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PubMed2006

Predictors of optical density of lutein and zeaxanthin in retinas of older women in the Carotenoids in Age-Related Eye Disease Study, an ancillary study of the Women's Health Initiative.

BACKGROUND: Lifestyle, diet, and physical and health predictors of xanthophyll carotenoids in the retina are poorly understood. OBJECTIVE: We aimed to investigate the predictors of the density of lutein and zeaxanthin in the macula of the retina. DESIGN: Macular pigment optical density (MPOD) was measured by heterochromatic flicker photometry. Relations to dietary lutein and zeaxanthin and to other predictors were measured in 1698 women aged 53-86 y. The women were members of observational study cohorts of the Women's Health Initiative at Iowa City, IA, Madison, WI, or Portland, OR, and participated in the Carotenoids in Age-Related Eye Disease Study (2001-2004). RESULTS: MPOD at 0.5 degrees from the foveal center was 30% higher in women in the highest quintile for lutein and zeaxanthin intake [x (+/-SD): 0.40 +/- 0.21] than in women in the lowest quintile (0.31 +/- 0.21) and 20% higher after adjustment for other predictors. Dietary intake of lutein, zeaxanthin, fiber, and polyunsaturated fatty acids (% of energy) together explained 3% of the variability in MPOD. Higher waist circumference and diabetes, which are related to lower MPOD, together with study site explained an additional 5% of variation. The total explained variability increased to 12% when lutein and zexanthin concentrations obtained from the serum, which were collected 4-7 y earlier, were added to the model. CONCLUSIONS: MPOD is directly related to dietary intake of lutein and zeaxanthin but even more strongly to serum concentrations, which may reflect unmeasured physical and medical factors that influence the uptake, distribution, and utilization of lutein and zeaxanthin. Higher abdominal body fat and diabetes are related to lower MPOD. Unknown predictors of retinal carotenoids remain.

Aged↗
PubMed2003

Lutein and zeaxanthin dietary supplements raise macular pigment density and serum concentrations of these carotenoids in humans.

Age-related macular degeneration (AMD) is thought to be the result of a lifetime of oxidative insult that results in photoreceptor death within the macula. Increased risk of AMD may result from low levels of lutein and zeaxanthin (macular pigment) in the diet, serum or retina, and excessive exposure to blue light. Through its light-screening capacity and antioxidant activity, macular pigment may reduce photooxidation in the central retina. Lutein supplements, at 30 mg/d, were shown previously to increase serum lutein and macular pigment density in two subjects. In this study, we compared the effects of a range of lutein doses (2.4- 30 mg/d), as well as a high zeaxanthin dose (30 mg/d), on the serum and macular pigment in a series of experiments. Serum carotenoids were quantified by HPLC. Macular pigment densities were determined psychophysically. Serum lutein concentrations in each subject reached a plateau that was correlated with the dose (r = 0.82, P < 0.001). Plateau concentrations ranged from 2.8 x 10(-7) to 2.7 x 10(-6) mol/L. Zeaxanthin was less well absorbed than an equal lutein dose, resulting in plateaus of approximately 5 x 10(-7) mol/L. The rate of increase in macular pigment optical density was correlated with the plateau concentration of carotenoids in the serum (r = 0.58, P < 0.001), but not with the presupplementation optical density (r = 0.13, P = 0.21). The mean rate of increase was (3.42 +/- 0.80) x 10(5) mAU/d per unit concentration (mol/L) of carotenoids in the serum. It remains to be demonstrated whether lutein or zeaxanthin dietary supplements reduce the incidence of AMD.

Adult↗
PubMed2004

Assessment of lutein bioavailability from meals and a supplement using simulated digestion and caco-2 human intestinal cells.

Lutein and zeaxanthin are selectively accumulated in the lens and macular region of the retina. It was suggested that these xanthophylls protect ocular tissues from free-radical damage that can cause cataracts and age-related macular degeneration. Insights regarding the absorption of dietary xanthophylls for delivery to ocular tissues are limited. Our primary objective was to examine factors affecting the transfer of lutein from foods to absorptive intestinal epithelial cells during digestion. Lutein and other carotenoids present in spinach purée and lutein from a commercial supplement were relatively stable during in vitro digestion. Micellarization of lutein and zeaxanthin during the small intestinal phase of digestion exceeded that of beta-carotene and was greater for xanthophylls in oil-based supplements than in spinach. Apical uptake of lutein from micelles by Caco-2 human intestinal cells was linear for at least 8 h, and accumulation from synthetic micelles exceeded that from micelles generated during simulated digestion. Stimulation of chylomicron synthesis resulted in the secretion of 7.6 +/- 0.1% of cellular lutein into the triglyceride-rich fraction in the basolateral chamber. These data support the use of simulated digestion and the Caco-2 cell model as effective tools for identifying factors affecting absorption of dietary carotenoids.

Biological Availability↗
PubMed2004

Correlates of serum lutein + zeaxanthin: findings from the Third National Health and Nutrition Examination Survey.

The determinants of blood levels of carotenoids were previously investigated in small or select samples. The relations of serum lutein + zeaxanthin to possible diet, lifestyle, and physiological determinants in 7059 participants of the Third National Health and Nutrition Examination Survey (1988-1994), > or = 40 y old, were examined. In a fully adjusted, multiple linear regression model, lower serum lutein + zeaxanthin was significantly associated with smoking, heavy drinking, being white, female, or not being physically active, having lower dietary lutein + zeaxanthin, higher fat-free mass, a higher percentage of fat mass, a higher waist-hip ratio, lower serum cholesterol, a higher white blood cell count, and high levels of C-reactive protein (P < 0.05). The model explained 24% of the variation present in serum lutein + zeaxanthin for the current sample. The correlation between dietary and serum lutein + zeaxanthin was 0.17 and increased to 0.18 after adjusting for the effects of given covariates. Each 10% increase in dietary lutein + zeaxanthin was associated with a 1% increase in serum conditional on other terms in the model. Many factors that influence the level of serum lutein + zeaxanthin remain unknown.

Alcohol Drinking↗
PubMed1995

Interleukin-1 beta (IL-1 beta) is increased in the follicular fluids of patients with premature luteinization.

PROBLEM: Most, but not all, studies indicate that premature luteinization correlates with poor pregnancy outcome in in-vitro fertilization (IVF) programs. It remains unclear whether cytokines (IL-1 beta, TNF alpha), the established immune mediators, play a role in regulation or initiation of an abnormal follicular or embryo development in patients with premature luteinization. METHODS: Levels of cytokines (IL-1 beta, TNF alpha), estradiol (E2) progesterone (P4), and androstenedione (A'ione) were examined in 18 preovulatory follicular fluid (FF) samples from patients with premature luteinization (group 1) and 3 FF samples from patients without premature luteinization (group 2). The number of oocytes recovered, fertilization rate, and pregnancy outcome were evaluated in these two groups. RESULT: IL-1 beta (25.4 +/ 11.9 pg/ml, mean +/ SD) and TNF alpha (13.4 +/ 10.7 pg/ml) were present in these FF samples. The mean level of IL-1 beta in group 1 was significantly higher than that in group 2 (37.3 +/ 12.3 vs. 20.0 +/ 7.6 pg/ml; P < 0.00001) and the mean level of E2 was significantly lower in group 1 than that in group 2 (1064 +/ 686 vs. 1570 +/ 641 ng/ml; P = 0.02). The levels of TNF alpha, P4, and A'ione showed no distinction between these two groups. There was no correlation between the levels of either IL-1 beta or TNF alpha and P4, E2 or A'ione. The fertilization rate in group 1 (62/77; 80%) was similar to that in group 2 (124/160; 78%). Five of 7 patients in group 1 and seven of 20 patients in group 2 achieved pregnancy following embryo transfer. One of five pregnancies in group 1 aborted. CONCLUSION: The exaggerated levels of IL-1 beta in patients with premature luteinization may arise from accumulation of this cytokine owing to sustained high LH stimulation, and this may be a protective response to the abnormal LH surge and function to inhibit prematurely increased secretion of P4. These data indicate the important role of LH in the induction of IL-1 beta secretion and the possible regulatory action of IL-1 beta in luteinization. According to the diminution of E2 in group 1, there may be a subtle atretic process progressing in follicles primed with prematurely elevated LH. However, the detrimental effect of premature luteinization, if it exists, may work at the stage ¿during or after implantation.

Abortion, Spontaneous↗
PubMed2006

The effect of lutein and zeaxanthin supplementation on metabolites of these carotenoids in the serum of persons aged 60 or older.

PURPOSE: To investigate the effect of lutein supplementation at doses of 2.5, 5.0, and 10 mg/d for 6 months on distribution of these carotenoids and their metabolites in the serum of elderly human subjects, with and without age-related macular degeneration. To determine whether supplementation with lutein can interact with the serum levels of other dietary carotenoids, retinol, and alpha-tocopherol. METHODS: Forty-five subjects received daily supplements of lutein (containing 5% zeaxanthin) for 6 months and were followed up for another 6 months after supplementation. Blood was collected at various intervals and lutein, zeaxanthin, and their metabolites in the sera were quantified by normal-phase high-performance liquid chromatography (HPLC)-UV/visible detection. Other dietary carotenoids, retinol, and alpha-tocopherol were identified and quantified on a C18 reversed phase HPLC column. RESULTS: After 6 months of supplementation with 10 mg of lutein, the increases in the mean serum levels from baseline were: 210 to 1000 nM/L (P < 0.0001) for lutein and 56 to 95 nM/L (P < 0.0001) for zeaxanthin. Similarly, the mean concentrations (nM/L) of carotenoid metabolites increased from 49 to 98 (P < 0.0001) for 3-hydroxy-beta,epsilon-caroten-3'-one (3'-oxolutein); 31 to 80 (P < 0.0001) for 3'-hydroxy-epsilon,epsilon-caroten-3-one; and 19 to 25 (P < 0.0001) for epsilon,epsilon-carotene-3,3'-dione. The serum levels of these carotenoids gradually decline within 6 months after supplementation. CONCLUSIONS: The increase in the serum levels of lutein/zeaxanthin correlates with increases in the serum levels of their metabolites that have previously been identified in the ocular tissues. Elderly human subjects with and without AMD can safely take supplements of lutein up to 10 mg/d for 6 months with no apparent toxicity or side effects.

Aged↗
PubMed1975

The morphological transformation and inhibition of growth of bovine luteal cells in tissue culture induced by luteinizing hormone and dibutyryl cyclic AMP.

The luteal cells obtained from bovine corpus luteum by enzymatic treatment have been maintained in tissue culture. When the cells were maintained in the absence of luteinizing hormone or dibutyryl cyclic AMP, they grew parallel to one another and were elongated, thus giving to the culture a fibroblastic appearance. No contact inhibition was observed and the progestin secretion rate was low (3 pg per cell per day). In contrast, when luteinizing hormone or dibutyryl cyclic AMP was present, the cells became polygonal, growing as a monolayer and taking the appearance of epithelial cells. In this case contact inhibition was observed. The rate of progestin secretion was 250 pg per cell per day. As soon as luteinizing hormone or dibutyryl cyclic AMP was removed from the media, the cells reverted to a fibroblastic appearance. Agents such as colcemid, vinblastin or cytochalasin B inhibited the morphological effect of luteinizing hormone or dibutyryl cyclic AMP. Since those agents are known to inhibit the assembly of microtubules, the data suggest that LH and dibutyryl cyclic AMP act by promoting the organization of microtubules from protein monomers. This microtubular system (cytoskeleton) is responsible for the morphological appearance of the cells. Concomitant with the morphological changes induced by luteinizing hormone and dibutyryl cyclic AMP an inhibition in the growth rate of luteal cells was observed. It suggests that by raising the intracellular level of cyclic AMP the luteinizing hormone inhibits the division of luteal cells and is not, for that reason, a mitogenic agent. A similar effect was obtained with other agents known to stimulate cyclic AMP production such asthe prostaglandins. Steroids such as glucocorticoids and testosterone but not progesterone also inhibited the growth rate. It is concluded that luteinizing hormone by controlling the level of cyclic AMP within the luteal cells is responsible for the expression of the phenotype of the cells and the maintenance of differentiation.

Animals↗
PubMed1986

Enhanced precision of estrus and luteinizing hormone after progesterone and prostaglandin in heifers.

Objectives were to determine if low progesterone and increased basal luteinizing hormone for 3 d after injecting prostaglandin F2 alpha would affect precision of preovulatory surges of luteinizing hormone and onset of estrus in Holstein heifers. In experiments 1 and 2, heifers received progesterone devices for 10 d and prostaglandin F2 alpha on the 7th d after inserting progesterone device. For controls, progesterone devices were removed when prostaglandin F2 alpha was injected, and control devices were installed for 3 d. In experiment 1, jugular blood was sampled every 2 or 4 h from injection of prostaglandin F2 alpha until 108 h after removing progesterone to determine basal and peak secretion of luteinizing hormone. In treatment heifers, basal luteinizing hormone tended to increase, and intervals to peak secretion of luteinizing hormone were shorter and more precise than for controls. In experiment 2, heifers were observed for estrus for 30 min every 4 h for 96 h after removing progesterone devices. Intervals to onset of estrus for experimental heifers were shorter and more precise than for controls. After exogenous prostaglandin F2 alpha, 1 to 2 ng of progesterone per milliliter of serum for 2 to 3 d allows increased basal luteinizing hormone and is associated with increased precision of preovulatory secretion of luteinizing hormone and onset of estrus. This may be an acceptable method to control ovulation precisely for fixed time insemination of cattle.

Animals↗
PubMed2000

Lutein and zeaxanthin concentrations in rod outer segment membranes from perifoveal and peripheral human retina.

PURPOSE: In addition to acting as an optical filter, macular (carotenoid) pigment has been hypothesized to function as an antioxidant in the human retina by inhibiting the peroxidation of long-chain polyunsaturated fatty acids. However, at its location of highest density in the inner (prereceptoral) layers of the foveal retina, a specific requirement for antioxidant protection would not be predicted. The purpose of this study was to determine whether lutein and zeaxanthin, the major carotenoids comprising the macular pigment, are present in rod outer segment (ROS) membranes where the concentration of long-chain polyunsaturated fatty acids, and susceptibility to oxidation, is highest. METHODS: Retinas from human donor eyes were dissected to obtain two regions: an annular ring of 1.5- to 4-mm eccentricity representing the area centralis excluding the fovea (perifoveal retina) and the remaining retina outside this region (peripheral retina). ROS and residual (ROS-depleted) retinal membranes were isolated from these regions by differential centrifugation and their purity checked by polyacrylamide gel electrophoresis and fatty acid analysis. Lutein and zeaxanthin were analyzed by high-performance liquid chromatography and their concentrations expressed relative to membrane protein. Preparation of membranes and analysis of carotenoids were performed in parallel on bovine retinas for comparison to a nonprimate species. Carotenoid concentrations were also determined for retinal pigment epithelium harvested from human eyes. RESULTS: ROS membranes prepared from perifoveal and peripheral regions of human retina were found to be of high purity as indicated by the presence of a dense opsin band on protein gels. Fatty acid analysis of human ROS membranes showed a characteristic enrichment of docosahexaenoic acid relative to residual membranes. Membranes prepared from bovine retinas had protein profiles and fatty acid composition similar to those from human retinas. Carotenoid analysis showed that lutein and zeaxanthin were present in ROS and residual human retinal membranes. The combined concentration of lutein plus zeaxanthin was 70% higher in human ROS than in residual membranes. Lutein plus zeaxanthin in human ROS membranes was 2.7 times more concentrated in the perifoveal than the peripheral retinal region. Lutein and zeaxanthin were consistently detected in human retinal pigment epithelium at relatively low concentrations. CONCLUSIONS: The presence of lutein and zeaxanthin in human ROS membranes raises the possibility that they function as antioxidants in this cell compartment. The finding of a higher concentration of these carotenoids in ROS of the perifoveal retina lends support to their proposed protective role in age-related macular degeneration.

Aged↗
PubMed2001

Absorption and tissue distribution of zeaxanthin and lutein in rhesus monkeys after taking Fructus lycii (Gou Qi Zi) extract.

PURPOSE: To study serum and tissue levels of zeaxanthin and lutein after feeding rhesus monkeys an extract of Fructus lycii (gou qi zi). METHODS: A carotenoid-containing fraction (P1) from an extract of F. lycii (equivalent to 2.2 mg zeaxanthin) was fed to three rhesus monkeys for 6 weeks as a daily dietary supplement through a nasogastric tube. Three other monkeys were fed with the vehicle (olive oil) similarly for 4 weeks as a control. Another three animals were fed with normal diet only. All animals were killed 4 hours after the last dose. Samples of serum, liver, spleen, brain, and retina were analyzed for zeaxanthin and lutein by high-pressure liquid chromatography. RESULTS: The basal levels of zeaxanthin and lutein in the monkey sera were 3.0 +/- 1.6 ng/ml (range, 2.3-4.8) and 31.5 +/- 12.2 ng/ml (range, 22.3-42.5), respectively. Serum levels of zeaxanthin and lutein in the P1-fed group were significantly higher than those of vehicle control (P<0.05). Besides the retina, the liver had the highest zeaxanthin and lutein levels, whereas the levels in the brain were undetectable. P1 supplement appeared to elevate zeaxanthin levels in liver and spleen. The level of lutein was higher than that of zeaxanthin in the maculae of rhesus monkeys. However, there were no detectable carotenoids in the peripheral and the equatorial regions of the monkey retina. P1 treatment elevated zeaxanthin density but not lutein in the macula. CONCLUSIONS: Serum levels and macular density of zeaxanthin was raised by feeding a carotenoid-containing fraction of F. lycii. Therefore, F. lycii is a good dietary source of zeaxanthin supplement.

Animals↗
PubMed1975

On the regulation of rat testicular steroidogenesis. Short term effect of luteinizing hormone and cycloheximide in vivo and Ca2+ in vitro on steroid production in cell-free systems.

An attempt has been made to correlate the rapid effect of luteinizing hormone on testicular steroid production in vivo with testicular steroid concentrations and in vitro steroid production rates in testis tissue preparations. Within 20 min after intravenous administration of 25 mug luteinizing hormone, increases were observed in testosterone concentrations in testicular venous plasma and in whole testis tissue and in pregnenlone concentrations isolated testis mitochondrial fractions. Testosterone production by whole testis homogenates and pregnenolone production by isolated mitochondrial fractions were significantly increased within 5 min after in vivo administration of luteinizing hormone. Injection of cycloheximide 10 min prior to luteinizing hormone prevented the stimulating effect of luteinizing hormone to steroid levels in testicular venous plasma and testis tissue and on steroid production rates by preparations of rat testis tissue. Cycloheximide treatment of control animals did not significantly alter testosterone concentrations and testosterone production rates vitro, although mitochondrial pregnenolone concentrations and production rates were decreased. Testosterone production by whole testis homogenates as well as the pregnenolone production by isolated mitochondrial fractions obtained from luteinizing hormone treated testes and control glands showed a biphasic time curve A period (5-10 min) of high steroid production was followed by a period lower steroid production. Addition of 25 mug luteinizing hormone or 10(-8)--10(-5) M adenosine 3':5'-monophosphate (cyclic AMP) to the incubation medium had no effect pregnenolone production by isolated mitochondrial fractions. Administration of leuteinizing hormone in vivo markedly enhance the stimulating effect of Ca2+ on testosterone production by whole testis homogenates and on pregnenolone production by isolated mitochondrial fractions.

Animals↗
PubMed1989

Differential role of protein kinase C in the action of luteinizing hormone-releasing hormone on hormone production in rat ovarian cells.

This study was undertaken to determine the involvement of arachidonic acid and protein kinase C in the actions of luteinizing hormone-releasing hormone on steroid and prostaglandin formation in the ovary. In primary culture of rat granulosa cells, treatment with 3 x 10(-7) mol/L melittin stimulates progesterone and prostaglandin E2 accumulation after a 5-hour culture period. Concomitant treatment of the cells with melittin and luteinizing hormone-releasing hormone or 12-0-tetradecanoylphorbol 13-acetate further enhances the stimulatory action of either luteinizing hormone-releasing hormone or 12-0-tetradecanoylphorbol 13-acetate by itself on prostaglandin E2 production. In contrast, no synergistic effects are observed on progesterone production by the same treatments. Treatment with luteinizing hormone-releasing hormone for 24 hours significantly decreases follicle-stimulating hormone-induced progesterone production by approximately 50%. Treatment of the cells with either follicle-stimulating hormone or luteinizing hormone-releasing hormone stimulates prostaglandin E2 production at least tenfold in the same cultures. When follicle-stimulating hormone and luteinizing hormone-releasing hormone are present concomitantly, they synergistically enhance prostaglandin E2 formation (p less than 0.01). Similar effects are observed with the phorbol ester, 12-0-tetradecanoylphorbol 13-acetate, which causes a dose-dependent inhibition of progesterone production by follicle-stimulating hormone whereas follicle-stimulating hormone-stimulated prostaglandin E2 formation is enhanced. Thus luteinizing hormone-releasing hormone-induced activation of protein kinase C may play multiple roles (stimulatory or inhibitory) in hormone production in the ovary.

Animals↗
PubMed1985

Effects of an analog of PGF2(alpha) (ONO-1052) on cows with luteinized ovarian cysts following treatment with GnRH analog (fertirelin acetate).

Effects of PGF2(alpha) analog (ONO-1052) on cows with luteinized cysts following treatment with GnRH analog (fertirelin) in inducing estrus and shortening an interval from treatment to conception were investigated in a field trial. Seventy-five cows with follicular cysts diagnosed by rectal palpation were treated intramuscularly (i.m.) with 400 mug fertirelin (an analog of GnRH). Luteinization of follicular cysts were tentatively judged by rectal palpation. Forty-one cows were considered to have luteinized cysts and were either treated i.m. with ONO-1052 (28 cows) or left untreated as controls (13 cows). Thirty-four other cows were considered to have not responded to fertirelin and retreated with 10,000 MU hCG (19 cows) or fertirelin (five cows). This tentative judgment of luteinization of the cysts by rectal palpation after treatment was later confirmed by determining serum progesterone concentration before and 10 to 14 days after treatment. Only in the cows with luteinized cysts which were confirmed by serum progesterone analysis; increased from a pretreatment level below 1.0 ng/ml to a value of 1.0 ng/ml or higher 10 to 14 days after treatment, effects of ONO-1052 combined with fertirelin were investigated. Of the 18 cows with luteinized cysts thus confirmed following fertirelin injection and treated with ONO-1052, 15 (83.3 %) cows came into estrus within 26 +/- 14 (mean +/- SD) days after the first treatment; eight cows within three to five days and four cows within 22 to 28 days, and 14 cows (77.8 %) conceived within 100 days (42 +/- 26 days). On the other hand, the five control cows with luteinized cysts that were not treated with ONO-1052 required significantly longer to exhibit normal estrus (54 +/- 13 days; P<0.05) and to conceive (54 +/- 13 days). These results indicate that ONO-1052 combined with fertirelin may be useful to shorten the interval from treatment to normal estrus and to conception in cows with follicular cysts.

Journal Article↗
PubMed1985

Demonstration of serotoninergic axons terminating on luteinizing hormone-releasing hormone neurons in the preoptic area of the rat using a combination of immunocytochemistry and high resolution autoradiography.

The synaptic relationship between serotoninergic terminals and luteinizing hormone-releasing hormone-containing neurons was investigated in the medial preoptic area using a combined technique. Axon terminals selectively taking up 5-[3H]hydroxytryptamine were labelled autoradiographically and luteinizing hormone-releasing hormone-containing neuronal elements were identified by means of immunocytochemistry. Synaptic contacts were observed between tritiated 5-hydroxytryptamine-labelled boutons and luteinizing hormone-releasing hormone-immunoreactive dendrites. About 5% of the boutons which formed synapses with luteinizing hormone-releasing hormone-immunoreactive dendrites were found to be labelled by the tritiated indolamine. Luteinizing hormone-releasing hormone-immunoreactive axon terminals occurred as presynaptic elements in contact with unidentified dendritic spines, shafts or perikarya. These observations provide morphological basis for the idea that 5-hydroxytryptamine-containing neurons can act directly on luteinizing hormone-releasing hormone release. Further, they support the assumption that luteinizing hormone-releasing hormone is not only a neurohormone but may also function as a neurotransmitter or neuromodulator.

Animals↗
PubMed1992

Electron microscopic identification of luteinizing hormone-releasing hormone-immunoreactive neurons in the medial olfactory placode and basal forebrain of embryonic mice.

Luteinizing hormone-releasing hormone is a decapeptide found in the brain and nose of all vertebrates that have been examined by immunocytochemical procedures with antiserum to luteinizing hormone-releasing hormone. It regulates the release of both luteinizing hormone and follicle-stimulating hormone from the gonadotropes of the anterior pituitary gland and promotes mating behavior. After about 11 days of embryogenesis in mice, luteinizing hormone-releasing hormone-immunoreactive cells are detected by immunocytochemical procedures in the medial olfactory placode, in the primordium of the vomeronasal organ. As they leave the olfactory placode, they run under the epithelial layer of the nasal septum associated with vomeronasal and terminalis nerves. Clustered, they stream toward the primordium of the olfactory bulb, passing along its ventromedial surface. Eventually, the largest numbers reach the septal and preoptic areas of the brain. Electron microscopic immunocytochemistry showed that luteinizing hormone-releasing hormone-immunoreactive product is accumulated just outside the nuclear envelope and in the lumen of rough endoplasmic reticulum adjacent to the cell nucleus of cells in and adjacent to the olfactory placode. As luteinizing hormone-releasing hormone-immunoreactive neurons migrate, they assume a fusiform shape and the immunoreaction product extends from the area around the nucleus throughout the cytoplasm, notably in processes which extend toward the direction of migration. Before and during migration, luteinizing hormone-releasing hormone was not detected in the Golgi apparatus or neurosecretory granules. It is inferred that as far as ultrastructural evidence is concerned, these neurons do not have a secretory function before they attain their target organs.

Animals↗
PubMed1984

A comparison of a powerful luteinizing hormone releasing hormone analogue agonist and estrogen in the treatment of advanced prostatic cancer.

Luteinizing hormone releasing hormone agonists presently are being evaluated in the treatment of patients with metastatic prostatic cancer. To determine the comparative benefits of a specific luteinizing hormone releasing hormone agonist [6-leu (1-9) luteinizing hormone releasing hormone nonapeptide ethylamide] relative to conventional estrogen therapy 23 patients with stage D2 prostatic cancer were randomized to receive either 1 mg. luteinizing hormone releasing hormone agonist daily (12) or 3 mg. diethylstilbestrol per day (11). Both agents were effective in inducing a remission in all patients, although diethylstilbestrol was slightly faster. The early phase of treatment with the luteinizing hormone releasing hormone agonist was dominated by a transient reversible deterioration (the flare) of the patient, which was believed to be related to the agonist-induced increase in serum androgens. At 1 year of followup adverse effects in both groups have been minor but the proportion of patients with progression in the luteinizing hormone releasing hormone agonist group (6 of 12) was significantly higher than that in the diethylstilbestrol group (0 of 11). Further investigation is required to determine the role of luteinizing hormone releasing hormone agonist in the treatment of patients with advanced prostatic cancer.

Aged↗
PubMed1983

The treatment of metastatic prostatic cancer with a potent luteinizing hormone releasing hormone analogue.

Metastatic prostatic cancer generally is treated by either castration or the administration of exogenous estrogens, both of which have significant clinical disadvantages. Luteinizing hormone releasing hormone analogues have been shown to suppress gonadal steroidogenesis in animals and humans. To assess the effect of the administration of a potent luteinizing hormone releasing hormone analogue, (D-Leu-6)luteinizing hormone releasing hormone (1-9) nonapeptide ethylamide, 9 patients with previously untreated stage D2 prostatic cancer were treated with this agent for 3 to 8 months. By 3 months of treatment all patients demonstrated a significant decrease in serum testosterone and a decreased peak serum luteinizing hormone and testosterone response to the acute administration of the analogue, with no change in baseline serum luteinizing hormone or prolactin. These data suggest that this analogue acts by decreasing the pituitary release of luteinizing hormone. No major adverse effects were noted with this treatment modality, and all patients were symptomatically improved and demonstrated a decrease or stabilization in tumor activity as measured by prostatic computerized tomography or ultrasound scan, prostatic acid phosphatase and bone scan. A representative case is presented. Luteinizing hormone releasing hormone analogues may prove to be valuable new agents in the treatment of advanced prostatic cancer.

Aged↗
PubMed1999

Insulin and insulin-like growth factor-I and -II modulate human granulosa-lutein cell steroidogenesis: enhancement of steroidogenic acute regulatory protein (StAR) expression.

Insulin and insulin-like growth factors (IGF)-I and -II stimulate granulosa cell steroidogenesis. Since steroidogenic acute regulatory protein (StAR) regulates the rate-limiting step in steroid hormone biosynthesis, the ability of insulin and IGF to modulate StAR protein and mRNA expression was examined in two human granulosa cell culture systems: (i) proliferating granulosa-lutein cells and (ii) luteinized-granulosa cells derived during in-vitro fertilization (IVF). In proliferating granulosa-lutein cells, IGF-I and IGF-II increased StAR protein approximately 4-5-fold, while insulin and 8-bromoadenosine 3',5'-cAMP (8-Br-cAMP) increased amounts of StAR protein 2.5- and 6-fold respectively. A combination of IGFs/insulin and 8-Br-cAMP increased StAR 7-9-fold. Luteinized granulosa cells also had increased StAR expression after treatment with IGF-I (2. 8-fold), IGF-II (3-fold), insulin (2.5-fold) and 8-Br-cAMP (4. 5-fold). Progesterone production generally followed a pattern similar to StAR protein in both cell systems. In proliferating granulosa-lutein cells, both IGF-I and insulin increased StAR mRNA (3-fold) and 8-Br-cAMP increased StAR mRNA 4-fold, whereas a combination of IGF-I and 8-Br-cAMP had an additive effect on StAR mRNA expression (7-fold). Transient transfection of proliferating granulosa-lutein cells with StAR promoter-luciferase reporter constructs demonstrated that IGF-I, IGF-II, and insulin had no effect on the StAR promoter activity, while 8-Br-cAMP stimulated StAR promoter function. The results indicate that: (i) IGFs and insulin stimulate StAR mRNA and protein expression in human granulosa-lutein cells; (ii) IGF-I and 8-Br-cAMP have an additive effect on StAR gene expression; and (iii) IGF-I increases StAR mRNA and protein by a mechanism that does not involve activation of the proximal StAR gene promoter.

Blotting, Northern↗