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Biomedical subjects

W B Zipf

Publications and source records attributed to W B Zipf.

51 records · Page 3Linked to original sources
PubMed1981

Blunted pancreatic polypeptide responses in children with obesity of Prader-Willi syndrome.

Serum pancreatic polypeptide (PP), gastric inhibitory polypeptide (GIP), insulin and glucose responses to meal stimulation were studied in 10 normal weight patients, 13 normal obese patients and 7 patients with Prader-Willi syndrome (PWS) associated obesity. Serum and plasma concentrations of PP, glucose, insulin and GIP were obtained at 15 min intervals from 0-180 min. after a 275 K calorie meal. Basal and peak responses of glucose, for patients with PWS were significantly lower when compared to normal or obese controls. Basal and peak insulin responses in PWS were significantly greater than those of the normal controls but still less than those of the obese controls. Basal GIP concentrations in the patients with PWS were significantly less than normals and their peak response was less than the obese control group. No significant differences in basal or peak PP responses were noted between normal and obese controls. All 7 patients with PWS had abnormal PP responses. Five failed to show significant PP release after the stimulation; one had a peak response to 130 pg/ml while the 7th patient (PB) had an exaggerated response to 2000 pg/ml. The 6 patients with low or no response had basal PP values of 62 +/- 12 pg/ml and a mean PP peak response of 78 +/- 15 pg/ml. This observation of blunted PP response in a human model of hyperphagia and obesity parallels the animal models and suggests PP may have a significant role in appetite control.

Adolescent↗
PubMed1980

Hormonal and clinical responses to prednisone treatment in adolescents with congenital adrenal hyperplasia.

The effects of prednisone therapy and the withdrawal of prednisone for 3 days on hormonal relationships was investigated in 6 adolescent patients, age 10--19 years with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency. Prednisone continuously suppressed adrenal release of 17 alpha-hydroxyprogesterone (17-OHP) in 4 patients and adequately controlled 17-oxosteroid (17-OS) excretion in 5. Serum dehydroepiandrosterone sulfate (DS) concentrations were not elevated during or 3 days after withdrawal of medication. Growth hormone (GH) secretion was not suppressed by prednisone. Withdrawal of treatment was associated with a decrease in the follicle-stimulating hormone (FSH) to luteinizing hormone (LH) ratio in 5 patients and a rise in serum testosterone in 4. The clinical courses of these patients emphasize the difficulty in achieving optimum control.

17-Ketosteroids↗
PubMed1979

The effect of synthetic androgens on the hypothalamic-pituitary-gonadal axis in boys with constitutionally delayed growth.

Serial concentrations of basal serum LH, FSH, testosterone, and LH and FSH responses to intravenous gonadotropin-releasing hormone were measured before and during six months of administration of fluoxymesterone or oxandrolone in 14 boys with constitutionally delayed growth and adolescence, in order to assess the effects of these androgens on maturation of the hypothalamic-pituitary-gonadal axis. Before therapy all boys had normal hormonal responses based on bone age. At the end of six months therapy 10 of the 14 boys had lower LH responses (34 to 89% reduction) to GnRH without consistent changes in FSH responses. With both androgens, there there was significant suppression of both basal serum FSH and testosterone. Eleven boys were restudied six months after completion of therapy; basal serum LH, FSH, and testosterone and responses to GnRH were equal to or greater than pretreatment levels, indicating recovery or progressive maturation of the HPGA. All boys had increased growth velocity and imporved weight gain without excessive bone age advancement; all had improved psychosocial adjustment.

Adolescent↗
PubMed1979

Suppressed responsiveness to gonadotropin-releasing hormone in girls with unsustained isosexual precocity.

Eleven girls, ages 10/12 to 76/12 years, were evaluated because of early and rapid breast development. Initial clinical presentations and serum gonadotropin or estradiol determinations did not differentiate patient types. However, patients could be divided into two groups based on their responses to synthetic gonadotropin-releasing hormone: Group A consisted of seven girls with suppressed or prepubertail-type responses, and Group B consisted of four girls with pubertal or adult-type responses. Subsequent evaluation revealed that Group A patients had intermittent or unsustained isosexual precocity, whereas Group B patients had isiopathic prococious puberty. During initial evaluation, increased serum or urinary estrogen values were noted in ten of ten patients who were studied. The greatest serum E2 values (162 and 117 pg/ml) were noted in two Group A patients; three months and two years later, those patients had normal prepubertal responses to GnRH and serum E2 values of less than 4 and 14 pg/ml, respectively. Unsustained sexual precocoity in girls may be secondary to autonomous ovarian production of estrogens, and the GnRH test may be useful in evaluation of girls with isosexual precocity.

Child↗
PubMed1978

Dissociation of lutropin-induced loss of testicular lutropin receptors and lutropin-induced desensitization of testosterone synthesis.

The relationship between changes in testicular lutropin receptors, as measured by specific binding of 125I-labeled human chorionic gonadotropin, and testosterone synthesis in response to lutropin (testicular responsiveness) was studied in intact and hypophysectomized rats. Administration of a single 200-microgram dose of ovine lutropin to intact rats results at 3 days in a 58% decrease in lutropin receptors associated with a parallel decrease in testicular responsiveness. A single 30-microgram dose of lutropin to intact rats resulted in a comparable decrease in lutropin receptors with a transient increase in testicular responsiveness. Rats receiving twice-daily injections of 15 microgram lutropin for 10 days exhibited a 48% decrease in lutropin receptors by day 3 which persisted during the 10-day treatment period, but was accompanied by a progressive increase in testicular responsiveness to lutropin. Hypophysectomy resulted in an 80% loss of receptors and a 72% loss in responsiveness 7 days after surgery. Daily treatment with lutropin initiated immediately following surgery resulted in a further dose-dependent decrease in lutropin receptors and a dose-dependent increase in testicular responsiveness. Loss of lutropin receptors was not due to occupancy of the receptor by exogenous lutropin. These studies demonstrate a dissociation between the negative regulation of lutropin receptors and testicular responsiveness to lutropin. Furthermore, the studies in hypophysectomized rats indicate that lutropin is the only hormone essential for maintenance of steroidogenesis and that this is independent of lutropin receptor concentration.

Animals↗
PubMed1978

Sexual precocity in association with septo-optic dysplasia and hypothalamic hypopituitarism.

Sexual precocity in association with abnormalities of the central nervous system is well known, but its occurrence with hypothalamic hypopituitarism is most unusual. We report five females with septo-optic dysplasia, blindness, and multiple pituitary tropic hormone deficiencies: all were growth hormone and adrenocorticotropic hormone deficient; two had diabetes insipidus; one had sexual precocity, and one had early pubertal maturation, whereas three were prepubertal and responded to administration of synthetic gonadotropin-releasing hormone. These children retained ability to secrete gonadotropins despite the presence of anterior hypothalamic disease. Experimental data from primates plus our observations on these patients raise questions about the role of the anterior hypothalamus in gonadotropin secretion in man.

Adolescent↗
PubMed1977

Variable X-linked recessive hypopituitarism with evidence of gonadotropin deficiency in two pre-pubertal males.

Two half-brothers with short stature secondary to growth hormone deficiency and a family history implicating X-linked transmission were studied extensively for other endocrine abnormalities. The proband had a normal physical examination, except for small stature and small external genitalia. ACTH and TSH release were normal. LH and FSH responses during an i.v. GnRH test were severely blunted. His half-brother also had a normal physical examination, except for severe short stature and very small external genitalia. Deficiencies of ACTH, and TSH as well as GH were documented. An i.v. GnRH test showed no LH or FSH response. These studies support the existence of an X-linked recessive form of hypopituitarism and portend the clinical usefulness of the i.v. GnRH test in evaluating gonadotropin reserve.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Characteristics of prolactin-modulated LH induction of LH/hCG receptors. Transient inhibition of receptor induction following prolactin exposure.

The temporal relationship between exposure to prolactin (PRL) and luteinizing hormone (LH) induction of LH receptors was investigated in hypophysectomized adult male rats. Testicular homogenate membrane preparations were incubated with [125I]hCG for analysis of LH/hCG binding. Seven days after hypophysectomy, the rats were injected with 100 micrograms/day of PRL for another 7 days and then given a single 10-micrograms dose of LH at 2, 4, 6, 12, 24, or 36 hours after the last PRL injection. The priming effect of PRL on LH induction of receptors was not observed if LH was administered 2 to 12 hours from the last PRL injection. However, after this inhibitory period, injections of LH to PRL-primed rats resulted in induction of LH receptors and the effect persisted for 36 hours. This study supports previous reports demonstrating a unique dependence upon PRL for LH up-regulation of the LH receptor and characterizes the brief refractory period following exposure to PRL.

Animals↗
PubMedDate not supplied

Sex steroid inhibition of LH induction of the LH receptor.

Testosterone and estrogen were tested as possible mediators of the prolactin-dependent LH induction of LH receptors in hypophysectomized adult male rats. Animals were injected s.c. with saline, prolactin (100 micrograms/day), or combinations of testosterone (1 mg/day) or estrogen (1 mg/day) and prolactin for 7 days following a 7-day period of hypophysectomy. Twenty-four hours after the last saline or prolactin injection, the animals were given a single i.p. injection of either saline or oLH (10 micrograms) to evaluate LH-induced LH receptor induction. Membrane preparations from testicular homogenates were incubated with [125I]hCG as the binding ligand for determination of the receptor response and capacity. Neither testosterone nor estrogen were able to mimic the ability of prolactin to allow LH to induce the LH receptor. However, both testosterone and estrogen significantly inhibited prolactin-mediated, LH induction of its homologous receptor.

Animals↗
PubMedDate not supplied

Pancreatic polypeptide infusions reduce food intake in Prader-Willi syndrome.

Prader-Willi syndrome is characterized by dramatic hyperphagia and morbid obesity, and is associated with a deficiency in basal and meal-stimulated serum pancreatic polypeptide (PP) levels. Intravenous infusions of pancreatic polypeptide (90 min, 50 pmol/kg/h) restored normal serum PP levels, and a regimen of morning and afternoon PP infusions was found to significantly reduce food intake in Prader-Willi subjects. Food intake was evaluated in a 60-min free-feeding test that shows high reliability and validity. Basal food intake during saline infusions was striking (approximately 60 chicken sandwich quarters), and this intake was reduced overall by approximately 12% during PP infusions. This reduction was apparent only for female subjects, and may have reflected enhanced satiation rather than an overall suppression of food intake. No differences were apparent across subjects, in either basal food intake or the PP-related decrease in food intake, in the presence or absence of the widely recognized chromosomal marker for this syndrome [deletion of 15(q11-q13)]. More specific gene defects as recently reported in these subjects, however, suggest that the Prader-Willi syndrome may represent an important model for the study of food intake regulation.

Child↗
PubMedDate not supplied

Feeding-induced changes in energy expenditure in children with cystic fibrosis.

Seven children with cystic fibrosis (aged 7 to 12 years) were studied in the fasted and fed states. Using a primed, constant, intravenous infusion of NaH13CO3, the rate of appearance of CO2 (RaCO2) was estimated. Net CO2 excretion (VCO2) was also measured. Energy expenditure was calculated using the food quotient. RaCO2 (mean +/- SD) (mumol.kg-1.min-1) in the fasted and fed states (297 +/- 59 and 359 +/- 67) was 117% and 105% of VCO2 (259 +/- 48 and 352 +/- 72). Feeding induced a 23% and a 37% increase in RaCO2 and VCO2, respectively, and respective 19% and 33% increases in energy expenditure (p < .05). Measurement of CO2 production by isotopic dilution is a useful index of group changes in energy expenditure, including those induced by feeding.

Body Temperature Regulation↗
PubMedDate not supplied

Hypocalcemia, hypomagnesemia, and transient hypoparathyroidism during therapy with potassium phosphate in diabetic ketoacidosis.

The effects of intravenous administration of potassium phosphate in the treatment of diabetic ketoacidosis were studied in nine children, ages 9 9/12 to 17 10/12 yr. During phosphate infusion (20--40 meq/L of fluid), all children maintained normal serum concentrations of phosphorus. Transient hypocalcemia occurred in six and transient hypomagnesemia in five patients. One child developed carpopedal spasms refractory to intravenous infusion of calcium gluconate but responsive to intramuscular injection of magnesium sulfate. In three patients, serum levels of intact parathyroid hormone were low at the time of hypocalcemia, an observation that suggests transient hypoparathyroidism. This study indicates that the use of potassium phosphate as the sole source of potassium replacement might potentiate ketoacidosis-induced hypocalcemia through multiple mechanisms.

Adolescent↗