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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We produced antiserum to insulin-like growth factor I (IGF-I), and developed a specific and sensitive radioimmunoassay (RIA) for IGF-I using the biosynthetic IGF-I. This antiserum to IGF-I was specific for IGF-I; no cross-reactivities with multiplication stimulating activity, porcine insulin or human growth hormone (hGH) were detected. The sensitivity was 10-25 pg/tube with 50% displacement at 125 pg/tube. The intra- and inter-assay coefficients of variation for IGF-I were 5.4 and 9.7%, respectively. The plasma IGF-I levels as determined by RIA in normal adults (N = 46), patients with active acromegaly (N = 31), and pituitary dwarfs (N = 31) were 21.6 +/- 1.0, 157.3 +/- 17.0, and 2.5 +/- 0.3 ng/ml (Mean +/- SEM), respectively, indicating the levels were GH-dependent. The plasma IGF-I levels were significantly increased from 2.2 +/- 0.2 to 26.5 +/- 3.2 ng/ml after hGH administrations for three consecutive days in five pituitary dwarfs. The IGF-I levels were low in patients with hypothyroidism and liver cirrhosis, but were normal in patients with chronic renal failure. These data confirm previous reports and this radioimmunoassay proves useful in evaluating plasma IGF-I levels.
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PMID:Radioimmunoassay for insulin-like growth factor I (IGF-I) using biosynthetic IGF-I. 358 65

Thirty-one children who were short but not GH deficient, whose serum GH responses to provocative tests were normal, and whose spontaneous GH secretion was low received daily sc injections of human GH (Crescormon; 0.1 IU/kg BW) for 1 yr. Their initial serum insulin-like growth factor I (IGF-I) and IGF-II responses to GH were compared with their 1-yr growth response to therapy. In the prepubertal group (n = 18) the growth rate of all but two children increased 3.4 +/- 0.2 (+/- SEM) cm (from 4.1 +/- 0.2 to 7.5 +/- 0.3 cm/yr). The mean increment in the growth rate of the pubertal group was 5.2 +/- 0.5 cm. In both groups the growth increase was strongly correlated with both the percent increase in serum IGF-I and the percent increase in serum IGF-II during the first 10 days of treatment. No correlation was found between the basal growth rate and basal serum IGF-I or IGF-II levels. In the prepubertal group of children, both the percent increase in serum IGF-I levels in response to GH and the age at start of treatment were predictors of long term growth. We conclude that this subgroup of normal short children with low spontaneous GH secretion and high percent increase in serum IGF values benefits from GH treatment with an increased growth rate.
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PMID:Growth hormone treatment in short children: relationship between growth and serum insulin-like growth factor I and II levels. 365 12

The renal excretion of radioimmunoassayable somatomedin-C/insulin-like growth factor I (Sm-C/IGF-I) was measured in 12-h overnight urine samples obtained from 88 subjects, aged 3-19 yr. The participants included 34 healthy children (group 1), 29 children with idiopathic growth failure and normal GH stimulation tests (group 2), and 25 GH-deficient subjects (group 3). The mean (+/- SEM) urinary Sm-C/IGF-I excretion in group 1 (28.4 +/- 2.1 mU/kg) was significantly greater than that in group 2 (8.1 +/- 1.6 mU/kg) or group 3 (8.6 +/- 1.3 mU/kg). Twenty-two of the 29 subjects in group 2 had urinary Sm-C/IGF-I values less than 8 mU/kg. After the administration of biosynthetic GH to 12 GH-deficient subjects, urinary Sm-C/IGF-I excretion rose from 10.3 +/- 2.3 to 21.4 +/- 4.2 mU/kg within 12 h (P less than 0.05), indicating that renal excretion of Sm-C/IGF-I is GH dependent. One woman with acromegaly had markedly elevated urinary Sm-C/IGF-I excretion (420 mU/kg). The authenticity of urinary Sm-C/IGF-I was confirmed by high pressure liquid chromatography (HPLC). Assay of serial dilutions of urinary Sm-C/IGF-I demonstrated a direct proportionality between concentration and dilution. Although it is not possible to identify whether urinary Sm-C/IGF-I reflects local or generalized synthesis of the peptide, we hypothesize that quantitation of Sm-C/IGF-I in timed urine collections will yield additional information about GH production and action in children with normal and abnormal growth.
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PMID:Quantitation of urinary somatomedin-C in children with normal and abnormal growth. 368 Apr 79

To investigate the possible role of somatomedin-C/insulin-like growth factor I (Sm-C/IGF I) in early human development, we measured this peptide by radioimmunoassay in extracts of multiple tissues and in plasma from fetuses during the first half of gestation (9-19 wk). All tissues contained Sm-C/IGF I far in excess of that which could be accounted for by Sm-C/IGF I derived from blood entrapment. Lung and intestine had the highest concentrations (166 +/- 35 mU/g, n = 25 and 160 +/- 20 mU/g, n = 19, respectively; mean +/- SEM) and liver the lowest (67 +/- 16 mU/g, n = 26). Plasma concentrations were 270 +/- 20 mU/ml (n = 20). Neither fetal weight (6-258 g) nor gestational age correlated with Sm-C/IGF I concentrations in any tissue or in plasma. These findings suggest that Sm-C/IGF I is synthesized in many human fetal tissues from as early as the 1st trimester. They also provide further evidence for an autocrine/paracrine role of this peptide growth factor.
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PMID:Tissue and plasma somatomedin-C/insulin-like growth factor I concentrations in the human fetus during the first half of gestation. 370 13

The roles of plasma insulin-like growth factor I (IGF I) and growth hormone (GH) were studied in 7 beagle dogs before and during starvation and during refeeding. IGF I levels significantly decreased from 75.2 +/- 5.9 ng/ml at 7 days prior to the start of starvation to 9 +/- 1.7 ng/ml at 19 days after the commencement of starvation (mean +/- SEM; P less than 0.0001). During refeeding IGF I significantly rose from 9 +/- 1.7 ng/ml to 55.5 +/- 7.5 ng/ml within 9 days (mean +/- SEM; P less than 0.002). During starvation plasma GH levels significantly increased (P less than 0.05) and these elevated levels returned to normal during refeeding. The dogs' GH secretory capacity significantly increased during starvation (P = 0.012) and became normal again during refeeding. The following conclusions can be drawn from this study: 1) starvation in the dog leads to a significant and drastic reduction of the circulating levels of IGF I, and 2) starvation in the dog, as in man, leads to increased circulating GH levels and to an increased GH-secretory capacity possibly brought about by a lack of a negative feedback normally exerted by IGF I.
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PMID:Insulin-like growth factor I and growth hormone in canine starvation. 388 84

Plasma somatomedin-C (Sm-C)/insulin-like growth factor I (IGF-I) concentrations have been shown to reflect changes in nitrogen balance induced by manipulation of nutrient intake. To assess the Sm-C/IGF-I response to refeeding a protein restricted diet in which the nitrogen source was supplemented with essential amino acids, six normal adults were fasted for five days, then refed for nine days diets consisting of 35 kcals/kg and 0.48 g protein/kg body weight. In one diet, 80% of the nitrogen was supplied as essential amino acids, and in the other, 80% was supplied as nonessential amino acids. Following the first fast/refeed cycle, a control diet was eaten for two weeks before the fast was repeated and the other test diet was ingested. The refeeding diets were given a random order. Plasma Sm-C/IGF-I fell from a pre-fast mean of 1.64 +/- 0.24 U/mL (mean +/- 1 SEM) to 0.67 +/- 0.18 (P less than 0.001) following fasting, and rose to 1.41 +/- 0.19 U/mL (P less than 0.001) following ingestion of the diet with supplemental essential amino acids. In contrast, when the same subjects were refed a diet in which 80% of the nitrogen was in the form of nonessential amino acids, the plasma Sm-C/IGF-I concentrations rose from 0.74 +/- 0.17 to 1.15 +/- 0.15 U/mL (P less than 0.01). This increase was significantly less than that observed after ingestion of the essential amino acid supplemented diet (0.74 +/- 0.10 U/mL v 0.40 +/- 0.11 U/mL; P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Supplemental essential amino acids augment the somatomedin-C/insulin-like growth factor I response to refeeding after fasting. 388 68

Growth hormone (GH) responses to growth-hormone-releasing hormone (GRH) and thyrotropin-releasing hormone (TRH) were studied in 17 diabetic patients. Ten patients (group 1) had retinopathy corresponding to stage III-V (Scott's classification), and the remaining seven patients (group 2) had no retinopathy despite longer duration of diabetes in comparison with the patients in group 1. There were no differences in age, percent of ideal body weight, and serum HbA1 levels between the two groups. Basal serum GH levels were 1.9 +/- 0.4 ng/ml (mean +/- SEM) in group 1, and not different from the values in group 2 (1.6 +/- 0.7 ng/ml). However, GH responses to synthetic human GRH-44 (1 micrograms/kg body wt, i.v. bolus) were significantly greater in group 1, as judged by the maximal response or integrated GH secretion after the administration of GRH. There were no differences in serum insulin-like growth factor I (IGF-I) levels between group 1 (262 +/- 35 ng/ml) and group 2 (232 +/- 30 ng/ml), and no significant correlation was found between serum IGF-I levels and GH responses to GRH in either of the two groups. Paradoxical GH responses to TRH (500 micrograms, i.v. bolus) were found in only one patient in each group. We have thus demonstrated that GH responses to GRH are more pronounced in diabetic patients with retinopathy than in patients without this complication, although it remains to be determined whether or not greater GH responses to GRH are causally related to the development of diabetic retinopathy.
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PMID:Growth hormone responses to growth-hormone-releasing hormone and thyrotropin-releasing hormone in diabetic patients with and without retinopathy. 392 95

The factors responsible for the elevation of circulating somatomedin-C/insulin-like growth factor I (Sm-C) during normal pubertal development are uncertain. To assess the role of ovarian estrogen secretion during puberty, we examined the effect of estrogen deficiency due to primary hypogonadism on Sm-C levels in late childhood and early adolescence. The concentration of immunoreactive Sm-C was measured in 36 untreated patients with gonadal dysgenesis (age, 4-16 yr); results were compared with the pattern of change in Sm-C in 153 age-matched normal girls. Between ages 4-9 yr, patients with gonadal dysgenesis had Sm-C levels similar to those in the age-matched normal subjects. In contrast to the normal girls, Sm-C levels in patients with gonadal dysgenesis did not rise after 10 yr of age and were significantly lower than those in normal girls at 11-16 yr of age. The effect of low dose estrogen therapy was assessed in eight patients with Turner's syndrome. Their Sm-C levels were measured before and during 2-12 months of treatment with ethinyl estradiol (90-220 ng/kg X day). The mean Sm-C concentration rose from 0.72 +/- 0.06 U/ml (+/- SEM) before treatment to 1.17 +/- 0.17 U/ml during estrogen treatment (P less than 0.04). In three patients who had a similar increase in Sm-C during estrogen treatment, interruption of therapy was associated with a fall in Sm-C concentrations; when estrogen therapy was reinstituted in two of these patients, Sm-C levels rose again. These results suggest that increasing endogenous estrogen production is a major determinant of the rise of circulating Sm-C that occurs during pubertal development in normal girls. Chronic estrogen deficiency, as in untreated patients with gonadal dysgenesis, is associated with failure to manifest the elevation of Sm-C that occurs during normal puberty.
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PMID:Somatomedin-C levels in children and adolescents with gonadal dysgenesis: differences from age-matched normal females and effect of chronic estrogen replacement therapy. 403 32

Insulin-like growth factor II (IGF-II) is a human plasma peptide whose sequence is homologous to both insulin-like growth factor I/somatomedin C (IGF-I/SM-C) and human proinsulin in the A and B regions. However, there is no obvious homology in the C (connecting peptide) region. The synthetic 8-amino acid C-peptide segment of IGF-II (Ser-Arg-Val-Ser-Arg-Arg-Ser-Arg) was covalently linked to thyroglobulin to render it more antigenic. Antiserum against the IGF-II C-peptide was generated which had a titer of 1:2000 determined with [125I]IGF-II C-peptide. Half-maximum displacement was by 350 pg/ml IGF-II C-peptide or 80 ng/ml IGF-II. There was no displacement by IGF-I/SM-C, insulin, or a wide variety of peptides. There was also a high degree of species specificity of this antisera. Isoelectric focusing studies of immunoreactive IGF-II showed an apparent pI of 6-6.5. The mean (+/- SEM) level of IGF-II after acid chromatography of 28 normal adult males was 687.0 +/- 31.9 ng/ml. The mean of 8 acromegalics was 600.5 +/- 57.4 ng/ml, indistinguishable from normal. The IGF-II levels of 21 hypopituitary children were significantly lower (231.5 +/- 32.3 ng/ml). Thus, GH action appears to be necessary for normal levels of IGF-II, but excess GH does not cause an elevation above normal of IGF-II, unlike what is seen with IGF-I/SM-C. These structurally related IGF peptides have different control mechanisms and ultimately may play different functional roles. The availability of specific RIAs for the measurement of IGF-II will help to clarify its role in human physiology and disease states.
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PMID:A radioimmunoassay for insulin-like growth factor II specific for the C-peptide region. 617 44

The roles of growth hormone (GH) and insulin-like growth factor I (IGF I) were studied in 9 German Shepherd dwarf dogs. GH deficiency was evidenced in all dogs by an absence of increase in GH levels in response to clonidine administration. While the mean IGF I concentration in normal adult German Shepherds was 280 +/- 23 ng/ml and 345 +/- 50 ng/ml in immature animals, the mean IGF I concentration in the dwarf dogs was 11 +/- 2 ng/ml (mean +/- SEM, P less than 0.001). In the affected animals, plasma thyroxine (T4) levels were only slightly subnormal and there was an increase in these levels in response to thyroid stimulating hormone (TSH) administration. The findings indicate 1) that dwarfism in German Shepherds is caused by primary GH-deficiency resulting in low circulating levels of IGF I and 2) that IGF I levels in the dog as in man are subject to control by GH.
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PMID:Growth hormone and insulin-like growth factor I in German shepherd dwarf dogs. 632 93


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