胞内Ca2 + 浓度逐渐升高 ,其峰高 (峰值减去静息值 )分别为 7 1± 1 4、12 1± 1 7、16 8± 2 2。其达峰时间也逐渐增快 ,分别为 34 2± 6 4s、18 9± 1 2s、10 4± 2 3s。相邻两组间其峰高及达峰时间均存在显著性差异 (P <0 0 5 ) ,且呈明显剂量依赖性。 2 在D Hank液 (去除外钙 )中 ,阿拉瑞林可轻度短暂升高胞内Ca2 + ;用内罗啶孵育后再加入阿拉瑞林也可轻度短暂升高胞内Ca2 + ,二者无显著性差异。 3 当用拉西地平孵育后再加入阿拉瑞林 ,可明显抑制胞内Ca2 + 的增加     

重组人生长激素对烟雾吸入性损伤大鼠肺泡Ⅱ型细胞的增殖及Bcl-2和Bax蛋白表达的影响

目的 研究重组人生长激素(recombinant human growth hormone,rhGH)对烟雾吸人性损伤大鼠肺泡Ⅱ型细胞(ATⅡ)增殖及Bcl-2和Bax蛋白表达的影响.方法　清洁级雄性SD大鼠70只,体重160～180 g,采用随机数字表法随机分为3组:正常对照组(C组)、单纯吸人性损伤组(Ⅰ组)和吸人性损伤+rhGH治疗(R组),后2组各再分为6、10、14日亚组.烟雾造成吸人性肺损伤模型,rhGH经腹部皮下注入(1.33 U/kg),连续应用7 d.各时相点剖胸取肺,行常规病理切片进行病理形态学观察并用免疫组化方法观察肺泡Ⅱ型细胞(ATⅡ)增殖以及Bcl-2和Bax蛋白表达的变化.结果 rhGH能显著增加新增殖ATⅡ数量;正常大鼠肺组织Bcl-2和Bax mRNA无表达,皮下注射rhGH后6、10、14日R组Bcl-2蛋白表达阳性细胞分别为(31.01±2.70)、(52.34±3.44)、(50.15±4.00)个/HP,明显高于I组的(24.76±2.82)、(37.92±4.28)、(35.58±3.64)个/HP(P<0.05);R组Bax蛋白表达阳性细胞为(21.16±2.79)、(31.22±5.62)、(26.27±5.41)个/HP,明显低于Ⅰ组[(26.51±2.61)、(41.50±4.14)、(34.55±2.94)个/HP,P<0.05].结论 经皮下注入外源性rhGH能有效刺激ATⅡ的增殖,上调Bcl-2蛋白表达及下调Bax蛋白表达,改变Bcl-2/Bax的比值从而抑制细胞凋亡.     

GnRH激动剂主动免疫母羊对生殖激素分泌的作用

目的:探讨GnRH激动剂(GnRHa)主动免疫对绵羊生殖激素合成与分泌的作用,并深入研究GnRH-A免疫调节动物生殖功能的机理。方法:42只5～6月龄母绵羊(Ovis aries)随机分为6组(n=7),EG-Ⅰ、EG-Ⅱ和EG-Ⅲ分别于0和14天皮下注射阿拉瑞林抗原200、300和400μg;EG-Ⅳ和EG-Ⅴ分别皮下注射阿拉瑞林抗原200、300、0、7、14和21天各一次,共4次;对照组在0和14天皮下注射抗原溶媒(除不用阿拉瑞林外,其余成分和制备方法与阿拉瑞林抗原相同)2.0 ml。无菌采集不同时段的血液,分离血清。以ELISA测定血清GnRH抗体浓度,用激素检测试剂盒(ELISA)分别测定血清GnRH、FSH、LH和E2浓度。结果:①阿拉瑞林首次免疫7天后,各实验组的抗体浓度逐渐升高,EG-Ⅰ、EG-Ⅱ和EG-Ⅲ分别在28、28和35天达到峰值(P<0.05),EG-IV和EG-V则在在45天达到峰值(P<0.01),至60天时仍明显高于对照组(P<0.05)。14～60天间EG-IV和EG-V抗体浓度均高于EG-Ⅰ、EG-Ⅱ和EG-Ⅲ(P<0.05)。②EG-Ⅰ、EG-Ⅱ的GnRH在21和28天抵谷值(P<0.05),EG-Ⅲ、EG-Ⅳ和EG-Ⅴ则在45天抵谷值(P<0.01),且以EG-Ⅴ为最低。谷值之后逐渐上升趋势,70天时达到免疫注射前水平。③实验组血清FSH浓度始终高于对照组(P<0.05)。EG-Ⅰ、EG-Ⅱ和EG-Ⅲ于28、28和35天达到峰值(P<0.05),而EG-IV和EG-V在60天达到高峰值(P<0.01)。④实验组绵羊血清LH呈下降趋势,EG-Ⅰ、EG-Ⅱ和EG-Ⅲ分别在21、21和28天达到谷值(P<0.01),EG-Ⅳ和EG-Ⅴ在35天达到谷值(P<0.01)。35天时EG-Ⅳ和EG-Ⅴ低于EG-Ⅰ、EG-Ⅱ和EG-Ⅲ。⑤各组的血清E2含量无显著差异。结论:GnRH激动剂(阿拉瑞林)抗原主动免疫可促进GnRH抗体的生成,抑制母羊GnRH和LH的合成与分泌,增强FSH的合成与分泌,且随着注射剂量和注射次数的增加,这种作用更加明显,而对血清E2无明显影响。     

Prenatal expression of growth hormone receptor/binding protein and insulin-like growth factor-I (IGF-I) in the enamel organ

Immunohistochemistry was used to study the ontogeny of GH receptor/binding protein (GHR/BP) and IGF-I from the 13-day-old embryo (E13) to the E19 rat fetus in the developing incisor and molar. Analysis of serial sections revealed diffuse staining of GHR/BP and IGF-I at the bud and early cap stages within both the mesenchyme of the dental papilla and the ectodermal-erived enamel organ. Just before transition to the cap stage, immunoreactivity of GHR/BP and IGF-I increased in the epithelial bud and extended to the condensed dental mesenchyme. At the cap stage, the dental epithelium showed an intense expression of GHR/BP and IGF-I, whereas the dental mesenchymal cells showed very weak staining. The inner enamel epithelium and the outer enamel epithelium were positive for both GHR/BP and IGF-I in the bell stage. Differentiating ameloblasts, odontoblasts and the secretory ameloblasts and odontoblasts continued to express GHR/BP and IGF-I in incisors. These findings support the premise that growth hormone and IGF-I may play a role in embryonic tooth development by regulating the epithelial-mesenchymal interactions that influence events in growth and cytodifferentiation.     

Effects of growth hormone releasing hormone on rat ovarian steroidogenesis

During the last decade, it has been shown that each part ofthe somatotrophic axis can influence granulosa cell function.Growth hormone releasing hormone (GHRH) may be effective throughthe release of hypophyseal growth hormone (GH) and the subsequentincrease of insulin-like growth factors (IGF). There is alsosome evidence that GHRH could act directly on ovarian function.The aim of this study was to determine the mechanism throughwhich GHRH affects granulosa cell steroidogenesis in the ovary.Granulosa cells were obtained from immature, oestrogen-treatedrats supplemented with or without follicle stimulating hormone(FSH) in vivo and were cultured for 48 h to evaluate steroidproduction. GHRH was administered either in vivo at the sametime as FSH, or in vitro in the presence or absence of testosteroneand FSH. Our results show that co-treatment with GHRH and FSHin vivo induced significant increases in plasma IGF-I concentrationsand steroid production by cultured granulosa cells. The additionof GHRH to culture medium did not significantly alter steroidproduction by either non-differentiated (no FSH in vivo) ordifferentiated (FSH in vivo) granulosa cells. In contrast, treatmentin vitro with IGF-I significantly increased steroidogenesisha both cases. Our results suggest that any physiologicallysignificant effect of GHRH on ovarian function is probably tobe exerted via activation of the somatotrophic axis and thesubsequent amplification of ovarian FSH responsiveness by IGF-I.     

Serum and tissue level of insulin-like growth factor-I (IGF-I) and IGF-I binding proteins as an index of pancreatitis and pancreatic cancer

Previously we have found deregulation of collagen metabolism in human pancreatitis and pancreatic cancer tissues. Insulin-like growth factor-I (IGF-I) is known to stimulate collagen biosynthesis through interaction with IGF-I receptor. IGF-I binding proteins (BPs) regulate the activity of IGF-I. We investigated whether serum and tissue IGF-I and IGF-BPs as well as tissue IGF-I receptor expression may reflect disturbances of collagen metabolism in patients with pancreatitis and pancreatic cancer. In pancreatitis tissue, a significant increase in IGF-I and IGFBP-3 content was accompanied by a distinct increase in IGF-I receptor expression, compared to control pancreas tissue. In contrast, serum from patients with pancreatitis did not show significant increases in IGF-I and IGFBP-3 levels, however, significant increases in IGFBP-1 level (2.5 fold). Moreover, a distinct decrease in radioactive IGF-binding to the BPs, compared to control serum, was found. Pancreatic cancer tissue and serum of patients with pancreatic cancer showed significant increases in IGF-I, IGFBP-3 and IGFBP-1 content, accompanied by dramatic increases in IGF-I tissue receptor expression, compared to controls. In serum of patients with pancreatic cancer distinct increases in radioactive IGF-binding to 46 kDa BP, compared to control serum, were observed. The data suggest that disturbances in tissue collagen metabolism during pancreatic diseases may result from deregulation of IGF-I homeostasis and that elevated serum levels of IGF-I, IGFBP-3 and IGFBP-1 may serve as markers of pancreatic cancer.     

Neuroprotective effects of IGF-I against TNFalpha-induced neuronal damage in HIV-associated dementia

Human immunodeficiency virus type 1 (HIV-1) infection often results in disorders of the central nervous system, including HIV-associated dementia (HAD). It is suspected that tumor necrosis factor-alpha (TNFalpha) released by activated and/or infected macrophages/microglia plays a role in the process of neuronal damage seen in AIDS patients. In light of earlier studies showing that the activation of the insulin-like growth factor I receptor (IGF-IR) exerts a strong neuroprotective effect, we investigated the ability of IGF-I to protect neuronal cells from HIV-infected macrophages. Our results demonstrate that the conditioned medium from HIV-1-infected macrophages, HIV/CM, causes loss of neuronal processes in differentiated PC12 and P19 neurons and that these neurodegenerative effects are associated with the presence of TNFalpha. Furthermore, we demonstrate that IGF-I rescues differentiated neurons from both HIV/CM and TNFalpha-induced damage and that IGF-I-mediated neuroprotection is strongly enhanced by overexpression of the wt IGF-IR cDNA and attenuated by the antisense IGF-IR cDNA. Finally, IGF-I-mediated antiapoptotic pathways are continuously functional in differentiated neurons exposed to HIV/CM and are likely supported by TNFalpha-mediated phosphorylation of I(kappa)B. All together these results suggest that the balance between TNFalpha and IGF-IR signaling pathways may control the extent of neuronal injury in this HIV-related experimental setting.     

Effects of growth hormone on muscle regeneration and IGF-I concentration in old rats

A study was made of regeneration of skeletal muscle in young adult and old rats and of the effects of administration of growth hormone to old rats. Regeneration was achieved by subjecting the right extensor digitorum longus muscle to ischaemic necrosis. The level of insulin-like growth factor I in serum was markedly decreased in old rats of 27 months of age compared with young adult rats aged 6 months. Daily injections of 4 IE recombinant human growth hormone during the 10 weeks of regeneration increased the level of insulin like growth factor I to almost the same levels as in rats aged 6 months. The body weight increased by 13% in the old rats treated with recombinant human growth hormone, while the weight of the untreated old rats was constant. The regenerating right and the normal left extensor digitorum longus muscles were studied 10 weeks after the ischaemic necrosis. The absolute and relative weights of regenerating muscle were decreased in 27-month-old rats compared with the rats aged 6 months. No significant difference between normal old rats and old rats treated with recombinant human growth hormone was observed either in muscle weight or in maximum contraction force. The results show that old rats have reduced levels of circulating insulin-like growth factor I. Administration of recombinant human growth hormone raises the level of insulin-like growth factor I to that of young adult rats, and causes an increased body weight. Muscle regeneration after ischaemic necrosis is impaired in old rats apparently by the formation of large amounts of connective tissue. Supplementation with growth hormone does not reverse this impairment.     

兔抗人重组生长激素rhGH多克隆抗体的制备、纯化及鉴定

目的制备抗人生长激素(growth hormone,GH)的多克隆抗体并鉴定其性能。方法真核细胞表达质粒pcDNA3.0-GHcDNA免疫家兔,制备rhGH多克隆抗体;ELISA法检测抗体效价。亲和层析法纯化后,进行Western blot、免疫组织化学和激光共聚焦显微镜检测,鉴定抗体的特异性与适用范围。结果得到兔抗人重组人生长激素rhGH多克隆抗体,效价达1:40000。纯化后的抗体可特异识别超表达的hGH和人内源性GH,可用于免疫组织化学实验、Western blot及激光共聚焦。结论用质粒免疫家兔制备的抗GH抗体具有较高的效价以及特异性,为hGH的功能性研究提供了有力的支持。     

Changes in growth hormone status related to body weight of growing cattle

The growth hormone (GH) status of 24 castrated male cattle was studied over a range of body weights by measuring GH in the blood plasma and anterior pituitary and by calculating metabolic clearance (MCR) and secretion rates after injection of GH. As the cattle increased in size, pituitary weight and GH content, MCR of GH and secretion of GH decreased relative to body weight. Plasma concentrations of GH did not decrease as markedly as secretion because MCR/body weight was also lower in the larger animals. At all sizes, more than 99% of the total GH in the body was located in the anterior pituitary. It was calculated that the pituitary releases 0.58% of its GH content per hour. This rate of release did not significantly change with body weight. It is suggested that basal secretion of GH by the anterior pituitary is related to GH content and that, as animals grow, there is gradually less GH available per unit of body mass.     

Effects of recombinant chicken growth hormone in randombred meat-type chickens

Recombinant chicken growth hormone (rcGH) was administered subcutaneously twice daily to male and female Athens-Canadian randombred meat-type chickens between 2 and 14 days posthatch. Treatment groups consisted of non-injected controls, saline-injected controls, and those injected with either 50 or 250 micrograms/kg rcGH per injection. Body weight, body weight gain, feed consumption, and feed efficiency were determined. Body weight or body weight gain was not significantly affected by rcGH through 28 d. Feed consumption and efficiency were not significantly affected by treatment through 21 d. It was concluded that rcGH failed to demonstrate any significant growth-promoting effects in young, slow-growing randombred chickens.     

The effects of treatment with recombinant human growth hormone on body composition and metabolism in adults with growth hormone deficiency

In a double-blind, placebo-controlled trial, we studied the effects of six months of growth hormone replacement in 24 adults with growth hormone deficiency. Most of the patients had acquired growth hormone deficiency during adulthood as a consequence of treatment for pituitary tumors, and all were receiving appropriate thyroid, adrenal, and gonadal hormone replacement. The daily dose of recombinant human growth hormone (rhGH) was 0.07 U per kilogram of body weight, given subcutaneously at bedtime. The mean (+/- SE) plasma concentration of insulin-like growth factor I increased from 0.41 +/- 0.05 to 1.53 +/- 0.16 U per liter during rhGH treatment. Treatment with rhGH had no effect on body weight. The mean lean body mass, however, increased by 5.5 +/- 1.1 kg (P less than 0.0001), and the fat mass decreased by 5.7 +/- 0.9 kg (P less than 0.0001) in the group treated with growth hormone; neither changed significantly in the placebo group. The basal metabolic rate, measured at base line and after one and six months of rhGH administration, increased significantly; the respective values were 32.4 +/- 1.4, 37.2 +/- 2.2, and 34.4 +/- 1.6 kcal per kilogram of lean body mass per day (P less than 0.001 for both comparisons). Fasting plasma cholesterol levels were lower (P less than 0.05) in the rhGH-treated group than in the placebo group, whereas plasma triglyceride values were similar in the two groups throughout the study. We conclude that growth hormone has a role in the regulation of body composition in adults, probably through its anabolic and lipolytic actions.