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Biomedical subjects

A D Rogol

Publications and source records attributed to A D Rogol.

At least 109 records · Page 6Linked to original sources
PubMed1990

Release of luteinizing hormone and growth hormone after recovery from maximal exercise.

Pulsatile properties of luteinizing hormone (LH) and growth hormone (GH) release were evaluated in 19 eumenorrheic untrained females [mean age 31.1 +/- 1.1 yr, height 165.2 +/- 1.4 cm, weight 64.8 +/- 2.1 kg, peak oxygen uptake (Vo2) 41.6 +/- 1.4 (SE) ml.kg-1.min-1] during the early follicular phase of the menstrual cycle (days 3-4 after the onset of menses). Each subject was studied during two consecutive menstrual cycles under each of two conditions in random order: 1) no formal exercise for 72 h (C) and 2) 12-24 h after two maximal exercise bouts (peak Vo2/lactate threshold treadmill evaluation and a 3,200-m time-trial run or a maximal Vo2 inclined treadmill test) performed on consecutive days (EX). Blood sampling was performed every 10 min for 12 h. LH and GH pulsatile parameters were identified and characterized by the Cluster pulse detection algorithm. No significant differences were noted in the number of peaks, peak amplitude, interpeak interval, peak increment, or 12-h integrated concentrations between C and EX for LH or GH. We conclude that maximal exercise protocols typically used for exercise evaluation do not have an effect on the pulsatile characteristics of LH or GH release in untrained women during the early follicular phase of the menstrual cycle if 12-24 h of recovery are allowed before evaluation of the pulsatile secretion of gonadotropins or GH.

Adult↗
PubMed1990

Variations of pulsatile growth hormone release in healthy short prepubertal boys.

Overnight growth hormone (GH) concentrations obtained by frequent venous sampling of 20 healthy, short prepubertal boys were evaluated using the objective pulse detection algorithm, CLUSTER. The resulting pulsatile characteristics were compared with those of 11 healthy prepubertal boys of normal stature and with those of nine prepubertal children with documented GH deficiency. Although no significant differences of pulsatile GH release were found between the normal and short subjects, a subset of the short prepubertal boys with significantly delayed skeletal ages had subnormal sum of GH pulse areas and sum of GH pulse amplitudes. The finding of a significant correlation in all subjects between growth velocity and the sum of GH pulse amplitudes is important, as the results are compatible with the hypothesis that alterations of amplitude-modulated GH release underlie the pathophysiology of suboptimal growth in some short prepubertal children.

Adolescent↗
PubMed1990

Increased hGH production rate after low-dose estrogen therapy in prepubertal girls with Turner's syndrome.

Low-dose estrogen therapy significantly increases radioimmunoassayable serum hGH concentrations in the prepubertal hypogonadal female. In this study, we have examined the effects of short- and long-term low-dose ethinyl estradiol therapy on the endogenous production rates and metabolic clearance rates of hGH. We used deconvolution mathematical modeling to provide quantitative estimates of individual secretory parameters and to calculate subject-specific hGH metabolic clearance rates, by using all serum hGH concentrations and their variances considered simultaneously. Nine girls with Turner's syndrome (mean age 7.7 +/- 0.5 y) were studied on three separate nights by drawing blood every 20 min from 2200 to 0800 h before (I), after 1 wk (II), and 5 wk (III) of 100 ng/kg/d ethinyl estradiol therapy orally. We found that the endogenous hGH production rate more than doubled in all patients studied after 5 wk of ethinyl estradiol therapy (194 +/- 22 (I), 290 +/- 43 (II), and 412 +/- 66 (III) micrograms/L/12 h; p less than 0.05 for I and III). The half-life of endogenous hGH was not altered in the estrogen treatment paradigm with a mean of 19 +/- 1.6 min in study I and 18 +/- 1.2 min in both studies II and III. Our results suggest that even prepubertal concentrations of gonadal steroids in the hypogonadal female may be physiologically relevant to the maintenance of normal somatotrope secretory function.

Child↗
PubMed1990

Atenolol enhances nocturnal growth hormone (GH) release in GH-deficient children during long term GH-releasing hormone therapy.

The effect of the selective beta 1-adrenergic blocking agent atenolol (50 or 100 mg, orally) on spontaneous and GH-releasing hormone (GHRH)-stimulated GH release was evaluated in six GH-deficient children during long term therapy with GHRH. Nocturnal GH concentrations were determined every 20 min for 12 h under the following four conditions: 1) control, 2) atenolol administration only, 3) sc GHRH administration only, and 4) combined GHRH and atenolol administration. The mean 12-h nocturnal GH concentrations after administration of atenolol alone [2.4 +/- 0.6 microgram/L (mean +/- SEM)] or GHRH alone (2.7 +/- 1.0 micrograms/L) were indistinguishable from baseline values (2.0 +/- 0.5 microgram/L; P greater than 0.05). In contrast, the addition of atenolol to ongoing GHRH therapy caused a clear augmentation of 12-h overnight GH release compared to that during all other study periods (5.0 +/- 1.3 micrograms/L; P less than 0.05). In a subset of three subjects for whom GH pulse characteristics were determined, the primary mode of the enhanced GH release was through an increase in the amplitude of serum GH pulses. These results are consistent with the hypothesis that beta-adrenergic blocking compounds enhance the responsivity of the pituitary gland to agents that permit GH release by inhibiting hypothalamic somatostatin secretion or action. They suggest that atenolol may have potential as an adjunctive therapy in some children with abnormalities of GH secretion when GHRH is the primary therapeutic agent.

Age Determination by Skeleton↗
PubMed1990

Testosterone and oxandrolone, a nonaromatizable androgen, specifically amplify the mass and rate of growth hormone (GH) secreted per burst without altering GH secretory burst duration or frequency or the GH half-life.

We investigated the mechanisms by which androgens increase mean circulating GH concentrations in boys. We tested two hypotheses: 1) testosterone increases serum GH concentrations at least in part via an androgen receptor-mediated mechanism, rather than exclusively by way of aromatization to estrogen; 2) androgen augments one or more specific features to GH secretion (secretory burst number, amplitude, and/or duration) and/or prolongs the half-life of GH removal. To examine these hypotheses, prepubertal boys with constitutionally delayed development and/or growth were given injections of testosterone (100 mg monthly; n = 7) or treated with oral oxandrolone, a nonaromatizable androgen (1.25 mg twice daily; n = 5). Pulsatile GH release was studied before and during androgen administration by sampling blood at 20-min intervals for 24 h. The immunoreactive GH time series were subjected to a novel deconvolution technique, which revealed that 1) testosterone and oxandrolone each increased mean (24-h) serum GH concentrations significantly; 2) both androgens augmented the daily endogenous GH secretory rate significantly; 3) increased GH production resulted from a higher mass of GH secreted per burst and a higher maximal rate of GH secretion within each burst; and 4) androgens amplified the magnitude of the nyctohemeral rhythm in the mass (but not frequency) of GH secretory pulses. The observed effects of androgen were specific, since the number and duration of GH secretory bursts and the subject-specific GH half-life were unaltered by androgen treatment. We conclude that androgen acting apart from conversion to estrogen is capable of specifically activating the somatotropic axis via distinct neuroendocrine secretory mechanisms.

Adolescent↗
PubMed1990

Reliability of estimates of pulsatile characteristics of luteinizing hormone and growth hormone release in women.

The test-retest reliability of estimates of pulsatile LH and GH release was evaluated in 23 eumenorrheic women during the early follicular phase of the menstrual cycle. Each subject was studied during two successive or near-successive menstrual cycles by repetitive blood sampling every 10 min for 24 h. Pulsatile parameters for LH and GH release were identified and characterized using the Cluster pulse detection algorithm. For LH, no significant differences existed in any parameter mean between the two 24-h admissions. Correlation coefficients for consecutive 24-h studies ranged from r = 0.22 (P less than 0.32) for number of LH peaks to r = 0.79 (P less than 0.0001) for 24-h integrated LH values (area under the concentration vs. time curve). No significant mean differences in any parameter were observed for consecutive 24-h GH evaluations. Correlation coefficients for 24-h GH ranged from r = 0.25 (P less than 0.34) for nadir to r = 0.71 (P less than 0.002) for incremental peak increase. Cosinor analysis was used to determine significant 24-h variations in LH and GH concentrations. Statistically significant differences existed between admissions for the amplitude of the nyctohemeral LH rhythm and its acrophase (time at which maximal hormone value was attained), but no mean differences were found for mesor (mean concentration). Correlation coefficients for LH were r = 0.10 (P less than 0.65), r = 0.43 (P less than 0.08), and r = 0.78 (P less than 0.0001) for phase, amplitude, and mesor, respectively. No significant mean differences existed for any parameter of nyctohemeral GH rhythms. Correlation coefficients were r = -0.18 (P less than 0.52), r = 0.49 (P less than 0.72), and r = 0.14 (P less than 0.80) for 24-h GH amplitude, phase, and mesor, respectively. We conclude that comparisons of mean and integrated LH and GH concentrations over a 24-h interval in the early follicular phase of the menstrual cycle are reliable; however, certain pulsatile properties responsible for the achievement of the mean daily concentrations of LH and GH may be nonuniform from menstrual cycle to menstrual cycle. In addition, nonuniformities may exist in the nyctohemeral rhythms of serum concentrations of LH and GH in the adult woman between cycles when a single 24-h time series is the basis for the analysis.

Adult↗
PubMed1990

Physical exercise and menstrual cycle alterations. What are the mechanisms?

The prevalence of menstrual cycle alterations in athletes is considerably higher than in sedentary controls. There appears to be a multicausal aetiology, which makes it extremely difficult to dissociate the effects of physical exercise on the menstrual cycle from the other predisposing factors. From cross-sectional studies it appeared that physical training eventually might lead to shortening of the luteal phase and secondary amenorrhoea. Prospective studies in both trained and previously untrained women have shown that the amount and/or the intensity of exercise has to exceed a certain limit in order to elicit this phenomenon. We hypothesise, therefore, that apart from a certain predisposition, athletes with a training-induced altered menstrual cycle are overreached (short term overtraining, which is reversible in days to weeks after training reduction). Menstrual cycle alterations are most likely caused by subtle changes in the episodic secretion pattern of luteinising hormone (LH) as have been found in sedentary women with hypothalamic amenorrhoea as well as in athletes after very demanding training. The altered LH secretion then, might be caused by an increased corticotrophin-releasing hormone (CRH) secretion which inhibits the gonadotrophin-releasing hormone (GnRH) release. In addition, increased CRH tone will lead to increased beta-endorphin levels which will also inhibit the GnRH signaller. Finally, the continuous activation of the adrenals will result in a higher catecholamine production, which may be converted to catecholestrogens. These compounds are known to be potent inhibitors of GnRH secretion. In conclusion, menstrual cycle alterations are likely to occur after very demanding training, which causes an increase secretion of antireproductive hormones. These hormones can inhibit the normal pulsatile secretion pattern of the gonadotrophins.

Amenorrhea↗
PubMed1989

Anabolic steroid therapies for growth disorders.

Until recently, human growth hormone was the only endocrine therapy available for promotion of growth and development. Dramatic progress in understanding the secretory and regulatory pathways pertinent to the anabolic steroids has led to multiple pharmacologic approaches. Growth hormone dynamics and its impact on therapy are discussed.

Anabolic Agents↗
PubMed1989

Treatment of the young child with postoperative central diabetes insipidus.

A continuous intravenous infusion of aqueous vasopressin (dosage range, 1.0 to 3.0 mU/kg/h) was administered to two patients (respective ages, 2 weeks and 3 years 1 month) who had postoperative central diabetes insipidus to determine if this mode of therapy is helpful in the very young patient. In both patients the polyuria and serum hyperosmolality were corrected. These findings suggest that an intravenous infusion of aqueous vasopressin can provide satisfactory control of the polyuria and electrolyte disturbances found in young children with acute postoperative central diabetes insipidus.

Brain↗
PubMed1989

Enhanced clearance of vancomycin by hemodialysis in a child.

Clearance of vancomycin by hemodialysis has previously been reported to be negligible. We describe a child undergoing chronic hemodialysis using a hollow fiber dialyzer with cellulose acetate membrane. When the patient was treated with intravenous vancomycin for staphylococcal bacteremia, the serum vancomycin half-life was found to decrease by more than 90% during each course of hemodialysis. We conclude that, contrary to prevailing opinion, vancomycin can be rapidly cleared by hemodialysis in the small pediatric patient, and that the dosage should be adjusted accordingly.

Child↗
PubMed1989

Androgen-dependent somatotroph function in a hypogonadal adolescent male: evidence for control of exogenous androgens on growth hormone release.

A 14(10/12)-year-old white male with primary gonadal failure following testicular irradiation for acute lymphocytic leukemia was evaluated for poor growth. He had received 2400 rad of prophylactic cranial irradiation. The growth velocity had decelerated from 7 to 3.2 cm/yr over 3 years. His bone age was 12(0/12) years (by TW2-RUS), and his peak growth hormone (GH) response to provocative stimuli was 1.4 ng/mL. The 24-hour GH secretion was studied by drawing blood every 20 minutes for 24 hours. The resulting GH profile was analyzed by a computerized pulse detection algorithm, CLUSTER. Timed serum GH samples were also obtained after a 1 microgram/kg IV bolus injection of the GH releasing factor (GRH). The studies showed a flat 24-hour profile and a peak GH response to GRH of 3.9 ng/ml. Testosterone enanthate treatment was started, 100 mg IM every 4 weeks. Ten months after the initiation of therapy the calculated growth rate was 8.6 cm/yr. The 24-hour GH study and GRH responses were repeated at the time, showing a remarkably normal 24-hour GH secretory pattern and a peak GH response to GRH of 14.4 ng/mL. Testosterone therapy was discontinued, and 4 months later similar studies were repeated. A marked decrease in the mean 24-hour GH secretion and mean peak height occurred, but with maintenance of the GH pulse frequency. The GH response to GRH was intermediate, with a peak of 8 ng/mL. There was no further growth during those 4 months despite open epiphyses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Growth hormone secretion by individual somatotropes of the testicular feminized rat.

To investigate the cellular mechanisms underlying the unique GH secretory apparatus of the androgen-resistant testicular feminized (Tfm) rat we employed a reverse hemolytic plaque assay to assess GH secretion by individual cells from normal male, normal female, and Tfm rats. Acutely dispersed pituitary cells were incubated for 90 min with GH anti-serum in the presence of medium alone, 0.01, 0.1, 1, 10, or 100 nM GHRH, or 3 microM forskolin after which hemolytic plaques were developed over an additional 30 min. Body weights of the Tfm rats [318 +/- 7 g (mean +/- SEM)] were intermediate between intact males (372 +/- 18 g) and females (218 +/- 7 g). The total number of cells recovered from dispersion of Tfm rat pituitaries [3.20 +/- 0.42 X 10(6) (mean +/- SEM)] was greater than that from males (1.43 +/- 0.12 X 10(6); P = 0.001), but not distinguishable from that from females (2.31 +/- 0.30 X 10(6); P = 0.06). However, the absolute population of recovered somatotropes from the Tfm animals (1.24 +/- 0.22 X 10(6) exceeded both male (0.56 +/- 0.10 X 10(6); P = 0.002) and female (0.80 +/- 0.14 X 10(6); P = 0.046) values. Mean basal and maximal GH plaque areas were greater for cells from male rats than for those from either female or Tfm rats (P less than 0.05) regardless of whether GHRH or forskolin was used as the secretagogue. Plaque areas from female and Tfm cells were indistinguishable under all study conditions. These data suggest that a deficiency of androgen receptors prevents establishment of the greater GH secretory capacity of individual somatotropes characteristic of the adult male rat. This androgen receptor-dependent modulation of GH secretory capacity appears to occur at a step distal to the GHRH receptor. The data also suggest that an increase in the absolute population of somatotropes is an additional consequence of androgen receptor deficiency. This combination of individual somatotropes, each possessing a GH secretory capacity similar to that of cells from normal females, but present in greater absolute numbers, may explain the intermediate values found during previous studies of the Tfm rat GH axis which were based on assessment of large mixed populations of pituitary cells.

Aging↗
PubMed1989

Somatostatin inhibition of growth hormone secretion by somatotropes from male, female, and androgen receptor-deficient rats: evidence for differing sensitivities.

To investigate the role of somatostatin (SRIF) in regulating sexually dimorphic GH secretion, we used a reverse hemolytic plaque assay and acutely dispersed somatotropes from age-matched normal male, normal female, and androgen receptor-deficient, testicular feminized (Tfm) rats. Hemolytic plaques were developed after a 90-min incubation in the presence of GH antiserum, 10 nM GH-releasing hormone (GHRH), and the following concentrations of SRIF: 0, 0.001, 0.003, 0.01, 0.03, 0.1, 0.3, 1, 3, 10, 30, and 100 nM. Additional studies were performed with 0 or 100 nM SRIF in the absence of GHRH. The absolute number of somatotropes (x10(6); mean +/- SEM) recovered from the pituitaries of Tfm rats (1.73 +/- 0.18) was significantly greater than that from the males (1.11 +/- 0.13; P = 0.01); the number from female rats (1.30 +/- 0.15) was not different from that of either male or Tfm animals. GHRH-stimulated GH secretion, as estimated by the mean GH plaque area (micron2 x 10(4); mean +/- SEM) in the absence of SRIF, was greater for somatotropes from male rats (3.36 +/- 0.41) than that for either Tfm (2.27 +/- 0.32; P = 0.02) or female (1.78 +/- 0.24; P = 0.001) rats; values for the latter two groups did not differ. However, mean GH plaque areas for each group during maximal SRIF inhibition in either the presence or absence of GHRH were indistinguishable from each other and from mean plaque areas obtained under basal conditions. As demonstrated by a lesser EC50 value (0.04 +/- 0.02 nM; mean +/- SEM), somatotropes from female rats were more sensitive to the inhibitory effect of SRIF than were those from either male (EC50 = 1.82 +/- 0.45; P = 0.0001) or Tfm (EC50 = 0.74 +/- 0.22, P = 0.0001) rats; values for the latter two groups were indistinguishable. These observed differences suggest that gender and/or the gonadal hormone environment may be important determinants of the inhibitory effects of SRIF on GH secretion by the somatotrope. While these gender-associated differences may represent effects of the gonadal hormones directly on the somatotrope, they could reflect modulation of the secretion of hypothalamic SRIF and/or GHRH by the prevailing gonadal hormone environment. Such gender-related differences may contribute to the overall sex-dependent patterns of GH secretion in the intact animal.

Androgen-Insensitivity Syndrome↗
PubMed1989

Alterations in the pulsatile properties of circulating growth hormone concentrations during puberty in boys.

To investigate the mechanisms subserving physiological alterations in circulating GH concentrations during puberty, we assessed the GH pulse characteristics of 60 24-h serum GH profiles obtained from healthy male volunteers of normal stature (aged 7-27 yr) whose physical development spanned the entire pubertal range. Subjects were divided into five study groups based on degree of sexual maturation. The mean 24-h concentration of GH was greater in late pubertal boys than in all other groups (P less than 0.001). This elevation primarily reflected a greater size, rather than number, of GH pulses, whether assessed as mean GH pulse area (P = 0.004 vs. all other groups), mean GH pulse amplitude (P = 0.001), or sum of the GH pulse areas (P less than 0.001). GH pulse frequency was indistinguishable among all groups (P greater than 0.05). However, circadian GH rhythms varied significantly in amplitude and mean values (but not in phase) throughout puberty. Plasma insulin-like growth factor-I levels were greatest in the late pubertal boys (1.98 +/- 0.15 U/mL) and remained elevated in the postpubertal group (1.44 +/- 0.18). The mean value for the adult men (0.74 +/- 0.06) was indistinguishable from that of prepubertal boys (0.90 +/- 0.13). In addition, all assessed characteristics of GH pulses and circadian rhythms in adults were equal to or less than corresponding values in prepubertal boys. We conclude that circulating GH concentrations transiently increase during mid- to late puberty in normal boys, primarily through augmentation of the size of GH pulses, but return to or below prepubertal levels during early adulthood.

Adolescent↗
PubMed1989

Specific, time-dependent actions of low-dose ethinyl estradiol administration on the episodic release of growth hormone, follicle-stimulating hormone, and luteinizing hormone in prepubertal girls with Turner's syndrome.

To investigate the actions of acute and chronic low doses of ethinyl estradiol (EE) on the pulsatile characteristics of GH and gonadotropin release we studied seven girls with Turner's syndrome [mean age, 7.5 +/- 0.75 (+/- SE) yr] on 3 separate study days. At baseline (study I), blood was drawn every 20 min from 2000-0800 h for GH, LH, and FSH determinations. One month after study I the patients were started on 100 ng/kg EE, orally, daily, and an identical study was repeated 1 week (study II) and 5 weeks (study III) from the initiation of low dose EE therapy. A pulse detection algorithm, Cluster, was used to objectively analyze pulsatility profiles. There were consistent and significant increases in all seven patients after 5 weeks of low dose EE therapy in mean GH concentrations (study I, 7.0 +/- 1.1 micrograms/L; study III, 13.4 +/- 1.7; P = 0.008), mean area under the GH pulse (study I, 602 +/- 52 micrograms/L.min; study III, 1350 +/- 261; P = 0.026), and mean GH pulse amplitude (study I, 14.0 +/- 2.2 micrograms/L; study III, 32.8 +/- 6.0; P = 0.018); with no detectable changes in GH pulse frequency (study I, 5.3 +/- 0.6 pulses/12 h; study III, 5.3 +/- 0.4). These findings were not accompanied by any significant changes in plasma somatomedin-C or serum estradiol concentrations or urinary cytological maturation indexes. Conversely, the amount of radioimmunoassayable FSH activity was suppressed after low dose EE therapy, with a decrease in mean FSH concentrations (study I, 23.5 +/- 6.6 IU/L; study III, 5.9 +/- 1.2; P = 0.035) and mean pulse amplitude (study I, 28.6 +/- 8.6 IU/L; study III, 8.2 +/- 1.8; P = 0.038), with no detectable changes in FSH pulse frequency (study I, 7.6 +/- 0.6 pulses/12 h; study III, 7.3 +/- 0.6). Similar qualitative changes in LH pulsatility were observed after low dose estradiol administration. In conclusion, our results demonstrate that low dose EE therapy results in a significant augmentation of pulsatile GH activity, with reciprocal decreases in gonadotropin concentrations in girls with Turner's syndrome. Such observations indicate an exquisite sensitivity of gonadotrope and somatotrope function to low dose estrogen action in this prepubertal hypogonadal model.

Adolescent↗
PubMed1989

Insulin and phorbol ester induce distinct phosphorylations of pp60c-src in the BC3H-1 murine myocyte cell line.

Insulin and phorbol esters have been shown to produce similar, non-additive metabolic effects in BC3H-1 murine myocytes. Recently, it has been demonstrated that insulin stimulation of these cells increases production of diacylglycerol, a known activator of protein kinase C (PK-C). To determine if insulin stimulation results in the activation of PK-C, we have examined the effects of insulin and the tumor promoting phorbol ester, 12-0-tetradecanoyl-phorbol-13-acetate (TPA), on the phosphorylation of a known PK-C substrate in vivo, the cellular proto-oncogene product, pp60c-src. Differentiated BC3H-1 monocytes showed an approximate twofold elevation in the [32P] content of pp60c-src following stimulation with insulin or TPA for 20 min, with no detectable change in the level of immunoprecipitable c-src protein. The enhanced phosphorylation in response to each agent localized to serine residues in the amino terminal 16 kD staphylococcal V8 proteolytic fragment. Tryptic phosphopeptide analysis revealed that TPA stimulation resulted in an approximate 18-fold increase in phosphorylation of the serine 12-containing tryptic fragment. Insulin stimulation, however, resulted in an approximate 10-fold increase in phosphorylation of the serine 17-containing tryptic fragment with little or no accompanying increase in serine 12 phosphorylation. In cells exposed to high concentrations of TPA for 16 h to deplete PK-C activity, insulin, but not TPA, stimulated phosphorylation of pp60c-src. These data suggest that insulin and phorbol ester induce phosphorylation of pp60c-src by distinct protein kinases.

Animals↗