Effects of oral administration of insulin-like growth factor-I on circulating concentration of insulin-like growth factor-I and growth of internal organs in weanling mice

Insulin-like growth factor (IGF)-I is a polypeptide that mediates the growth-promoting action of growth hormone in postnatal animals. The present study was conducted to examine whether orally administered IGF-I would be absorbed into the general circulation and also whether ingested IGF-I would enhance the growth of whole body as well as internal organs, and tissues in 3-week-old ICR-strain female weanling mice. In experiment (Exp) 1, a total of 70 mice received IGF-I orally at 1 microg.g-1 in 0.2-ml PBS or the vehicle alone. Concentrations of IGF-I and glucose in heart blood were measured after killing 5 animals in each group every fourth hour during a 24-hour period. In Exp 2, a total of 40 mice received oral IGF-I administration at 1 microg.g-1 or vehicle every third day beginning from day 0 for a 13-day period. Half the animals were killed at day 7 and the other half at day 13. Weights of whole body and organs/tissues (small intestine, liver, thigh muscle, and brain) were measured every day and at slaughter, respectively. In Exp 1, following the oral IGF-I administration, serum IGF-I concentration increased at hour 4 (p<0.01) and returned to the hour 0 level by hour 8, whereas glucose concentration was lowest at hour 4 and returned to the hour 0 level by hour 16. In the PBS-fed group, neither IGF-I nor glucose concentration changed during the 24-hour period. In Exp 2, weight of small intestine increased (p<0.05) in response to the oral IGF-I, whereas weights of liver and thigh muscle of the IGF-I-fed group were greater (p<0.01) and tended to be greater (p=0.06), respectively, than those of the PBS-fed only at day 13. However, brain weight and serum concentrations of IGF-I and IGF-II were not affected by oral IGF-I administration. Results suggest that although orally administered IGF-I mainly acts at the intestine, a portion of ingested IGF-I is absorbed into the general circulation to enhance the growth of selective organs/tissues in weanling mice.     

Activity of the growth hormone/insulin-like growth factor-I axis in critically ill children

Critical illness has an important impact on the human endocrine system. Very few studies have been performed to elucidate the alterations of the GH/IGF-I axis in acutely ill children. The aim of this study was to investigate several parameters of this axis in children with trauma (TRA) and sepsis (SEP) requiring admission to the pediatric intensive care unit (PICU). A total of 16 children, ten with TRA and six with SEP (age 1-10 years) as well as 18 healthy children (CS) of similar age and gender were included in the study. Two children, one with TRA and one with SEP, died. Serum IGF-I and -II, IGFBP-1 and -3, and GH levels were measured on days 1, 3 and 7 after admission. GH levels were higher in the patients than in CS (p = 0.04), with no difference between TRA and SEP, and were elevated during PICU stay (p = 0.05). Serum IGF-I, -II and IGFBP-3 were lower in the patients than in CS (p = 0.03, 0.02 and 0.001, respectively) with a tendency to increase up to day 7. Finally, IGFBP-1 levels were similar in the patients and CS. These findings indicate that critically ill children are characterized by low levels of IGF-I and -II as well as IGFBP-3 accompanied by elevated levels of GH, probably reflecting the development of peripheral GH resistance. No significant differences were found between the different catabolic conditions, sepsis and trauma.     

Serum zinc, insulin-like growth factor-I and insulin-like growth factor binding protein-3 levels in children with type 1 diabetes mellitus

BACKGROUND: Growth is impaired during the course of diabetes mellitus (DM). Derangement of the growth hormone/insulin-like growth factor (IGF) axis, insulinopenia and zinc deficiency are the possible causative factors of this impairment. Zn supplementation is proven to attenuate hyperglycemia in mice but its use to ameliorate impaired height is still a matter of discussion. OBJECTIVE: To investigate serum Zn, IGF-I and IGF binding protein-3 (IGFBP-3) levels and to emphasize the potential beneficial effects of Zn supplementation for the prevention of growth failure in children with type 1 DM (DM1). Patients and Methods: Twenty-eight patients with DM1 and 15 control children were included in the study. Zn levels were measured by flame atomic absorption spectrophotometry; IGF-I and IGFBP-3 levels were measured by immunoradiometric assay. RESULTS: Mean serum Zn levels were significantly lower in diabetic children taken as a whole and as their pubertal subgroup compared to the controls. Mean serum IGF-I and IGFBP-3 levels were significantly lower in both prepubertal and pubertal diabetic groups compared to those of control groups. CONCLUSION: From the results of our study, it can be hypothesized that serum Zn levels should be closely monitored during the course of DM1 and supplementation may be given to patients, especially at the time of puberty. This hypothesis needs to be confirmed by further studies.     

Relationship of insulin-like growth factor-I, insulin-like growth factor binding protein-3, insulin, growth hormone in cord blood and maternal factors with birth height and birthweight

BACKGROUND: To determine whether the following factors are related to birthweight or birth height, we measured insulin-like growth factor (IGF)-I, insulin-like growth factor binding protein (IGFBP)-3, insulin and growth hormone (GH) levels in cord blood and also observed the relationship between birthweight, birth height and maternal factors. METHODS: One hundred and ninety-four cord bloods were collected, 106 from males and 88 from females. Three newborns were small for gestational age (SGA), 168 were appropriate (AGA) and 23 were large (LGA); 21 newborns were preterm and 172 were term. RESULTS: Levels of IGF-I and IGFBP-3, measured by enzyme-linked immunosorbent assay, were significantly lower in preterm babies (35.3 +/- 15.1 and 1025.6 +/- 562.8 ng/mL, respectively) than in term babies (61.6 +/- 39.5 and 1252.6 +/- 403.2 ng/mL, respectively; P < 0.01), but neither insulin nor GH levels, measured by radioimmunoassay, showed any significant difference between the two groups (P > 0.05). Among term babies, IGF-I and IGFBP-3 levels were significantly higher in the LGA group (96.1 +/- 34.1 and 1544.7 +/- 418.1 ng/mL, respectively) than in the AGA group (56.4 +/- 37.6 and 1212.8 +/- 383.4 ng/mL, respectively; P < 0.01). Levels of IGF-I and IGFBP-3 showed significant correlation with birthweight and length, respectively (P < 0.01), although GH and insulin levels did not (P > 0.05). There was a significant correlation between IGF-I and IGFBP-3 levels (P < 0.01, r = 0.64), but IGF-I and IGFBP-3 levels showed no relationship with GH or insulin levels. Birthweight correlated significantly with prepartum maternal weight, maternal weight gain and maternal height (P < 0.05), but birth length correlated significantly only with maternal height (P < 0.05). CONCLUSIONS: Our results suggest that fetal growth depends on fetal levels of IGF-I and IGFBP-3 and maternal factors, not on insulin or GH. Levels of IGF-I and IGFBP-3 may not be regulated by insulin alone, but by the complex interactions between several factors, such as insulin, GH and maternal factors.     

Serum concentrations of insulin, insulin-like growth factor-I and insulin-like growth factor binding proteins are different between white and African American girls.

OBJECTIVES: To determine whether serum insulin-like growth factor (IGF)-I and IGF binding protein (IGFBP) concentrations are different between African American and white girls. STUDY DESIGN: Serum glucose and hormone concentrations were measured in blood samples collected after a 12-hour fast from 79 white and 57 African American healthy girls between 9 and 17 years of age. Tanner stages of pubic hair development were evaluated by physical examination, and body composition by dual energy x-ray absorptiometry. RESULTS: The African American girls were older and sexually more mature and had higher fat mass, higher serum insulin and free IGF-I concentrations, higher serum free IGF-I to total IGF-I ratio, but lower serum IGFBP-1 concentrations than the white girls. After controlling for sexual maturation and fat mass, the serum concentrations of total IGF-I, bound IGF-I, and IGFBP-3 in the white girls became significantly higher than those in the African American girls. The higher concentrations of total IGF-I in the white girls were due to a proportional increase in the concentrations of bound IGF-I that coincided with a similar increase in serum IGFBP-3 concentrations. CONCLUSIONS: Higher serum insulin concentrations in the African American girls are associated with lower serum IGFBP-1 concentrations and increased bioavailability of free IGF-I, which may contribute to their accelerated growth compared with their white counterparts.     

Effects of growth hormone (GH) and insulin-like growth factor-I therapy in patients with gene defects in the GH axis

We report on four patients (3 F) who were diagnosed as having either a 6.7 kb GH1 gene deletion, a GH1 signalling peptide mutation, or a GH receptor mutation, with particular regard to treatment modalities (GH, rhIGF-I) and final height. Patients with GH1 gene defects developed anti-GH antibodies (GH-Ab) following GH treatment. Surprisingly, growth response to GH was unrestricted in one girl, who reached a final height within her target height range, whereas her cousin with the identical genetic defect responded far less favourably. Variability in the growth inhibiting potency of GH-Ab may therefore depend on genetic disposition, specific epitopes, or induction of immunological tolerance. Growth response during rhIGF-I treatment carried out in three of the patients was moderate, but pubertal development and bone age acceleration occurred in the two patients treated at pubertal age. GH resistance, either caused by GH-Ab or GH receptor mutations, is still difficult to treat and results in a heterogeneous outcome.     

出生后长期缺锌对大鼠生长发育及生长激素的影响

目的 研究出生后长期缺锌对大鼠生长发育的影响及其机制。方法 选取刚出生的SD大鼠3窝,每窝1只母鼠、10只仔鼠,3窝母鼠与仔鼠体重相近,仔鼠雌雄各半。随机分为3组,缺锌组（ZD）、配饲组（PF）、对照组（ZA）。实验期60 d。测定大鼠身长、股骨长度、直径、重量,血清生长激素（GH）含量。结果 ZD组身长[（16.15&#177;0.67）cm]明显低于PF组[（20.94&#177;0.98）cm]及ZA组[（23.08&#177;0.11）cm]（P〈0.01）;ZD组股骨长度[（2.61&#177;0.22）cm]明显低于PF组[（3.38&#177;0.10）cm]及ZA组[（3.54&#177;0.08）cm]（P〈0.01）;ZD组股骨直径[（0.30&#177;0.03）cm]明显低于PF组[（0.37&#177;0.33）cm]及ZA组[（0.42&#177;0.01）cm]（P〈0.01）;ZD组股骨重量[（0.65&#177;0.10）g]明显低于PF组[（1.07&#177;0.07）g]及ZA组[（1.28&#177;0.08）g]（P〈0.01）;ZD组血清生长激素水平[（0.47&#177;0.04）ng/ml]明显低于PF组[（0.66&#177;0.11）ng/ml]及ZA组[（0.75&#177;0.07）ng/ml]（P〈0.01）。结论 出生后长期缺锌可导致动物体内生长激素水平下降,是导致生长迟缓的原因之一。     

The effects of metabolic acidosis on jejunal phosphate and glucose transport in weanling rats

To investigate the effects of metabolic acidosis on jejunal phosphate and glucose absorption, in vivo and in vitro transport studies were performed on weanling rats fed 1.5% NH4Cl for three days and on group pair-fed controls. Both in vivo and in vitro, acidosis significantly depressed phosphate transport without effecting glucose transport. In vitro, the decrease of phosphate transport was due to a depression of sodium-phosphate cotransport, but not of sodium independent phosphate transport. This corresponded to a significant increase of the Km of sodium-phosphate cotransport with no change of the Vmax. Treatment of the acidotic animals with intraperitoneal 1,25 dihydroxycholecalciferol did not restore phosphate transport to control levels. These studies indicate that in weanling rats, metabolic acidosis selectively suppresses jejunal phosphate transport independent of circulating levels of 1,25 dihydroxycholecalciferol.     

Serum insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 levels in severe iodine deficiency

Iodine deficiency is an important public health problem worldwide. It is well known that it has severe consequences such as brain damage, developmental delay, deficits in hearing and learning and lower intellectual attainment. It also has a negative impact on growth. In this study, we aimed to address this issue and we assessed height standard deviation scores of children living in an area of severe iodine deficiency in comparison to those living in a mild iodine deficiency area. Serum levels of insulin-like growth factor-I (IGF-I), IGF-binding protein-3 (IGFBP-3), thyroxine (T4), and thyroid stimulating hormone (TSH) were also analyzed to investigate the mechanisms by which iodine depletion leads to growth failure. Pubertal children in a severe iodine deficient SID area had lower height standard deviation scores (HSDS), IGF-I and IGFBP-3 levels than those living in mild iodine deficient MID area. Similar findings could not be elucidated in the prepubertal age group. The major determinants of HSDS were age, IGF-I, IGFBP-3 and TSH. IGF-I and IGFBP-3 were negatively correlated with T4. These findings suggest that iodine deficiency has a negative impact on growth, as well as IGF-I and IGFBP-3 levels. This effect seems to be due to the derangements in thyroid hormone economy arising from iodine depletion. The degree of this impact may be related to the duration of iodine depletion or may be dependent on the developmental stage of the organism at the time of iodine depletion.     

胰岛素样生长因子-I和血糖在脓毒症中的变化及意义

目的探讨脓毒症患儿血清胰岛素样生长因子-I(IGF-I)和血糖的变化及相关意义。方法选择2009年1月至2010年1月入住PICU的脓毒症患儿42例,检测入院次日清晨血糖和血清IGF-I、皮质醇、胰岛素、IL-6、IGF结合蛋白-I(IGFBP-I)及入院第3、5天晨血清IGF-I水平,根据入院次日血糖水平分为血糖升高组和血糖正常组;以同期健康体检儿童60例为对照组,分别比较三组间各指标的差异。结果入院次日,脓毒症血糖升高组、血糖正常组和对照组三组间血糖、IGF-I、皮质醇、胰岛素、IL-6水平的差异有统计学意义(P均0.001),而IGFBP-I水平差异无统计学意义(P0.05)。两两比较发现,与对照组相比,脓毒症血糖升高组和血糖正常组患儿的皮质醇、IL-6显著升高,IGF-I显著降低,差异有统计学意义(P均0.05);血糖升高组的血糖和胰岛素水平均高于血糖正常组和对照组,差异有统计学意义(P均0.05)。脓毒症血糖正常及血糖升高组患儿IGF-I水平随时间变化(入院次日,第3、5天)的差异无统计学意义(P均0.05);在入院次日,第3、第5天,两组脓毒症患儿之间IGF-I水平的差异也无统计学意义(P均0.05)。入院次日,脓毒症患儿血糖与IGF-I水平无明显相关性(r=0.152,P=0.267)。结论脓毒症患儿IGF-I降低,并在病程中保持稳定,血糖变化与IGF-I无显著联系。     

Effects of dietary zinc deficiency on hepatic ornithine carbamoyltransferase and alcohol dehydrogenase activities in rats

Hepatic ornithine carbamoyltransferase (OCT) and alcohol dehydrogenase (ADH) activities were measured in six groups of rats: (A) fed a severe zinc-(Zn-) deficient diet (1.98 ppm) for 5 weeks; (B) pair-fed control for group (A); (C) fed a less severe Zn-deficient diet (6.10 ppm) for 5 weeks; (D) pair-fed control for group (C); (E) fed a Zn-supplemented control diet (90.4 ppm) for 5 weeks; and (F) first fed the severe Zn-deficient diet for 5 weeks and then replaced on the Zn-supplemented control diet until a body weight corresponding to the final weight of group (E) was obtained. Hepatic OCT was similar in all these six groups. On the contrary, hepatic ADH was significantly reduced in groups (A) and (C) and in each of the corresponding pair-fed groups, (B) and (D). No differences were found between groups (A) and (B) or between groups (C) and (D). In group (F), ADH activity improved to a level equivalent to that in group (E). The changes in ADH activities were accompanied by changes in the hepatic Zn content. Thus, it is clear that: (1) the hepatic Zn content may not be affected by the amount of Zn intake alone, but by the combination of Zn and food intake; and (2) ADH, and not OCT, reflected the hepatic Zn content.     

Transport of electrolytes, water, and glucose in zinc deficiency

Zinc deficiency in humans and animals results in failure to thrive, skin lesions, loss of hair, and diarrhea. The mechanism underlying the diarrhea seen in zinc deficiency is not known. Therefore, the current study was designed to investigate net transport of water, electrolytes, and glucose from segments of small and large intestine in zinc-deficient, pair-fed control, and ad libitum-fed rats. An in vivo single-pass perfusion study was used. The results indicate that net water and sodium transport from the small and large intestine of zinc-deficient rats was significantly decreased compared to corresponding mean values for pair-fed controls and for ad libitum-fed rats. Net absorption of glucose and net secretion of potassium were not significantly different in the three groups. The results are in agreement with previous investigations showing decreased sodium transport in leukocytes and renal tubules of zinc-deficient animals and suggest that zinc may have a role in modulating membrane permeability.     

A case of macroprolactinoma and elevated insulin-like growth factor-I in a young boy

We report a case of a 10-y-old boy who presented with persistent headache and was found to have a giant prolactinoma. Laboratory evaluation revealed markedly elevated prolactin (PRL) level, thyroid-stimulating hormone (TSH) deficiency, and elevated insulin-like growth factor-I (IGF-I). He had normal random growth hormone (GH) but non-suppressible GH during oral glucose tolerance test (OGTT). Cabergoline treatment was initiated and was well tolerated. Therapy successfully reduced PRL levels, normalized IGF-I levels, and reduced tumor size. CONCLUSION: Our patient presented with a GH-PRL-secreting tumor. Dopamine agonists are recommended as the treatment of choice for prolactinomas. However, there should be careful attention to GH status when treating GH-PRL-secreting tumor with dopamine agonists alone. IGF-I levels should be followed in all patients with prolactinoma, even in those with normal basal GH concentrations, because of the possibility of GH co-secretion.     

Effects of insulin-like growth factor-I deficiency and replacement therapy on the hematopoietic system in patients with Laron syndrome (primary growth hormone insensitivity)

BACKGROUND: Primary insulin-like growth factor-I (IGF-I) deficiencies, such as in Laron syndrome (LS), are a unique model in man to study the consequences resulting from defects in growth hormone (GH) signal transmission. OBJECTIVE: To assess retrospectively the effect of IGF-I deficiency and its therapy on the various cells of the hematopoietic system as reflected by peripheral blood counts. PATIENTS AND METHODS: Two groups of patients were studied. The first group consisted of 11 untreated patients with LS, seven males and four females, who were followed from childhood into adult age. Average age at the time of data analysis was 45.4 +/- 9.6 years. The second group included ten children with LS, six males and four females, who received IGF-I replacement therapy for an average period of 6 years, ranging in age from 0.9-11 years. The mean age at initiation of therapy was 6.9 +/- 4.28 years. Only the seven children treated for 5 years or more were included in the analysis. Data on blood counts were collected from the patients' charts. Blood samples were drawn at baseline, weekly during the first month, once a month during the first year, and once every 3 months thereafter. Statistical analysis of the change over time was performed using repeated measures ANOVA. RESULTS: Children with LS had red cell indices in the lower normal range and an elevated monocyte count. A statistically significant rise in red blood cell (RBC) indices was seen in children during IGF-I therapy: RBC rose from 4.66 x 10(6)/ml to 4.93 x 10(6)/ml (p = 0.011); hemoglobin from 11.55 g/dl to 13.01 g/dl (p < 0.001); hematocrit from 34.94% to 38.52% (p = 0.007), and mean corpuscular volume from 72.27 fl to 79.93 fl (p < 0.001). The platelet count diminished significantly during IGF-I therapy from 316 x 10(3)/ml to 219 x 10(3)/ml (p = 0.02), and the monocyte count from 0.74 x 10(3)/ml to 0.49 x 10(3)/ml (p < 0.001). CONCLUSIONS: The present investigation, the first of its kind in this syndrome, confirms that IGF-I has a strong stimulatory effect on erythropoiesis. In addition, IGF-I therapy had a reducing effect on monocytes and platelets, an effect not previously described. The mechanism by which IGF-I mediates these effects needs further elucidation.     

Changes in growth, growth hormone, and insulin-like growth factor-I (IGF-I) after orthotopic liver transplantation

Growth failure is an important consequence of chronic liver disease in childhood. Insulin-like growth factor-I (IGF-I), which is synthesized and released by the liver, plays an important role as a growth regulator in humans. We examined the growth hormone (GH)/IGF-I axis before and after orthotopic liver transplantation (LT) in 14 children aged between 2 and 11 years (mean 5.6 ± 1.1 years). Pre-transplantation serum GH levels (7.5 ± 1.2 ng/ml) were significantly higher (P < 0.001) compared with controls (5 ± 0.5 ng/ml). However, post-transplantation levels (1.8 ± 0.8 ng/ml) did not differ from those in the control group. Serum IGF-I levels showed a statistically significant increase after LT (20.1 ± 9.4 vs 190 ± 66.2 ng/ml; P < 0.001) and became indistinguishable from the levels in the control group (180 ± 96 ng/ml). In comparison with pre-transplantation data (z− 2.70), there was an increase in height 4 years postoperatively (z− 1.68). Catch-up growth was highly significant, in particular during the 1st year after LT (z−1.58 ± 1.63 vs 2.59 ± 5.29; P < 0.01). We conclude that a GH resistance state found in patients with severe chronic liver disease reverted following LT. Given that IGF-1 depends upon liver function, this could be one of the main factors in the significant catch-up growth in pediatric LT recipients.     

The relationship of the levels of leptin, insulin-like growth factor-I and insulin in cord blood with birth size, ponderal index, and gender difference

In humans, serum levels of leptin correlate with total body fat in both adults and children. After collecting cord blood from 156 term neonates (82 males, 74 females; 132 AGA and 22 LGA), we measured the cord levels of leptin, insulin and IGF-I to determine the relationships between these three hormones and relationships of these hormones with birth size (birth weight and ponderal index for adiposity in newborn) and gender. The leptin and IGF-I levels were significantly higher in the LGA group (9.2+/-4.0 ng/ml and 96.1+/-34.1 ng/ml, respectively) than in the AGA group (4.8+/-3.8 ng/ml and 56.4+/-37.6 ng/ml, respectively). A significant positive correlation was observed between leptin levels and birth weight, and a weaker correlation between leptin levels and birth height. IGF-I level significantly correlated with birth weight and birth height, but there was no correlation between the levels of insulin and birth weight. There was no relationship between the levels of IGF-I, insulin and leptin. Ponderal index was higher in LGA than in AGA. A significant correlation was also observed between the levels of leptin and ponderal index, but not between the levels of insulin or IGF-I and ponderal index. The levels of leptin and ponderal index were higher in females than males despite no gender differences in gestational age and birth weight. In conclusion, our results suggest that the level of IGF-I is a useful index for fetal growth during late gestation, and the development of adipose tissue is the major determinant of fetal serum leptin levels, the production of which is not regulated by insulin or IGF-I. In addition, a gender difference with a higher level of leptin in female neonates suggests that sexual dimorphism in adipose tissue already exists in utero.     

IGF-I及IGFBP-3对生长激素缺乏症患儿诊断及疗效判断的价值

为了探求一次性抽血确诊生长激素缺乏症 (GHD)的方法和寻找一个检测GH治疗效果的可靠而敏感的生化指标 ,分别用RIA法和IRMA法检测25例GHD患儿血清胰岛素样生长因子 -I(IGF -I)、胰岛素样生长因子结合蛋白 -3(IGFBP -3) ,同时进行生长激素 (GH)刺激试验 ;将GHD患儿分为2组 ,完全性缺乏组 (cGHD)及部分缺乏组 (pGHD) ,将2组血清IGF -I、IGFBP -3与年龄、性别配对的正常儿童 (C组 )均值对照 ,并对照不同年龄及不同发育期的50例正常儿童参考范围 ,计算GHD患儿血清IGF -I、IGFBP -3的降低率 ;将IGF -I与GH峰值做相关性分析。用rhGH治疗GHD3个月后将IGF -I增高值 (△IGF -I)与治疗后每年生长速度 (GV)做相关性分析。结果显示 ,GHD组血清IGF -I、IGFBP -3均显著低于正常对照组 ,两组无重叠 ,cGHD组与pGHD组比较 ,两者差异显著 ;IGF -I及IGFBP -3在GHD组及C组均呈显著正相关 ;GHD组血清IGF -I与GH峰值呈显著正相关 (r=0.85,P<0.001) ,回归方程 :y=0.1613 +0.0235x ,由此可根据血清IGF -I测定值求出GH峰值 ;治疗3个月后△IGF -I与治疗后GV呈显著正相关。提示IGF -I、IGFBP -3对GHD患儿的诊断有重要价值 ;GH峰值可根据所测IGF -I由回归方程求出 ,以代替传统的生长激素刺激试验 ;IGF—I是判断rhGH治疗效果的可靠而     

特发性矮小患儿生长激素-胰岛素样生长因子轴变化的研究

目的 观察特发性矮小(ISS)患儿血中生长激素(GH)、胰岛素样生长因子-l(IGF-1)、胰岛素样生长因子结合蛋白-3(IGFBP-3)及生长激素结合蛋白(GHBP)水平的变化.方法 2002年6月至2006年5月在中南大学湘雅二医院儿科就诊的37例ISS患儿为病例组,37例年龄性别相匹配的正常儿童为对照组.采用放射免疫分析法(RIA)测定血清GH,免疫放射计量法(IRMA)测定血清IGF-1及IGFBP-3,葡聚糖覆盖炭末吸附法(DCT)检测血清GHBP.结果 ISS组血清GHBP、IGF-1、IGFBP-3均明显低于对照组(均P＜0.01),而血清GH基础值在ISS组明显高于时照组(P＜0.05).结论 ISS患儿血中IGF-1和IGFBP-3降低可能是其矮小的原因之一.ISS患儿血中反映生长激素受体(GHR)水平的GHBP降低,而GH基础值升高,提示可能存在因GHR缺陷导致的GH不敏感.