bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spontaneous Nocturnal Growth Hormone Secretion in Anorexia Nervosa
Authors: Scacchi Massimo , Pincelli Angela I. , Caumo Andrea , Tomasi Paolo , Delitala Giuseppe , Baldi Gabriella , Cavagnini Francesco 
Published: January 2014

Abstract
In anorexia nervosa, serum GH levels are increased under basal conditions and respond abnormally to provocative stimuli. We report here, for the first time, an analysis of pulsatile GH secretion in these patients performed by Cluster algorithm. Seven anorectic and six normal weight, healthy women underwent serial blood sampling at 20-min intervals from 2030–0830 h for GH estimation. The total area under the curve (AUC; micrograms per L/min) was elevated 4-fold in anorectic patients compared to controls (4743.0 ± 1520.09 vs. 1148.6 ± 519.27; P &lt; 0.01), largely due to an increase in the nonpulsatile fraction (3212.5 ± 990.45 vs. 378.7 ± 123.27; P &lt; 0.01). Accordingly, the valley mean value was higher in anorectic than in control subjects (5.9 ± 2.25 vs. 1.0 ± 1.30 μg/L; P &lt; 0.01). Furthermore, pulsatile AUC was also greater in anorectic patients (1530.4 ± 654.72 vs. 769.8 ± 404.02; P &lt; 0.01) due to a significant increase in GH peak frequency (5.0 ± 0.81 vs. 3.0 ± 0.89; P &lt; 0.01). No correlations were observed in these patients between body mass index and any of the parameters of spontaneous GH release, whereas a positive correlation was found between insulin-like growth factor I levels and pulsatile AUC (r2 = 0.583; P &lt; 0.05), peak height (r2 = 0.743; P = 0.01), peak increment (r2 = 0.801; P &lt; 0.01), and GH valley mean (r2 = 0.576; P &lt; 0.05).
In conclusion, it appears that the enhanced GH secretion in anorexia nervosa is the result of an increased frequency of secretory pulses superimposed on enhanced tonic GH secretion. Although this latter is consistent with a reduction of hypothalamic SRIH tone, the former may be accounted for by an increased number of GHRH discharges. Considering that in normal weight and obese subjects parameters of GH release are negatively correlated with adiposity indexes, the lack of such a negative correlation in our patients suggests that the enhancement of spontaneous GH release in anorectic patients is not merely the consequence of malnutrition-dependent impairment of insulin-like growth factor I production, but reflects a more complex hypothalamic dysregulation of GH release.
Ovarian Origin of Plasma and Peritoneal Fluid Prorenin in Early Pregnancy and in Patients with Ovarian Hyperstimulation Syndrome*
Authors: Itskovitz-Eldor Joseph , Kol Shahar , Lewit Nathan , Sealey Jean E. 
Published: January 2014

AbstractProrenin is the major product of renin gene expression in the ovary. Plasma levels of prorenin are elevated in ovarian-stimulated patients and during early pregnancy. To further elucidate the source of the elevated plasma levels of prorenin, we measured prorenin, renin activity, angiotensinogen, and steroid hormone levels in the plasma, luteal fluids (luteal cysts), ascitic fluid, and in ovarian venous samples collected from a patient with severe ovarian hyperstimulation syndrome (OHSS) and ectopic pregnancy. Prorenin/renin was also measured in plasma and in peritoneal fluid obtained during therapeutic paracentesis from four patients with OHSS.Several corpora luteal fluids were obtained that were rich in estradiol (E2) and progesterone (P). Ovarian venous E2 and P were 20-fold higher than in arterial blood and as high or higher than the levels detected in the luteal fluids. The ratios of the hormonal levels in ascitic fluid and plasma were 1.9 for P and 1.4 for E2. A wide range of prorenin concentrations [1279 ± 918 sd ng/mL/hr, n = 6] were found in corpora luteal fluids, but in each the prorenin concentration was higher than in plasma (494 ng/mL/hr). Prorenin but not renin was higher (+23%) in ovarian venous than arterial blood. Prorenin in the 7 liters of ascitic fluid aspirated (2686 ng/mL/hr) was 5-fold higher than in plasma and similar to the levels measured in the corpora lutea with the highest prorenin concentrations. Renin in luteal cysts and ascitic fluid constituted 3% and 6% of the total renin (renin + prorenin), respectively. Total renin was also higher in peritoneal fluid (1538 ± 925 ng/mL/hr) than in plasma (375 ± 237 ng/mL/hr) of the 4 additional patients with severe OHSS.These findings indicate that the ovary secretes prorenin during early pregnancy and that its secretion is directed preferentially from the luteal cysts into the peritoneal cavity. In light of recent evidence of an effect of prorenin on the vascular system, the presence of a huge reservoir of prorenin in the peritoneal cavity of patients with OHSS suggests a potential role for prorenin in the pathogenesis of this syndrome.
Twenty-Four-Hour Profiles of Luteinizing Hormone, Follicle-Stimulating Hormone, Testosterone, and Estradiol Levels: A Semilongitudinal Study throughout Puberty in Healthy Boys*
Authors: Albertsson-Wikland Kerstin , Rosberg Sten , Lannering Birgitta , Dunkel Leo , Selstam Gunnar , Norjavaara Ensio 
Published: January 2014

Abstract
To follow and correlate gonadotropin and sex steroid changes throughout puberty, 24-h profiles of LH, FSH, testosterone, and estradiol were taken on several occasions for between 2–9.5 yr in 12 healthy boys, aged 8.7–18.2 yr. Serum concentrations of LH and FSH were measured every 20 min, whereas testosterone and estradiol were measured every 2–4 h during the 24-h period. The prepubertal boys (Tanner stage 1) were subdivided into two groups: Pre 1, with a testicular volume of 1–2 mL, and Pre 2, with a testicular volume of 3 mL. Pubertal stages were classified, according to testicular volume, as early puberty (pubertal stage 2; 4–9 mL), midpuberty (pubertal stages 3–4; 10–15 mL), and late puberty (pubertal stage 5; ≥16 mL). Mean levels of LH and FSH increased with pubertal development, although the increase in LH was greater than that in FSH. These increases were due to elevated basal levels of LH and FSH as well as to increases in the number of peaks and the peak amplitudes of LH. No diurnal rhythm was found in boys at stage Pre 1. Thereafter, a clear diurnal rhythm appeared for LH, and later in puberty, an ultradian rhythm was superimposed, as shown by time-sequence analyses. A diurnal rhythm also existed for FSH, but was much less marked than that for LH despite a clear covariation between LH and FSH, as shown from cross-correlation studies. Testosterone also showed diurnal variations from the late prepubertal stage, followed by increasing levels during both day and night in puberty.
We conclude that during puberty, gonadotropin levels rise differently for LH and FSH, which may be due to the development of differences in feedback mechanisms. Despite covariation between LH and FSH, only LH showed a clear diurnal variation. In parallel, nocturnal variations in testosterone and estradiol were found. Changes in mean levels of LH, testosterone, and estradiol as well as their mean daytime and nighttime levels follow each other from the prepubertal stages to late puberty.
Expression of Steroid Receptors and Steroidogenic Enzymes in the Baboon (Papio anubis) Corpus Luteum during the Menstrual Cycle and Early Pregnancy1
Authors: Hild-Petito Sheri , Fazleabas Asgerally T. 
Published: January 2014

Abstract
As estrogen and progesterone are proposed regulators of luteal function, this study was undertaken to correlate the presence of receptors for these steroids with luteal function during early pregnancy. Corpora lutea (CL) were obtained from nonpregnant baboons during the midluteal [ML; days 7–8 postovulation (PO)] and late luteal (LL; days 11–12 PO) phases of the menstrual cycle or from pregnant baboons on days 18, 25, 29, or 31–33 PO. Estrogen and progestin receptors (ER and PR, respectively) and 3β-hydroxysteroid dehydrogenase (3βHSD) were detected by immunocytochemistry using specific monoclonal (H222 for ER; JZB39 for PR) or polyclonal (S683 for 3βHSD) antibodies. In addition, ribonucleic acid (RNA) was extracted from CL, processed for Northern blot analysis, and probed with complementary DNAs to human PR, human 3βHSD, and rat aromatase. Levels of messenger RNA (mRNA) for 3βHSD were quantified by laser densitometric scanning, and the data were normalized to the expression of a housekeeping gene (glyceraldehyde-3-phosphate dehydrogenase) to correct for loading differences. CL did not demonstrate specific nuclear stain for ER at any stage of the menstrual cycle or pregnancy. In contrast, PR-positive cells were present during the ML phase, but decreased during the LL phase (P &lt; 0.05). PR-positive cells were maintained during early pregnancy at levels comparable to the ML phase (P &gt; 0.05). Staining for 3βHSD was present at all stages of the cycle and pregnancy. Although the percent of 3βHSD-positive cells appeared to decrease as pregnancy proceeded, this was not statistically different (P &gt; 0.05). The complementary DNA to PR hybridized to multiple transcripts (∼4.4, 3.1, 1.6, and 0.95 kilobases) in CL of the cycle. A single transcript (∼1.8 kilobases) for 3βHSD was present in CL at all stages of the cycle and pregnancy. The level of 3βHSD mRNA was highest during the ML phase and declined significantly (P &lt; 0.05) during the LL phase and early pregnancy. Three transcripts (∼3.6, 3.0, and 1.7 kilobases) for aromatase were detected in CL of the cycle and pregnancy. Aromatase mRNA increased during early pregnancy. These results support the concept of PR-mediated events, but not ER-regulated processes in the primate CL. Furthermore, the data suggest that the steroidogenic enzymes 3βHSD and aromatase are differentially regulated during early pregnancy.
Increased Plasma Leptin Concentration in End-Stage Renal Disease1
Authors: Merabet Eddine , Dagogo-Jack Samuel , Coyne Daniel W. , Klein Samuel , Santiago Julio V. , Hmiel S. Paul , Landt Michael 
Published: January 2014

Abstract
Leptin is a 16-kDa protein recently identified as the obese gene product involved in body weight regulation. Administration of recombinant leptin to ob/ob mice, which have a genetic defect in leptin production, reduces food intake and increases energy expenditure. Leptin is synthesized by fat cells, and in normal humans, plasma concentrations are proportional to adiposity. The physiological actions and the degradation pathways of leptin in humans are unknown. We investigated renal elimination of leptin by comparing plasma leptin concentrations in end-stage renal disease (ESRD) patients with normal controls. Our hypothesis was that if renal filtration is a significant route of elimination, the hormone would accumulate in ESRD patients. Mean plasma levels in 141 ESRD patients (26.8 ± 5.7 and 38.3 ± 5.6 μg/L for males and females, respectively) were significantly higher (P&lt; 0.001) than mean values obtained in normal controls (11.9 ± 3.1 and 21.2 ± 3.0 μg/L for males and females, respectively). Leptin concentrations in ESRD patients correlated directly with body mass index (BMI; r = 0.77 for men and 0.78 for women). The rate of increase in leptin concentrations with BMI was significantly greater in ESRD patients (5.5 and 6.6 μg/L/U BMI for men and women, respectively) than in normal controls (1.4 and 2.6 μg/L/U for men and women, respectively). Pre- and postdialysis leptin levels in hemodialysis patients were similar. Western blot of plasma from ESRD patients with high leptin levels showed bands corresponding to the intact protein (16 kDa) with no lesser or greater molecular mass species observed. Leptin concentrations in patients with ESRD did not correlate with measures of residual renal function (serum creatinine,β 2-microglobulin, PTH, or GH levels). Similarly, we found no correlation between leptin levels and the number of years patients had been on dialysis or with recent weight changes. We conclude that intact leptin is increased in ESRD patients, but does not appear to cause decreased weight. As leptin levels did not correlate with residual renal function, increased production may account for the high levels observed.
Immunohistochemical Localization of Gonadotropin and Gonadal Steroid Receptors in Human Pineal Glands1
Authors: Luboshitzky Rafael , Dharan Muralee , Goldman Dalia , Hiss Yehuda , Herer Paula , Lavie Peretz 
Published: January 2014

Abstract
Recently, we demonstrated that melatonin secretion was increased in male patients with GnRH deficiency and decreased to normal levels during testosterone treatment. These data suggested that gonadal steroids modulate melatonin secretion, probably by activating specific receptors in the pineal gland. We used immunohistochemistry to localize gonadotropin (LH and FSH) and gonadal steroid (androgens and estrogens) receptors in human pineal glands. Tissues were obtained at autopsy from 25 males, aged 19–87 yr, and five prepubertal children, aged 0.2–10 yr. Positive staining for all four types of receptors (LH, FSH, androgen, and estrogen) in the pineal parenchymal cells, pinealocytes, was evident in all 30 glands examined. Double staining revealed that nuclear receptors (androgen or estrogen) coexisted with cytoplasmatic receptors (LH or FSH) in the same cells. The results demonstrate the presence of gonadotropin and gonadal steroid receptors in human pinealocytes from infancy to old age.
Ribonucleic Acid Expression of the Clustered Imprinted Genes, p57KIP2, Insulin-Like Growth Factor II, and H19, in Adrenal Tumors and Cultured Adrenal Cells1
Authors: Liu Jianqi , Kahri Arvi I. , Heikkilä Päivi , Voutilainen Raimo 
Published: January 2014

Abstract
The recently cloned cyclin-dependent kinase inhibitor gene p57KIP2 is genomically imprinted and located on human chromosome 11p15.5. This region contains two other imprinted genes, insulin-like growth factor II (IGF-II) and H19, both of which seem to be implicated in adrenal neoplasms. We analyzed the expression of the putative tumor suppressor p57KIP2 gene by Northern blotting in normal and hyperplastic adrenals, adrenocortical tumors, and pheochromocytomas. The expression of p57KIP2 messenger ribonucleic acid (mRNA) correlated positively with H19 and negatively with IGF-II RNA in adrenocortical tissues. p57KIP2 mRNA (and H19 RNA) was abundantly expressed in normal human adrenals, adrenocortical adenomas from patients with Cushing’s or Conn’s syndrome or without clinical evidence of hormone overproduction, hyperplastic adrenals, and tumor-adjacent adrenal tissues, in which IGF-II mRNA expression was low. In most adrenocortical carcinomas and virilizing adrenal adenomas, very low levels of both p57KIP2 and H19 RNAs were observed, whereas IGF-II was highly expressed. In pheochromocytomas, p57KIP2 and H19 RNA expression was highly variable, but on the average it was about 45% and 27%, respectively, of that in normal and tumor-adjacent adrenals.
In cultured adrenocortical cells, ACTH and dibutyryl cAMP treatment slightly reduced the predominant 1.7-kilobase (kb) transcript of p57KIP2 gene, but induced a 2.5-kb transcript with a simultaneous increase in H19 RNA expression. The stimulatory effect of ACTH on the 2.5-kb p57KIP2 and H19 transcript accumulation was enhanced by exogenous IGF-II and IGF-I. Our data show that p57KIP2 and H19 RNAs are expressed usually in parallel in normal and pathological adrenocortical tissues. The decreased expression of both p57KIP2 and H19 RNAs in conjunction with elevated IGF-II mRNA expression in hormonally active adrenocortical carcinomas suggests that the loss of expression of the putative tumor suppressor genes p57KIP2 and H19 may be involved in the pathogenesis of these neoplasms.
Thyroid Hormone and Estrogen Receptor Expression in Normal Pituitary and Nonfunctioning Tumors of the Anterior Pituitary1
Authors: Gittoes Neil J. L. , McCabe Christopher J. , Verhaeg Julie , Sheppard Michael C. , Franklyn Jayne A. 
Published: January 2014

AbstractNonfunctioning tumors (NFTs) of the anterior pituitary often express elevated levels of the glycoprotein hormone α-subunit, which, under normal physiological conditions, is under negative feedback control by thyroid and gonadal steroid hormones. We postulate that inappropriately elevated levels of expression of α-subunit in the face of normal levels of these target organ hormones may reflect an abnormality of thyroid hormone receptors (TRs) and/or gonadal steroid receptors in NFTs. Using immunocytochemistry and Western blotting we have examined TR and estrogen receptor (ER) protein expression in normal human anterior pituitary glands and NFTs. Pretranslational expression of these receptors was examined using semiquantitative reverse transcriptase-PCR. Expression of all TR variant and ER proteins was reduced in pituitary tumors compared with that in normal pituitaries. The expression of messenger ribonucleic acids encoding the TRβ1 and TRβ2 isoforms and ER was also significantly reduced in tumors compared with normal tissues, although there was no difference between tumors and normals in the level of expression of TRα1 and α2 messenger ribonucleic acids. We suggest that reduced expression of TRs and ER may account for inappropriate expression of the glycoprotein hormoneα -subunit gene in some NFTs and may contribute to uncontrolled tumor growth.
Studies of the Impact of a Liver Glucokinase Promoter Variant on Glucose Tolerance and Insulin Sensitivity Index1
Authors: Urhammer Søren A. , Hansen Torben , Jensen Liselotte Brix , O. Clausen Jesper , Hansen Lars , Chui Ken C. , Pedersen Oluf 
Published: January 2014

Abstract
Because a frequently occurring nucleotide substitution at position− 258 in the liver glucokinase promoter has been reported to be associated with impaired promoter activity, we have examined in Danish Caucasians whether this variant is associated with alterations in glucose tolerance and/or the insulin sensitivity index (Si). Among 246 Danish Caucasian patients with noninsulin-dependent diabetes mellitus, the allelic frequency of the −258 promoter variant was 15.2% (95% confidence interval: 12.0–18.4%) vs. 16.5% (13.2–19.8%) among 242 matched control subjects. In the control group, the glucokinase variant was not related to serum insulin or plasma glucose levels before or during an oral glucose tolerance test. Neither was the gene variant among 380 young, healthy subjects associated with altered Si or altered insulin secretion after an iv glucose load. We conclude that in Danish Caucasians, the −258 glucokinase promoter variant has no impact on glucose tolerance, whole-body Si, or insulin secretion.
Testosterone Replacement in Older Hypogonadal Men: A 12-Month Randomized Controlled Trial
Authors: Sih Rahmawati , Morley John E. , Kaiser Fran E. , Perry Horace M. , Patrick Ping , Ross Candie 
Published: January 2014

Abstract
A decline in testicular function is recognized as a common occurrence in older men. However data are sparse regarding the effects of hypogonadism on age-associated physical and cognitive declines. This study was undertaken to examine the year-long effects of testosterone administration in this patient population.
Fifteen hypogonadal men (mean age 68 ± 6 yr) were randomly assigned to receive a placebo, and 17 hypogonadal men (mean age 65± 7 yr) were randomly assigned to receive testosterone. Hypogonadism was defined as a bioavailable testosterone &lt;60 ng/dL. The men received injections of placebo or 200 mg testosterone cypionate biweekly for 12 months. The main outcomes measured included grip strength, hemoglobin, prostate-specific antigen, leptin, and memory.
Testosterone improved bilateral grip strength (P &lt; 0.05 by ANOVA) and increased hemoglobin (P &lt; 0.001 by ANOVA). The men assigned to testosterone had greater decreases in leptin than those assigned to the control group (mean ± sem: −2.0 ± 0.9 ng/dL vs. 0.8 ± 0.7 ng/dL; P &lt; 0.02). There were no significant changes in prostate-specific antigen or memory. Three subjects receiving placebo and seven subjects receiving testosterone withdrew from the study. Three of those seven withdrew because of an abnormal elevation in hematocrit.
Testosterone supplementation improved strength, increased hemoglobin, and lowered leptin levels in older hypogonadal men. Testosterone may have a role in the treatment of frailty in males with hypogonadism; however, older men receiving testosterone must be carefully monitored because of its potential risks.
Insulin Secretion and Sensitivity in Black Versus White Prepubertal Healthy Children1
Authors: Arslanian Silva , Suprasongsin Chittiwat , Janosky Janine E. 
Published: January 2014

AbstractWe had previously demonstrated greater insulin secretion and lower insulin sensitivity in black pubertal adolescents compared with whites. This study aimed to investigate whether similar black/white differences are present in the prepubertal period or are characteristics of the pubertal period. Twelve black and 11 white healthy prepubertal children, matched for age, body mass index, and Tanner I pubertal development, underwent a 2-h hyperglycemic clamp (225 mg/dL). Physical fitness was assessed by maximal oxygen consumption (VO2max) measurement during graded bicycle ergometry, and resting energy expenditure was measured by indirect calorimetry after overnight fast.Fasting and first phase insulin concentrations were higher in blacks than in whites [14.7 ± 1.3 vs. 10.4 ± 1.2 (P = 0.02) and 76.9 ± 6.8 vs. 52.1 ± 6.4 μU/mL (P = 0.016)]. There were no differences in second phase insulin levels and insulin sensitivity index. Both maximal oxygen consumption (VO2max) and resting energy expenditure were lower in black children, whereas insulin-like growth factor I was higher. After controlling for these differences, race contributed significantly to basal insulin, but not to first phase insulin.In summary, previously reported black/white differences in insulin secretion and sensitivity during adolescence may have their origin in early childhood manifested as hyperinsulinemia. However, genetic (race) vs. environmental factors (physical activity/fitness and energy balance) should be carefully scrutinized as potential factors responsible for such differences.