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Biomedical subjects

W J Raum

Publications and source records attributed to W J Raum.

At least 19 recordsLinked to original sources
PubMed2000

The effect of an herbal dietary supplement containing ephedrine and caffeine on oxygen consumption in humans.

OBJECTIVE: To determine if an herbal dietary supplement for weight loss increases metabolism. DESIGN: Measurement of peak oxygen consumption in response to the supplement followed by a double-blind placebo-controlled crossover measurement of oxygen consumption in response to the supplement. SETTING: The study was conducted in an academic research clinic. SUBJECTS: Ten obese females (aged 41 +/- 4 years [body mass index (BMI)] 33.3 +/- 2.6 kg/m2) participated in the peak oxygen consumption test; six of these females participated in the crossover trial. INTERVENTIONS AND OUTCOME MEASURES: Peak oxygen consumption was measured for 45 minutes after taking two herbal dietary supplement capsules orally, each containing the equivalent of 10 mg of caffeine and 5 mg of ephedrine. The crossover trial measured oxygen consumption for 45 minutes after taking two herbal dietary supplement capsules or two placebo capsules orally. RESULTS: The herbal dietary supplement increased peak oxygen consumption 0.178 +/- 0.03 (SEM) kcal/min (8.01 +/- 1.35 kcal/min expressed over 45 minutes) above baseline (p < 0.0001), and 2.0 +/- 0.56 kcal/min over 45 minutes compared to placebo (p < 0.006). CONCLUSIONS: The herbal dietary supplement increased oxygen consumption when taken according to the package directions. The significance of this rise for weight loss requires further research.

Caffeine↗
PubMed1997

Potentially predictive and manipulable blood serum correlates of aging in the healthy human male: progressive decreases in bioavailable testosterone, dehydroepiandrosterone sulfate, and the ratio of insulin-like growth factor 1 to growth hormone.

A cross-sectional survey was made in 56 exceptionally healthy males, ranging in age from 20 to 84 years. Measurements were made of selected steroidal components and peptidic hormones in blood serum, and cognitive and physical tests were performed. Of those blood serum variables that gave highly significant negative correlations with age (r > -0.6), bioavailable testosterone (BT), dehydroepiandrosterone sulfate (DHEAS), and the ratio of insulin-like growth factor 1 (IGF-1) to growth hormone (GH) showed a stepwise pattern of age-related changes most closely resembling those of the age steps themselves. Of these, BT correlated best with significantly age-correlated cognitive and physical measures. Because DHEAS correlated well with BT and considerably less well than BT with the cognitive and physical measures, it seems likely that BT and/or substances to which BT gives rise in tissues play a more direct role in whatever processes are rate-limiting in the functions measured and that DHEAS relates more indirectly to these functions. The high correlation of IGF-1/GH with age, its relatively low correlation with BT, and the patterns of correlations of IGF-1/GH and BT with significantly age-correlated cognitive and physical measures suggest that the GH-IGF-1 axis and BT play independent roles in affecting these functions. Serial determinations made after oral ingestion of pregnenolone and data from the literature suggest there is interdependence of steroid metabolic systems with those operational in control of interrelations in the GH-IGF-1 axis. Longitudinal concurrent measurements of serum levels of BT, DHEAS, and IGF-1/GH together with detailed studies of their correlations with age-correlated functional measures may be useful in detecting early age-related dysregulations and may be helpful in devising ameliorative approaches.

Adult↗
PubMed1997

Dehydroepiandrosterone (DHEA) treatment of depression.

Dehydroepiandrosterone (DHEA) and its sulfate, DHEA-S, are plentiful adrenal steroid hormones that decrease with aging and may have significant neuropsychiatric effects. In this study, six middle-aged and elderly patients with major depression and low basal plasma DHEA f1p4or DHEA-S levels were openly administered DHEA (30-90 mg/d x 4 weeks) in doses sufficient to achieve circulating plasma levels observed in younger healthy individuals. Depression ratings, as well as aspects of memory performance significantly improved. One treatment-resistant patient received extended treatment with DHEA for 6 months: her depression ratings improved 48-72% and her semantic memory performance improved 63%. These measures returned to baseline after treatment ended. In both studies, improvements in depression ratings and memory performance were directly related to increases in plasma levels of DHEA and DHEA-S and to increases in their ratios with plasma cortisol levels. These preliminary data suggest DHEA may have antidepressant and promemory effects and should encourage double-blind trials in depressed patients.

Aged↗
PubMed1994

Higher calorie content preserves myocardial electrical activity during very-low-calorie dieting.

We investigated the effect of calorie and protein content of very-low-calorie diets for weight loss upon myocardial electrical activity. Patients were followed on very low calorie diets for up to 20 weeks. Study No. 1 had 16 obese patients (4 men and 12 women). Study No. 2 had 113 obese women. Both study groups were consecutive samples with patients who had BMI > 30. In Study No. 1 patients were given 400 kcal/d with 50 gm of protein and 45 gm of carbohydrates over 12 weeks. In Study No. 2 patients were given either Metabolic Nutrition Program (MNP) which contained 600 kcal/d with 70 gm protein and 70 gm carbohydrates, or Optifast-70 which contained 420 kcal/d with 70 gm protein and 32 gm carbohydrates, for up to 20 weeks. Electrocardiograms were obtained at baseline and during the third month in Study No. 1, and monthly in Study No. 2. The sum of the voltage in leads I+II+III and the length of the QT interval were derived from the electrocardiograms. In Study No. 1 the QRS voltage decreased from 2.77 +/- .18 mv to 2.45 +/- .17 mv (p < .02). Patients lost 18.1 kg +/- 4 kg and the QT interval remained unchanged. In Study No. 2 at 20 weeks the QRS voltage decreased on Optifast-70 (p < .001) in comparison to MNP, in which the QRS voltage remained unchanged. Patients on Optifast-70 lost 17.5 +/- .53 kg, patients on MNP lost 18.5 +/- .66 kg and the QT interval in both groups remained unchanged. The formula diets tested of less than 600 kcal/d were associated with a decrease in electrocardiographic voltage.

Adult↗
PubMed1994

Pheochromocytoma.

Explore the source record for details and available documents.

Adrenal Gland Neoplasms↗
PubMed1990

Prenatal inhibition of hypothalamic sex steroid uptake by cocaine: effects on neurobehavioral sexual differentiation in male rats.

Several adrenergically active drugs have been shown to prevent the masculinizing and/or defeminizing effects of testosterone on brain sexual differentiation. We examined the ability of the neuronal norepinephrine uptake blocker, cocaine, to produce similar effects. The ability of cocaine to inhibit sex steroid incorporation into the hypothalamus during a critical period for sexual differentiation of the brain was examined in females treated at birth with testosterone. Sixty minutes after administration, cocaine was observed to inhibit both testosterone and estradiol incorporation into the hypothalamus by approximately 50%. Long-term consequences of prenatal cocaine exposure were studied by injecting Sprague-Dawley dams twice daily with 3, 10 or 30 mg/kg of cocaine hydrochloride on days 15 through 20 of gestation and examining the offspring. In adulthood, cocaine-exposed males, but not females were found to exhibit significantly less marking behavior than controls. Cocaine-exposed males in the 10 mg/kg group tested for sex behavior exhibited demasculinization in some aspects of the behaviors tested. Measurement of plasma hormone levels in this group revealed elevated levels of plasma LH, but normal levels of FSH and testosterone. No differences were observed in cocaine-exposed males with respect to sex organ or adrenal weights, but thymus was approximately 25% smaller compared to control males at 80 days of age. In a separate experiment, dams were treated with 3 mg/kg of cocaine twice daily from days 15 through 21 of gestation and half of the male pups received additional injections twice a day for the first 5 days postnatally.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Lack of prenatal testosterone surge in fetal rats exposed to alcohol: alterations in testicular morphology and physiology.

Pregnant Sprague-Dawley rats were administered a liquid alcohol diet (35% ethanol-derived calories), a pair-fed isocaloric diet, or dry food pellets beginning on Day 14 of gestation and continuing until parturition. Testosterone levels in male fetuses were measured on Days 17 through 20 of gestation. The normal surge of testosterone on Days 18 and 19 was present in controls, but notably absent in male fetuses exposed to alcohol. Light microscopic examination of the testes at birth revealed a reduction in the number of leydig cells in the alcohol exposed group and the presence of a large number of vacuoles in the seminiferous tubules. In vitro studies of fetal testes at 18 and 22 days of gestation revealed that this in utero alcohol exposure regimen produced a marked insensitivity to rat LH (10 ng/ml) stimulation of testosterone secretion compared to controls. The response to ethanol (160 mg/dl) in alcohol exposed testes was characterized by a long-lasting suppression of testosterone compared to a large increase observed in control testes. No differences in anogenital distance were observed among the groups. Together, these data may explain some of the long-term feminizing and demasculinizing effects on reproductive and nonreproductive sexually dimorphic behaviors observed in adult males prenatally exposed to alcohol.

Anal Canal↗
PubMed1986

Norepinephrine turnover in brown adipose tissue is stimulated by a single meal.

A single meal stimulates brown adipose tissue (BAT) thermogenesis in rats. In the present study the role of norepinephrine in this thermogenic response was assessed from the rate of its turnover in BAT after a single test meal. For comparison, norepinephrine turnover was determined in the heart and spleen. A total of 48 male Wistar rats (200 g) were trained to eat during two feeding sessions per day. On the experimental day, one group (n = 24) was meal deprived and the other (n = 24) was given a low-protein high-carbohydrate test meal for 2 h. The synthesis inhibition method with alpha-methyl-p-tyrosine was employed to determine norepinephrine turnover from its concentration at four hourly time points after the meal. Tissue concentrations of norepinephrine were determined by radioimmunoassay. Norepinephrine concentration and turnover rate were increased more than threefold in BAT of the meal-fed compared with the meal-deprived rats (P less than 0.001 and P less than 0.005 for concentration and turnover, respectively). Neither were significantly altered by the meal in the heart or spleen. Other measures of turnover kinetics, turnover time and rate constant, were not significantly affected in any of the tissues examined. Our data suggest that norepinephrine mediates a portion of the thermic effect of meals that originate in BAT.

Adipose Tissue, Brown↗
PubMed1986

The effect of hypothalamic catecholamine synthesis inhibition by alpha-methyltyrosine on gonadotropin secretion during sexual maturation in the male Wistar rat.

alpha-Methyl-p-tyrosine (AMPT), a competitive inhibitor of tyrosine hydroxylase, was used to block the synthesis of hypothalamic catecholamines in six different age groups (15, 23, 30, 38, 56, and 72 days of age) in both intact and castrated male rats. Castrated rats received testosterone-filled Silastic capsules of various lengths to give four graded serum concentrations of testosterone in each age group. Intact and castrate animals of all ages were killed 1 week after the castrate group was orchiectomized and outfitted with Silastic capsules. On the day of death, 250 mg/kg BW AMPT base were given ip at zero time, and a second dose (125 mg/kg BW) was given 2 h after the first injection. Rats were killed at zero time and 2 and 4 h after the first AMPT injection. Serum was collected for LH, FSH, and testosterone determinations. AMPT had marked biphasic effects on LH and T secretion, causing both to increase (less than 70% above basal) in the intact immature rats (15 and 23 days of age) and fall (greater than 60% below basal) in the mature rats (38, 56, and 72 days of age). LH increased (up to 307%) in the castrated immature rats in response to AMPT, but no change occurred in the mature castrated rats until moderate concentrations of testosterone were present (1000-2000 pg/ml). Then, LH, as in intact rats, decreased (up to 90%) during exposure to AMPT. These data suggest that the ratio of stimulatory and inhibitory effects of hypothalamic norepinephrine and dopamine changes during sexual maturation, with inhibitory effects predominating in the prepubertal rat.

Age Factors↗
PubMed1986

Mechanism of action of dopamine on the in vitro release of gonadotropin-releasing hormone.

Controversy exists on whether dopamine (DA) stimulates or inhibits GnRH secretion and whether its effects are mediated via alpha-adrenergic receptors or dopaminergic receptors. As a means to examine this conflict, we have utilized an in vitro superfusion system to study the effects of DA, norepinephrine (NE), phentolamine (alpha-antagonist), pimozide (DA antagonist), and two DA agonists (apomorphine and bromocryptine) on GnRH release from isolated mediobasal hypothalami from adult male rats. In this dynamic system, graded concentrations of both NE and DA (2.0 nM to 2.0 microM) led to a dose-dependent increase in GnRH output during the 10 min interval that followed each pulse dose of NE (P less than 0.02) or DA (P less than 0.05). The DA-induced GnRH release was reproducible, consistent, and significant over five successive pulses (20 microM) at 30-min intervals (P less than 0.02). Coinfusion of phentolamine (20 microM) prevented the DA (20 microM) induced release of GnRH (P less than 0.03), but pimozide (20 microM) had no significant effect on DA-induced GnRH release (P greater than 0.3). The two DA agonists, apomorphine and bromocryptine, at doses up to 2.0 microM and 200 nM, respectively, had no significant effect on GnRH release. To determine whether DA was causing a direct stimulation of alpha-adrenergic receptors or being enzymatically converted to NE which could then stimulate alpha-receptors to induce GnRH release, rats were injected with sodium diethyldithiocarbamate (DDC) (550 mg/kg BW) ip, 1 h before death. DDC blocks the enzymatic conversion of DA to NE, and this was reflected by a 37% decrease in hypothalamic NE efflux during the superfusion. However, pulses of DA, even in the presence of DDC, were associated with a marked dose-dependent increase in hypothalamic NE efflux, and DDC failed to prevent the subsequent stimulation of GnRH release. We conclude that the apparent DA-induced release of GnRH is most probably attributable to DA-induced release of hypothalamic NE which, in turn, acts through alpha-adrenergic receptors on peptidergic neurons to stimulate GnRH release.

Animals↗
PubMed1984

Nuclear accumulation of estradiol derived from the aromatization of testosterone is inhibited by hypothalamic beta-receptor stimulation in the neonatal female rat.

We previously reported that hypothalamic beta-adrenergic receptor stimulation prevents testosterone (T)-induced androgenization (defeminization) of the female neonatal rat hypothalamus. It was hypothesized that hypothalamic beta-receptor stimulation blocks androgenization by reducing the nuclear accumulation of estradiol (E2) derived from the aromatization of T. Various adrenergic agonists and antagonists were injected intracerebrally in 4-day-old female rats. [3H] T and its 3H-metabolites (including E2) were extracted from hypothalamic nuclear pellets, and separated from one another with thin-layer chromatography and/or Celite chromatography. The ratio of recovered [3H] T and E2 in the control groups was arbitrarily assigned as a 100% conversion and nuclear accumulation. Phenoxybenzamine, an alpha-antagonist, and isoproterenol and isoxsuprine, beta-agonists, inhibited the nuclear accumulation of E2 to 66.7%, 69.0% and 85.0% of control, respectively. A nonadrenergic, specific, competitive aromatase inhibitor, 1,4,6-androstratrien-3,17-dione (ATD) inhibited aromatization (and subsequent nuclear accumulation) to 39.0% of control. The beta-antagonist, hydroxybenzylpindolol, specifically prevented the inhibition of nuclear accumulation produced by phenoxybenzamine, isoproterenol and isoxsuprine, but did not alter the inhibition of aromatization produced by ATD. These studies support the hypothesis that beta-receptor stimulation prevents androgenization of the brain by inhibiting either the aromatization of T to E2 or the nuclear uptake of E2.

Adrenergic beta-Agonists↗
PubMed1984

Chronic norepinephrine infusion and insulin and glucagon secretion in the dog.

The effect of epinephrine on glucose homeostasis has been studied extensively in many species, but there is little data on the effects of another catecholamine, norepinephrine. This study was designed to examine the alterations that occur in insulin and glucagon secretion during a chronic low-dose infusion of norepinephrine in free-roaming dogs. A total of four intravenous glucose tolerance tests and insulin-induced hypoglycemia tests were performed on each of five dogs infused with norepinephrine (1.4 g/min) for 3 mo and on each of eight control dogs. The infusion resulted in a threefold increase in plasma norepinephrine without a significant effect on blood pressure. Fasting serum glucose was elevated significantly in the norepinephrine-infused dogs [102.4 +/- 2.1 vs. 92.8 +/- 1.7 (SE) mg/100 ml]. Fasting plasma glucagon was elevated by the norepinephrine infusion (58.4 +/- 7.6 vs. 31.3 +/- 3.1 pg/ml), whereas fasting serum insulin was inhibited (12.3 +/- 1.3 vs 16.8 +/- 1.7 U/ml). Glucagon secretion in response to hypoglycemia was markedly enhanced in the infused dogs compared with controls. It has been reported that the infusion of norepinephrine in humans will inhibit insulin secretion and increase serum glucose concentrations but have no effect on serum glucagon concentrations. The stimulation of glucagon by norepinephrine has been demonstrated in the isolated, perfused canine pancreas but has not been reported previously in the free-roaming dog.

Adrenal Glands↗
PubMed1984

Methods of plasma catecholamine measurement including radioimmunoassay.

Fluorometric and radioenzymatic assays are presently the most widely used techniques for the estimation of plasma, urine, and tissue catecholamines. The fluorometric assay lacks specificity and sensitivity. The radioenzymatic assay is significantly more sensitive and specific but is technically very complex, time consuming, and expensive. A newer methodology has been developed by modification of a 125I radioimmunoassay for metanephrine. The assay utilizes an antibody that specifically binds metanephrine. Plasma and urinary epinephrine and norepinephrine are detected by conversion to metanephrine with the enzymes catechol-O-methyl-transferase (COMT) and phenylethanolamine-N-methyltransferase (PNMT). The major advantages of the radioimmunoassay are the savings in cost and time. The radioenzymatic assay utilizes an expensive tritium-labeled compound, S-adenosylmethionine, and requires multiple organic solvent-extraction steps, thin-layer chromatography, and liquid scintillation counting. The radioimmunoassay requires only one extraction with alumina to aid in specificity and to concentrate the catecholamines. Sample detection is by gamma counting. The radioenzymatic assay is presently the reference method for catecholamines and is best suited for small numbers of samples where sample volume is limited and exquisite sensitivity is required. The radioimmunoassay is rapid, has sufficient sensitivity, specificity, and precision for most applications and is best applied to the analysis of large numbers of samples.

Catechol O-Methyltransferase↗
PubMed1984

Norepinephrine increases beta-receptors and adenylate cyclase in canine myocardium.

Norepinephrine, a known inducer of myocardial hypertrophy, was found to have marked effects on the myocardial adrenergic system, which occurred prior to the development of a significant increase in heart weight. The chronic subhypertensive infusion (1.4 microgram/min) in free-roaming dogs produced a threefold increase in plasma norepinephrine (determined by radioimmunoassay). After 3 mo of infusion, right and left ventricular norepinephrine content (ng/mg protein) decreased significantly by twofold (right, 2.50 +/- 0.24; left, 2.08 +/- 0.36) compared with controls (right, 4.76 +/- 1.48; left, 4.65 +/- 1.49), and beta-receptor density (125I-pindolol) increased (right, 0.122 +/- 0.029; left, 0.153 +/- 0.021) over the controls (right, 0.082 +/- 0.015; left, 0.069 +/- 0.008 pmol/mg protein). Accompanying the beta-receptor changes, isoproterenol-stimulated adenylate cyclase activity also increased significantly [right, 29.2 +/- 2.1; left, 29.5 +/- 1.0 vs. controls, right, 13.8 +/- 1.1; left, 20.2 +/- 2.2 pmol adenosine 3',5'-cyclic monophosphate (cAMP) generated X min-1 X mg protein-1]. Because the above changes occurred in the absence of cardiac hypertrophy, it suggests that alterations in the myocardial adrenergic system are dependent on the stimulus (in this case norepinephrine) invoking the change and not the degree of hypertrophy. It also suggests that changes in the adrenergic system may not directly reflect the mechanism involved in the development of hypertrophy.

Adenylyl Cyclases↗
PubMed1983

Beta-adrenergic receptor and cyclic AMP alterations in the canine ventricular septum during long-term norepinephrine infusion: implications for hypertrophic cardiomyopathy.

Norepinephrine infusion in dogs has been shown to cause ventricular septal hypertrophy that mimics the syndrome of hypertrophic cardiomyopathy in humans. To characterize the mechanisms involved in septal hypertrophy, the adrenergic system of the right and left ventricles and the septum were analyzed before and after norepinephrine infusion. In the normal unperturbed state, the septum was found to be more sensitive to beta-adrenergic stimulation than either the right or left ventricles. That is, more cyclic AMP could be generated with a smaller dose of beta-agonist (isoproterenol) in septal tissue homogenate than in homogenates of the right or left ventricles. With infusions of norepinephrine (1.4 micrograms/min) to subhypertensive levels over 3 months, beta-receptor number increased twofold to threefold in the ventricles and septum. Adenylate cyclase activity also increased in the ventricles, but not in the septum. The sensitivity of adenylate cyclase to beta-agonist stimulation increased in the septum but remained unchanged in the right and left ventricles. We conclude that the alterations in the myocardial adrenergic system occur in response to the norepinephrine infusion and are not a consequence of hypertrophy. We formulated a hypothesis suggesting that depleted tissue stores of cyclic AMP and/or adenosine triphosphate may be one of the mechanisms involved in the development of hypertrophic cardiomyopathy.

Adenylyl Cyclases↗