T Salazar

University of Santiago, Chile, CiudadSantiago, Santiago, Chile

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Publications (17)43.8 Total impact

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    ABSTRACT: The biochemical mediators responsible for variations in stature among normal subjects are largely unknown. To obtain some initial information about potential endocrine factors, we measured the serum concentrations of GH, IGF-1, IGFBP-3 and GHBP in healthy young men shorter than 159 cm and taller than 187 cm. We studied 14 volleyball and basketball players (tall group), and 14 jockey students from a horse racetrack (short group). A careful medical history was taken, including dietary intake, and physical examination with special attention to the possible presence of genetic stigmata was performed. Serum prealbumin was determined as an index of nutritional status. A buccal smear was performed to exclude Klinefelter's syndrome. The BMI and serum prealbumin levels were comparable in both groups of individuals. The nutritional survey, however, revealed that the tall subjects had a higher intake of calories (42.2+/-11.2 vs. 30.1+/-15.15 kcal/kg, p<0.05), and protein (1.5+/-0.6 vs. 0.8+/-0.4 mg/kg, p<0.01). Serum concentrations of GHBP did not differ in the two groups (0.95+/-0.37 nmol/l in the tall, and 0.95+/-0.53 nmol/l in the short group), and did not correlate with height, serum IGF-I levels, or BMI. We observed a significant difference in the serum concentrations of IGF-I in the two groups of individuals (42.02+/-9.37 nmol/l in the tall and 31.79+/-3.18 nmol/l in the short group, p<0.05), and this growth factor showed a positive correlation with height (r = 0.5, p<0.01). These preliminary findings suggest that final height differences in young men do not appear to be mediated by variations in GHBP concentrations.
    No preview · Article · Jan 2011 · Journal of pediatric endocrinology & metabolism: JPEM
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    ABSTRACT: To assess normative data and the usefulness of spontaneous and LHRH analogue-stimulated serum LH and FSH levels measured by immunoradiometric assays (IRMA) in the evaluation of normal puberty. Prospective. Healthy girls in Tanner I and Tanner II from the local community were invited to participate (n = 47). A leuprolide acetate test (500 mcg/m(2); sc) was performed. LH and FSH levels were determined using IRMA. Tanner II girls were assessed every 6 months until Tanner V. Girls who progressed from Tanner II to Tanner III in the next 6 months were called Tanner II-2; otherwise, they were called Tanner II-1. The prepubertal upper limit (CI 95%) was 0.49 IU/l for basal LH and 5.1 IU/l for stimulated LH. Taking into account these LH cut-off limits, 72.2% and 66.7% of Tanner II-1 and 41.6% and 41.7% of Tanner II-2 subjects presented overlapping values for basal and stimulated LH, respectively, as compared with the Tanner I group. The cut-offs for basal and stimulated LH to predict progression from Tanner II to Tanner III in the next 6 months were a basal LH level > or =0.49 IU/l (Sensitivity = 0.58; 1-Specificity = 0.33) and a poststimulated LH level > or =4.75 IU/l (Sensitivity = 0.67; 1-Specificity = 0.44). According to an IRMA, the basal and leuprolide acetate gonadotrophin response patterns during the beginning stages of puberty overlapped between Tanner I and Tanner II, and the cut-offs of basal and stimulated LH levels to predict progress from Tanner II to Tanner III had low sensitivities for the following 6 months.
    Full-text · Article · Oct 2009 · Clinical Endocrinology
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    ABSTRACT: Small for gestational age (SGA) has been associated with decreased insulin sensitivity (IS). A possible mechanism is the postnatal development of a metabolically disadvantageous body composition (BC). To determine whether there are differences between IS and BC in girls in early puberty who were SGA (birth weight < 10th percentile) or appropriate for gestational age (AGA, 10th-90th percentile). Age-matched (SGA/AGA) early pubertal girls (Tanner II) were recruited from local schools. We determined waist circumference (WC), the sum of four skinfolds (S4S), and per cent fat mass (fat %) by impedanciometry. Leptin and OGTT assays were performed. The insulinogenic index (I-In), HOMA-IR (homeostasis model assessment of insulin resistance) and WBISI (whole body insulin sensitivity) were calculated. Median age (interquartile range) for 30 SGA and 35 AGA girls was 10.2 (1.1) vs. 9.8 (0.9), respectively (P = NS). BMI percentiles were 62.6 (56) vs. 67.4 (39); WC 60.5 (9.5) vs. 62.2 (6.5) cm; S4S 52 (30) vs. 52.2 (29.5) cm, and fat %[26.2 (6.7) vs. 28.5 (6.3)] was similar in both groups. SGA girls had higher leptin levels [15.4 (9.7) vs. 9.6 (11) ng/ml; P = 0.01] and I-In [2.05 (1.86) vs. 1.47 (1.27) microU/ml* mg/dl; P = 0.02]. No differences between HOMA-IR [2.07 (1.26) vs. 2.04 (1.4)] and WBISI [5.3 (3.3) vs. 5.1 (3.1)] were found between groups. The higher leptin level and I-In in girls born SGA at the beginning of puberty may be early indicators of an underlying subtle degree of insulin resistance, despite similar BMI and BC to AGA girls.
    No preview · Article · Oct 2007 · Clinical Endocrinology
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    ABSTRACT: There are limited and controversial data concerning puberty characteristics in girls born small for gestational age (SGA). The objective of the study was to document clinical, ultrasonographic, and biochemical characteristics at the beginning of puberty in matched healthy girls born either SGA or appropriate for gestational age (AGA) recruited from the community. Inclusion criteria were breast Tanner stage II and a body mass index between the 10th and 95th percentiles. Recruited subjects underwent a complete physical exam, bone age, and ultrasound measurements of the internal genitalia. Hormonal assessment included fasting early morning dehydroepiandrosterone sulfate, androstenedione, SHBG, inhibin-B, FSH, LH, estradiol (E2), 17-hydroxyprogesterone (17OH Prog), and testosterone. Thereafter, a GnRH agonist test (leuprolide 500 microg, sc) was performed with FSH and LH at time 3 and 24 h for E2, 17OH Prog, and testosterone. Sixty-five girls (35 AGA, 30 SGA) with a mean age of 9.9 +/- 1.03 (7.8-12.5) yr, similar bone age/chronological age (1.02 +/- 0.8 in AGA and 1 +/- 0.76 in SGA), median height of 1.35 +/- 0.06 cm, and similar waist to hip ratio were included. No differences in the presence of pubic hair, axillary hair, apocrine odor, or ultrasound measurements were found. SGA girls had increased baseline E2 as well as stimulated E2 and 17OH Prog. In a preliminary sample of lean, healthy girls recruited from the community born either SGA or AGA, we observed slight hormonal differences at the beginning of puberty. Longitudinal follow-up of this cohort will allow us to understand whether these differences are maintained and have a clinical impact in their pubertal development.
    Full-text · Article · Oct 2006 · Journal of Clinical Endocrinology & Metabolism
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    V Mericq · K K Ong · Bazaes RA · V Peña · A Avila · T Salazar · N Soto · G Iñiguez · D B Dunger
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    ABSTRACT: Insulin resistance and type 2 diabetes risk in human subjects who were small-for-gestational-age (SGA) at birth may be a consequence of rapid early postnatal weight gain. We prospectively studied early changes in fasting insulin sensitivity and insulin secretion, assessed by a short intravenous glucose tolerance test that was conducted several times from birth to 3 years of age in 55 SGA (birthweight below fifth percentile) newborns and in 13 newborns with a birthweight appropriate for gestational age (AGA). Most SGA infants showed postnatal upward weight centile crossing and by 3 years were similar in size to AGA infants. SGA infants had lower pre-feed insulin levels at postnatal age 48 h than AGA infants (median 34.4 vs 59.7 pmol/l, p<0.05), but by the age of 3 years they had higher fasting insulin levels (median 38.9 vs 23.8 pmol/l, p<0.005), which were related to rate of weight gain between 0 and 3 years (r=0.47, p=0.0003). First-phase insulin secretion did not differ between SGA and AGA infants, but SGA infants had a lower glucose disposition index (beta cell compensation) (median 235 vs 501 min mmol(-1) l(-1), p=0.02), which persisted after allowing for postnatal weight gain (p=0.009). SGA infants showed a marked transition from lower pre-feed insulin and increased insulin sensitivity at birth to insulin resistance over the first 3 years of life. This transition was related to rapid postnatal weight gain, which could indicate a propensity to central fat deposition. The additional observation of reduced compensatory beta cell secretion underlines the need for long-term surveillance of glucose homeostasis in all SGA subjects, whether or not they show postnatal catch-up growth.
    Full-text · Article · Jan 2006 · Diabetologia
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    ABSTRACT: We hypothesized that some children with idiopathic short stature in Chile might bear heterozygous mutations of the GH receptor. We selected 26 patients (3 females, 23 males) from 112 patients who consulted for idiopathic short stature at the University of Chile. Their chronological age was 8.3 +/- 1.9, and bone age was 6.1 +/- 1.0 yr. Their height was -3.0 +/- 0.7 SDS; IGF-I, -1.2 +/- 1.1 SD; IGF binding protein 3, -0.7 +/- 2.0 SDS; and GH binding protein, 0.4 +/- 0.8 SDS. Patients were admitted, and blood samples were obtained every 20 min to determine GH concentrations overnight. Coding sequences and intron-exon boundaries of exons 2-10 of GH receptor gene were amplified by PCR and subsequently analyzed through single-strand conformational analysis. Mean serum GH concentration, over 12-h, was 0.20 +/- 0.08 nM; pulse amplitude, 0.40 +/- 0.15 nM; number of peaks, 5.8 +/-1.5 peaks/12 h; peak value of GH during the 12-h sampling, 1.03 +/- 0.53 nM; and area under the curve, 151.4 +/- 56.1 nM/12 h. There were positive correlations between mean GH vs. area under the curve (P < 0.001) and GH peak (P < 0.01). The single-strand conformational analysis of the GH receptor gene showed abnormal migration for exon 6 in 9 patients and for exon 10 in 9 patients, which (by sequence analysis) corresponded to 2 polymorphisms of the GH receptor gene: an A-to-G transition in third position of codon 168 in exon 6 and a C-to-A transversion in the first position of codon 526 in exon 10. We further sequenced all coding exons and intron-exon boundaries in the most affected patients (nos. 6, 9, 11, 14, 15, 16, and 23). This analysis revealed a C-to-T transition in codon 161 of exon 6 in patient 23, which results in an amino acid change (Arg to Cys) in an heterozygous form in the patient and his father. In conclusion, the results of our study suggest that, in Chilean patients with idiopathic short stature, GH receptor gene mutations are uncommon, although we cannot exclude mutations that were missed by single-strand conformational analysis or mutations within introns or in the promoter regions of the GH receptor gene.
    Full-text · Article · Oct 2001 · Journal of Clinical Endocrinology & Metabolism
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    ABSTRACT: Circulating concentrations of the high affinity growth hormone binding protein (GHBP) may be a marker of GH receptor density as well as GH sensitivity. To determine values of GHBP for a normal Chilean pediatric population. We determined GHBP levels in 73 males and 73 females between 4 to 15.5 years and 4 to 16.8 years respectively, divided in 7 groups according to age and puberal status. The population was normally distributed in weight, height and body mass index (BMI). GHBP activity increased up to Tanner IV in males and Tanner III in females, and decreased slightly thereafter in Tanner V and IV respectively. There was a significant difference between GHBP levels of preschool children and those found in Tanner II to V in both sexes (p < 0.05). In addition, we found a positive correlation between GHBP vs weight, height and BMI (p < 0.001) in males and females. The availability of this methodology allows us to establish the normative value of GHBP in our population and provides useful information to interpret GH circulating levels in children with growth disorders.
    No preview · Article · Apr 2001 · Revista medica de Chile
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    ABSTRACT: The diagnosis of GH deficiency (GHD) is based upon the results of GH stimulation tests, which have several drawbacks. To evaluate the usefulness of IGF-1 and IGFBP-3 for the diagnosis of GHD in prepuberal children. We measured IGF-I and IGFBP-3 in three group of subjects: I. GHD (n: 24), height < -2SD for age (Z score, average +/- SD: -4.2 +/- 1.2), growth velocity < p10 (3.4 +/- 1.0 cm/year) and peak GH level on two GH stimulation tests < 7 ng/ml (1.2 +/- 0.6 ng/ml); II. Short non-GHD (NGHD, n: 32), height of -2.7 +/- 0.9 SD for age, growth velocity < p 25 (3.9 +/- 1.2 cm/year), and peak GH level on two GH stimulation tests > 7 ng/ml (15.3 +/- 6.9 ng/ml), y III. Normal school children (n: 35) with normal heights (-0.17 +/- 0.12 SD) were studied as controls. IGF-1 and IGFBP-3 were significantly lower in GHD than in NGHD and controls (p < 0.001), and in NGHD than in C (p < 0.001). We defined the normal range of both proteins as +/- 2 SD of the mean of the control group. Using this criteria, IGF-I was low in 21/24 GHD, and in 12/32 NGHD. IGFBP-3 was low in 22/24 GHD, and in 6/32 NGHD. Only 1 GHD patient had both exams in the normal range, suggesting that he is probably NGHD. 4/32 of the NGHD and both exams below normal range, suggesting that they are probably GHD. IGF-1 and IGFBP-3 are important tools for the diagnosis of GHD.
    No preview · Article · Jul 1999 · Revista medica de Chile
  • T. Salazar · V. Mericq · M. Eggers · A. Avila · F. Cassorla

    No preview · Article · Mar 1999 · Pediatric Research

  • No preview · Article · Mar 1999 · Pediatric Research

  • No preview · Article · Mar 1999 · Pediatric Research

  • No preview · Article · Feb 1998 · Pediatric Research
  • E Codner · V Mericq · M Espinoza · F Beas · A Avila · T Salazar · F Cassorla · H Garcia

    No preview · Article · Feb 1998 · Pediatric Research
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    ABSTRACT: The mechanisms by which zinc supplementation increase the growth rate in children of short stature are unknown. To study the effects of zinc supplementation on growth hormone in children with short stature and growth deficiency. A study was carried out in 33 eutrophic prepubertal boys, aged 7.8 ± 1.8 years, with height/age -2.6 ± 0.91 (NCHS), prior growth velocity of 4 ± 1 cm/year, with no other pathological condition nor GH deficiency and whose intake of zinc was, 10 mg/day. They were randomly assigned in a double blind fashion to groups A and B, who received zinc acetate 20 mg/day p.o. and placebo for periods of 6 months alternately. An anthropometric follow-up was carried out as well as plasma determinations of IGF-I, IGF-II, IGFBP-3, GHBP, urinary GH, zinc in plasma and hair, bone age at 0, 3, 6, 8, 11 and/or 14 months. The results were compared using the Student's t test, and p < 0.05 was considered significant. There were no significant differences in growth nor in the parameters studied between groups A and B in any of the time periods measured. Both groups increased their growth rate, which was 4.2 ± 1.1, 4.8 ± 1.2 and 5.3 ± 1.7 cm/year in group A and 3.9 ± 1, 5.1 ± 1.3 and 4.5 ± 2.1 cm/year in group B, in the basal period, 0-6 and 8-14 months respectively. GHBP increased at 3 months from 136.9 ± 32.1 to 204.4 ± 51.4 and from 130.7 ± 56.9 to 199.6 ± 89.5 pmol/L, in A and B (p < 0.001). The increase in growth rate and in GHBP observed in these patients is not attributable to zinc supplementation.
    No preview · Article · Jan 1998

  • No preview · Article · Feb 1997 · Pediatric Research
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    ABSTRACT: The growth hormone-releasing peptides (GHRP's) are a family of hexa- and heptapeptides which specifically stimulate GH release. Their mechanism of action has not been determined, but they may act at hypothalamic and pituitary sites. We have shown that GHRP's acutely stimulate GH secretion in GH deficient (GHD) children (JCEM 80:1681, 1995). With lower molecular weight than GH and GHRH, they may represent an attractive option for therapy. Our goal was to study the effects of the chronic administration of GHRP-2. We studied 6 prepubertal GH-deficient children (4 ♂, 2 ♀) over 6 months of treatment. GHD was defined as growth velocity below 4 cm/year, delayed bone age, and maximum GH response to 2 provocative tests below 4 μg/L. Ages were between 6 2/12 and 14 3/12 years, and bone ages ranged from 4 6/12 to 106/12. The patients received GHRP-2 sc at increasing doses every 2 months: 0.3 μg/Kg/day 0-2 months, 1 μg/Kg/day 2-4 months and 3 μg/Kg/day 4-6 months. Overnight 12-1 GH profiles were analyzed by Pulsar. Results are shown in the table (means ± SD). *=p<0.05 by ANOVA. Baseline 2 months 4 months 6 months Height Velocity, cm/y 2.5 ± 0.5 5.8 ± 3.4 * 4.7 ± 3.2 5.6 ± 1.5 * Mean GH, μg/L 2.8 ± 2.3 2.1 ± 1.5 3.4 ± 16 4.2 ± 3.3 Max GH, μg/L 12.7 ± 11 12.6 ± 7.7 19.4 ± 12 34.6 ± 28 * No. of GH peaks/12 hr 7.2 ± 2.0 5.7 ± 5.8 5.8 ± 1.3 7.2 ± 2.6 Peak amplitude, μg/L 4.7 ± 4.7 5.4 ± 3.3 7.6 ± 6.4 * 9.1 ± 7.3 * IGF-I, μg/L 148 ± 80 158 ± 79 157 ± 63 147 ± 66 IGFBP-3, mg/L 1.7 ± 0.5 1.8 ± 0,6 1.5 ± 0.4 1.6 ± 0.5 Conclusions: 1) There was a significant increase in growth velocity compared to baseline even at the lowest GHRP dose employed. 2) Maximum GH concentrations and the amplitude of GH peaks increased significantly at higher doses. 3) We did not observe any adverse reactions during the course of the study. We conclude that GHRP-2 holds promise as a therapeutic agent for GH-deficient children.
    No preview · Article · Jan 1996
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    T. Salazar · Y u Y · J. Sztein · S. Humphreys · F. Cassorla
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    ABSTRACT: Hypothyroidism induces growth retardation and decreases the circulating concentrations of GH and IGF-I. To study the effects of thyroid hormone on GHR and IGF-I expression, we measured rat liver and kidney GHR and IGF-I mRNA levels by solution hybridization RNase protection assay. Three to six 21 day-old castrated male rats per group were given either pure water or 0.025% methimazole in their drinking water, and subcutaneous pellet containing either placebo or thyroxine (T4) 2.5 mg. After 13 days, the animals were sacrificed. Serum free T4 and IGF-I levels were determined by RIA. Liver and kidney GHR and IGF-I, mRNA were measured by solution hybridization using specific antisense riboprobes. Protected bands corresponding to GHR and IGF-I mRNA were quantified using a Phosphorlmager.
    Full-text · Article · Nov 1994 · Pediatric Research