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Results for “Luteinization”

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PubMed1998

Effect of simultaneous, single oral doses of beta-carotene with lutein or lycopene on the beta-carotene and retinyl ester responses in the triacylglycerol-rich lipoprotein fraction of men.

The effects of lutein and lycopene on beta-carotene absorption and cleavage were investigated in 12 male subjects. Responses of carotenoids and retinyl palmitate in the triacylglycerol-rich lipoprotein (TRL) fraction after a separate 15-mg beta-carotene dose were compared with those after a dose of 15 mg beta-carotene combined with 15 mg lycopene or lutein (given as natural concentrates or extracts). After combined dosing with lutein, the areas under the curve (AUCs) of beta-carotene and retinyl palmitate in the TRL fraction, adjusted for the triacylglycerol response, were 66% (P = 0.019) and 74% (P < 0.059), respectively, compared with 100% after dosing with beta-carotene alone. After combined dosing with lycopene these percentages were 90% and 101%, respectively (NS). Beta-carotene conversion, estimated from the ratio between the AUC for retinyl esters and beta-carotene, assuming eccentric cleavage, was 69%, 71%, and 72% for treatment with only beta-carotene, beta-carotene combined with lycopene, and beta-carotene combined with lutein, respectively. In addition, a pilot study was performed to evaluate application of TRL response curves to measure absorption of carotenoids from vegetable sources (15 mg carotenoid as carrots, spinach, and tomato paste). As compared with the carotenoid concentrates, responses were considerably lower or hardly measurable (beta-carotene and retinyl palmitate after carrots, lutein after spinach), except for lycopene and retinyl palmitate after a single dose of tomato paste. In conclusion, this study showed that lutein, but not lycopene, negatively affected beta-carotene absorption when given simultaneously with beta-carotene but apparently had no effect on beta-carotene cleavage.

Absorption↗

PubMed2000

Amount of fat in the diet affects bioavailability of lutein esters but not of alpha-carotene, beta-carotene, and vitamin E in humans.

BACKGROUND: Fat-soluble vitamin E and carotenoids are regarded as being protective against chronic diseases. Little is known about the effect of dietary fat on the bioavailability of these compounds. OBJECTIVE: The objective of this study was to assess the effect of the amount of dietary fat on plasma concentrations of vitamin E and carotenoids after supplementation with these compounds. DESIGN: During two 7-d periods, 4 groups of 14-15 volunteers received daily, with a low-fat hot meal, 1 of 4 different supplements: vitamin E (50 mg), alpha- plus beta-carotene (8 mg), lutein esters (8 mg lutein), or placebo. The supplements were provided in a low- or high-fat spread supplied in random sequence during either of the 2 experimental periods. RESULTS: As anticipated, plasma concentrations of vitamin E, alpha- and beta-carotene, and lutein were significantly higher in the supplemented groups than in the placebo group. The amount of dietary fat consumed with the hot meal (3 or 36 g) did not affect the increases in plasma concentrations of vitamin E (20% increase with the low-fat spread and 23% increase with the high-fat spread) or alpha- and beta-carotene (315% and 139% with the low-fat spread and 226% and 108% with the high-fat spread). The plasma lutein response was higher when lutein esters were consumed with the high-fat spread (207% increase) than with the low-fat spread (88% increase). CONCLUSION: Optimal uptake of vitamin E and alpha- and beta-carotene requires a limited amount of fat whereas the amount of fat required for optimal intestinal uptake of lutein esters is higher. 2000;71:-93.

Adolescent↗

PubMed1998

Human follicle fluid vascular endothelial growth factor concentrations are correlated with luteinization in spontaneously developing follicles.

Vascular endothelial growth factor (VEGF) is a cytokine that induces angiogenesis. Angiogenesis is a prominent histologic component of the luteinization process. Luteinization is also characterized by granulosa cell progesterone secretion in response to the luteinizing hormone (LH) surge. Local VEGF production in human pre-ovulatory follicles, induced by LH, was postulated to be a luteinization mediator in women. To investigate this hypothesis, serum and fluid from the dominant follicle of 31 healthy regularly cycling multiparous women undergoing laparoscopic sterilization were obtained. VEGF was measured by enzyme-linked immunosorbent assay, and LH and progesterone were measured by radioimmunoassay. Follicle aspiration was performed at a median of 13 days from the last menstrual period (range 11-17 days). The median pre-ovulatory follicle diameter was 16 mm (range 11-23 mm). Follicle fluid VEGF concentrations (mean 6900 pg/ml, range 1200-17 100 pg/ml) were correlated positively with follicle fluid progesterone concentrations (mean 10 176 nmol/l, range 636-66780 nmol/l, r=0.62, P=0.002). This correlation was even tighter (r=0.87, P < 0.0001) when only samples from the 22 women in the earliest stages of follicle luteinization were considered. In these women serum LH concentrations were also correlated with follicle fluid VEGF concentrations (r=0.51, P=0.02). Our findings demonstrate the close dynamic relationship between VEGF production and early luteinization in human follicles during normal non-stimulated cycles.

Adult↗

PubMed2006

Hypo- and hyperresponse to egg cholesterol predicts plasma lutein and beta-carotene concentrations in men and women.

The purpose of this study was to determine whether the plasma response to dietary cholesterol from eggs is associated with the plasma carotenoid response and whether gender influences the carotenoid response. Using a crossover design, 40 subjects classified as either hyper- (10 men and 10 women) or hyporesponders (10 men and 10 women) to dietary cholesterol consumed an egg (EGG, 640 mg/d additional dietary cholesterol and 600 microg lutein + zeaxanthin) or placebo (SUB, 0 mg/d cholesterol, 0 microg lutein + zeaxanthin and 568 microg beta-carotene) diet for 30 d, followed by a 3-wk washout period and the alternate diet. Plasma concentrations of lutein and beta-carotene after each dietary period were then examined to determine whether the response to carotenoid intake was similar to that seen for dietary cholesterol. After the EGG period, the increase in plasma lutein in female hyperresponders (mean increase +/- SD; 0.32 +/- 0.19 micromol/L) and male hyperresponders (0.26 +/- 0.11 micromol/L) was significantly greater than that of their hyporesponsive counterparts (0.16 +/- 0.18 micromol/L for women and 0.14 +/- 0.11 micromol/L men). Gender was not a significant factor influencing lutein response. Both men and women classified as hyperresponders significantly increased plasma beta-carotene after the SUB period, whereas their hyporesponsive counterparts were not affected. The increase in plasma beta-carotene in female hyperresponders (0.29 +/- 0.48 micromol/L) was significantly greater than that in male hyperresponders (0.07 +/- 0.07 micromol/L). We conclude that plasma responses to cholesterol and carotenoids are related and that gender influences the beta-carotene response to a greater degree than the lutein response.

Analysis of Variance↗

PubMed2000

Spontaneous luteinization of antral marmoset follicles in vitro.

Large non-luteinized follicles of the marmoset monkey were cultured for up to 96 h in the presence of substances that are known to induce luteinization, i.e. LH, transforming growth factor (TGF)-beta and cyclic AMP. The state of the basal lamina, and the expression of connexin-43, alpha(2) integrin subunit and TGF-beta receptor type II (TbetaR-II) were chosen as parameters to judge the progress of luteinization. Antral follicles, cultured for 1 h, were not luteinized, as shown by an intact basal lamina, strong immunoreactivity of connexin-43 in granulosa cells, and no expression of TbetaR-II in the theca layer. After 12 h, most follicles showed a dissolution of the basal lamina, a faint reactivity of connexin-43, high expression of TbetaR-II in theca- and outer granulosa cells and high expression of alpha(2) integrin subunit in granulosa cells bordering at the basement membrane; all of which indicate luteinization. After 96 h of culture, luteal structures (e.g. corpora lutea accessoria) had developed. This was true for both non-stimulated and stimulated follicles. Our results strongly suggest that antral follicles luteinize spontaneously. The decisive determinant appears to be the follicular stage.

Animals↗

PubMed1996

Progesterone receptor messenger ribonucleic acid and protein in luteinized granulosa cells of rhesus monkeys are regulated in vitro by gonadotropins and steroids.

Previous studies in our laboratory indicated that the midcycle gonadotropin surge stimulates progesterone receptor (PR) expression in granulosa cells of the macaque preovulatory follicle. The current experiments were designed to determine whether gonadotropin or steroids continue to regulate PR in luteinized granulosa cells that contain these receptors after the LH surge. Luteinizing granulosa cells obtained from gonadotropin-treated rhesus macaques were cultured in chemically defined medium in the presence of low density lipoprotein (LDL; 100 micrograms/ml) with or without hCG (100 ng/ml) for up to 4 days. Cells were also cultured with various concentrations (0.25-250 ng/ml) of the 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) inhibitor trilostane to reduce progesterone (P) production in vitro. P and estradiol (E) in the media were assayed by RIA; PR mRNA was assessed by RNase protection assay, and cells expressing PR were identified by immunocytochemistry. Whereas hCG stimulated cellular P production through 4 days of culture, trilostane reduced hCG-stimulated P production in a dose-dependent fashion, with P levels decreasing more than 90% during incubation with 250 mg/ml trilostane (p < 0.05). When trilostane was removed from the media, P production returned to hCG-stimulated levels, indicating that trilostane (250 ng/ml) alone did not alter levels compared to those in controls. Before culture, 68 +/- 11% of luteinizing granulosa cells expressed PR; intense nuclear staining was typically observed. After 2 days of culture, 78 +/- 3% of cells remained PR-positive, but nuclear staining was more heterogeneous. Incubation with hCG did not alter the percentage of luteinized granulosa cells staining positive for PR but increased the intensity of PR staining. Trilostane treatment (25 ng/ml) in combination with hCG significantly reduced the percentage of PR-positive cells (54 +/- 9%) when compared with hCG treatment (83 +/- 2%, p < 0.05). These in vitro data suggest that macaque luteinized granulosa cells retain some PR expression in the absence of luteotropic hormones, but that gonadotropin stimulates PR mRNA levels and enhances PR expression as assessed by intensity of nuclear PR staining. In the presence of gonadotropin, trilostane effectively inhibited P production ad reduced the number of PR-positive cells, suggesting that P or a metabolite modulates PR expression in primate luteinized granulosa cells.

3-Hydroxysteroid Dehydrogenases↗

PubMed1999

Relaxin secretion and gene expression in porcine granulosa and theca cells are stimulated during in vitro luteinization.

During formation of the corpus luteum, the primary source of relaxin switches from theca cells (TC) to granulosa-derived, large luteal cells. What controls this shift in relaxin production is poorly understood. The objective of this study was to observe the effect of luteinization on relaxin gene expression and secretion by porcine granulosa (GC) and TC using an in vitro model. TC and GC from medium-sized porcine follicles (4-6 mm) were treated for up to 8 days with LH (250 ng/ml) and/or insulin-like growth factor-I (IGF-I; 10 ng/ml). Media were assayed for relaxin and progesterone by RIA, changes in cell morphology were recorded, and total RNA was subjected to reverse transciption-polymerase chain reaction to monitor relaxin gene expression. In vitro luteinization, induced with LH + IGF-I treatment, was confirmed in both GC and TC by a change in morphology and a sustained, significant rise in progesterone secretion. In luteinizing GC, relaxin secretion was first detected after 5 treatment days, and steadily rose until it became significantly higher (p < 0.001) by treatment Days 7-8. In contrast, relaxin release from luteinizing TC was significant after only 2 days of treatment (p < 0.05) and increased consistently over the 8-day culture period (p < 0.001). In GC, relaxin mRNA was not detected until treatment Day 4 and became significantly higher (p < 0.001) by Day 8, the final treatment day. Relaxin transcript in luteinizing TC was low on treatment Days 2-4 and significantly higher (p < 0.01) by treatment Days 6 and 8. In summary, the present study demonstrates that hormones important in the control of luteinization are essential for regulating relaxin gene expression and secretion by GC and TC in the porcine follicle.

Animals↗

PubMed1993

Luteinizing hormone (LH) surge in patients using buserelin spray during ovarian stimulation for assisted reproduction.

The incidence of luteinizing hormone surge was studied in patients who were downregulated with a short protocol of gonadotrophin releasing hormone agonist before ovarian stimulation for assisted reproduction. Buserelin nasal spray 100 micrograms was given 5 times daily from day 2 of the cycle, followed by ovarian stimulation with human menopausal gonadotrophin and follicle stimulating hormone from day 3 onwards. Of the 159 cycles studied, luteinizing hormone surge was detected in 9 cycles (5.7%). The occurrence of LH surge was usually (67%) but not always associated with a fall in serum oestradiol level before administration of human chorionic gonadotrophin. None of the patients developed luteinizing hormone surge after day 10. Even in patients without luteinizing hormone surge the serum luteinizing hormone levels on the day of administration of hCG were significantly higher than those on day 2 before administration of buserelin. It is concluded that a short protocol with intranasal buserelin 500 micrograms per day is inadequate to suppress endogenous luteinizing hormone surge.

Administration, Intranasal↗

PubMed2000

Natural tocopherols in a dietary supplement of lutein affect tissue distribution of tocopherols in young rats.

The effects of graded levels of Flora GLO (FG), a dietary supplement containing lutein derived from marigold flowers, on tissue concentrations of lutein and alpha- and gamma-tocopherol were determined. Six groups of male weanling Fischer 344 rats (15/group) were fed ad libitum modified AIN-93G diets containing 0%, 0.30%, 0.60%, 1.20%, 2.40%, or 4.80% FG for eight weeks. FG provided 0%, 0.015%, 0.030%, 0.060%, 0.120%, or 0.240% lutein; corresponding levels of tocopherols were approximately 0%, 0.006%, 0.012%, 0.023%, 0.046%, and 0.092%, respectively. Maximal uptakes of lutein in plasma, spleen, and liver were observed with 4.8% FG. Lutein was not detectable in brain, heart, lung, testes, and kidney. Concentrations of alpha-tocopherol in the plasma (microgram/mg triglycerides) were reduced in all rats fed FG (p < 0.05). alpha-Tocopherol increased nonlinearly in lung, heart, and spleen with increased FG level. alpha-Tocopherol in liver increased with increased dietary FG; alpha-tocopherol in kidney, testes, and brain did not increase. At each dietary level of FG, the spleen had a higher percentage of gamma-tocopherol, and testes and brain had a lower percentage of gamma-tocopherol than all other tissues. For all tissues, the concentrations of alpha-tocopherol were always higher than those of gamma-tocopherol. Tocopherols added to the dietary supplement for functional purposes appeared to have a significant effect on tissue levels of tocopherols. Therefore, changes in alpha- and gamma-tocopherol levels in tissues of rats fed FG cannot be attributed solely to effects of lutein.

Animals↗

PubMed2003

Dynamics of Myc/Max/Mad expression during luteinization of primate granulosa cells in vitro: association with periovulatory proliferation.

Granulosa cell luteinization involves the attenuation of gonadotropin-induced proliferation. Although recent evidence indicates that primate granulosa cells stop dividing within 12 h of an ovulatory stimulus, early events in cell cycle arrest remain unknown. In the current study an in vitro model of primate granulosa cell luteinization is established that allows assessment of early events in terminal differentiation. A luteinizing dose of human chorionic gonadotropin (hCG) results in a secondary rise in proliferation before cell cycle arrest that is paralleled by a transient increase in the expression of c-Myc. In contrast, the c-Myc antagonists Mad1, Mad4, and Mxi1 are transiently repressed by hCG. Max, the common dimerization partner for Myc and Mad, is similarly repressed by hCG, suggesting that changes in the expression of this gene may further regulate the activity of Myc and Mad. To determine whether other cell cycle regulatory families are involved in luteinization, the expression of p53 and the wild-type p53-inducible phosphatase (wip1) was examined. Similar to Mad and Max, p53 and wip1 are transiently repressed by hCG, suggesting that the p53 and Mad pathways have either parallel or cooperative roles in luteinization. Thus, luteinization of primate granulosa cells is preceded by a burst of proliferation that is regulated by changes in the relative levels of c-Myc, Max, and Mad as well as p53.

Animals↗

PubMed2004

Progesterone secretion by luteinizing human granulosa cells: a possible cAMP-dependent but PKA-independent mechanism involved in its regulation.

The corpus luteum formed after luteinization of follicular cells secretes progesterone under the control of luteinizing hormone (LH). Binding of LH to its G-protein-coupled receptor leads to the activation of the adenylate cyclase/ cyclic AMP (cAMP)/cAMP-dependent protein kinase (PKA) signalling pathway. The identification of a new class of cAMP-binding proteins termed 'guanine nucleotide exchange factors' (cAMP-GEFs) provides a means by which changes in cAMP could yield actions that are independent of PKA. Hence, in this study, we have explored the hypothesis that steroidogenesis in luteinizing cells is mediated in both a cAMP/PKA-dependent and cAMP-dependent, but PKA-independent, manner. Human granulosa cells were isolated from follicular aspirates of women undergoing assisted conception. Luteinizing human granulosa cells were cultured for up to 3 days in the presence of human (h)LH and the adenylate cyclase activator forskolin in the added presence or absence of increasing doses of the PKA inhibitors H89 (N-[2-(4-bromocinnamylamino)ethyl] 5-isoquinoline) and PKI (myristoylated protein kinase A inhibitor amide 14-22) or the cAMP antagonist, Rp-cAMP. Agonist-stimulated progesterone secretion was inhibited in a dose-dependent manner by the PKA inhibitors and the cAMP antagonist, with decreasing sensitivity as luteinization progressed. Pretreatment of granulosa cells for 4 h with human (h)LH reduced the effectiveness of H89 in inhibiting progesterone secretion. Under basal conditions, cAMP-GEFI expression increased progressively throughout culture, and this could be further enhanced when cells were incubated with increasing doses of LH and forskolin. Furthermore, incubation of cells in the presence of increasing concentrations of the novel cAMP-GEF-specific cAMP analogue, 8 CPT-2 ME-cAMP (8-(4-chloro-phenylthio)-2'-0-methyladenosine-3',5'-cyclic monophosphate), increased progesterone secretion in a dose-dependent manner. The results show that increases in cAMP generated by LH and forskolin, in addition to activating PKA, also induce increases in cAMP-GEFI protein expression in luteinizing human granulosa cells. In addition, activation of cAMP-GEFI results in increased progesterone secretion. Hence, increases in cAMP lead to the activation of PKA-dependent, as well as PKA-independent but cAMP-dependent (via cAMP-GEFI), signalling mechanisms. Since cAMP-GEFs have the capacity to activate the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3-K)/protein kinase B (PKB) signalling pathways, these may provide the potential mechanisms by which cAMP-dependent but PKA-independent progesterone synthesis is regulated.

Adenylyl Cyclases↗

PubMed1982

Effect of adrenocorticotropin and cortisol on luteinizing hormone surge and estrous behavior of cows.

In six cows, twice daily administration of 100 IU corticotropin for 3.5 days during the follicular phase delayed the preovulatory luteinizing hormone surge and onset of behavioral estrus. Corticotropin increased progesterone and decreased estradiol and basal luteinizing hormone concentrations of blood. Following corticotropin withdrawal, a shortened period of behavioral estrus (50% of control) was accompanied by an apparent luteinizing hormone surge and ovulation. To ascertain if these effects were caused by the elevated corticosteroid concentrations induced by corticotropin, we infused intravenously four heifers with cortisol sodium succinate. During this infusion, luteinizing hormone surge and estrous behavior were inhibited; however, estradiol and basal luteinizing hormone concentrations were not affected. Furthermore, there was no luteinizing hormone surge, ovulation, or behavioral estrus after cessation of cortisol treatment. These results are consistent with a role for corticosteroids in mediating inhibitory effects on reproduction produced by corticotropin administration.

Adrenocorticotropic Hormone↗

PubMed1992

Effect of coccidiosis on the distribution of dietary lutein in the chick.

A series of experiments was run to determine whether the distribution of dietary carotenoids in chick plasma and tissue was dependent upon a saturable carrier, and to observe how infection with Eimeria acervulina affected this distribution. Broiler (Hubbard x Hubbard) and Sex Sal (Rhode Island Red x White Rock) chicks were fed a white corn and soybean meal-based diet supplemented with varying levels of a commercial lutein concentrate. Plasma, small intestine, and liver were analyzed for lutein. In the first experiment, mean plasma values in control broiler chicks increased linearly from 0 to 200 ppm supplementation. Mean plasma values of infected chicks were decreased an average of 71% as compared with controls, and reached a plateau between 100 and 200 ppm dietary lutein. In the second experiment, plasma, small intestinal, and liver lutein levels in broiler chicks reached a plateau between 200 and 500 ppm. In the third experiment, plasma and liver values in Sex Sal chicks leveled off between 250 and 500 ppm whereas levels in the small intestine increased linearly. Infection of the Sex Sal chicks at 3 wk of age with E. acervulina caused plasma lutein levels to be reduced about 88%, small intestinal levels 76%, and liver levels 72%. Supplementation with 500 ppm resulted in higher proportions of lutein in tissues. Infection with E. acervulina shifted the ratios to even higher proportions in the tissues at all supplementation levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2002

Effect of dietary zeaxanthin on tissue distribution of zeaxanthin and lutein in quail.

PURPOSE: The xanthophyll carotenoids (lutein and zeaxanthin) are hypothesized to delay progression of age-related macular degeneration. The quail has a cone-dominant retina that accumulates carotenoids. The purpose of these experiments was to characterize the carotenoid composition of retina, serum, liver, and fat in quail and to determine whether dietary enrichment with zeaxanthin alters zeaxanthin or lutein concentrations in these tissues. METHODS: Quail were fed for 6 months with a commercial turkey diet (T group; n = 8), carotenoid-deficient diet (C- group; n = 8), or a carotenoid-deficient diet supplemented with 35 mg 3R,3'R-zeaxanthin per kilogram of food, (Z+ group; n = 8). Zeaxanthin was derived from Sphingobacterium multivorum (basonym Flavobacterium). Carotenoids in serum, retina, liver, and fat were analyzed by HPLC. RESULTS: As in the primate fovea, the retina accumulated zeaxanthin, lutein, and cryptoxanthin, and preferentially absorbed zeaxanthin (P < 0.005). In contrast, lutein was preferentially absorbed by liver (P < 0.01) and fat (P < 0.0001). In supplemented females, zeaxanthin increased approximately 4-fold in retina, and 74-, 63- and 22-fold in serum, liver, and fat, respectively. In males, zeaxanthin was elevated approximately 3-fold in retina, and 42-, 17-, and 12-fold in serum, liver, and fat, respectively. Birds fed the Z+ diet absorbed a higher fraction of dietary lutein into serum, but lutein was reduced in the retina (P < 0.05). CONCLUSIONS: Xanthophyll profiles in quail mimic those in primates. Dietary supplements of zeaxanthin effectively increased zeaxanthin concentrations in serum, retina, liver, and fat. The robust response to zeaxanthin supplementation identifies the quail as an animal model for exploration of factors regulating delivery of dietary carotenoids to the retina.

Adipose Tissue↗

PubMedDate not supplied

Effects of lutein from marigold extract on immunity and growth of mammary tumors in mice.

The effects of dietary lutein from marigold extract on the development and growth of a transplantable murine mammary tumor and on lymphocyte function were investigated. Mice were fed a diet containing 0.1% or 0.4% of lutein. In experiment 1, mice were fed the diets for 3 weeks and infused with mammary tumor cells into the mammary gland. Dietary lutein increased tumor latency and inhibited mammary tumor growth in a dose-dependent manner. The incidence of palpable tumors on day 28 post-infusion and final tumor weight were lower in mice fed lutein. In experiment 2, dietary lutein enhanced phytohemagglutinin-induced lymphocyte proliferation but had no effect on interleukin-2 production or lymphocyte cytotoxicity. Therefore dietary lutein increased tumor latency, suppressed mammary tumor growth and enhanced lymphocyte proliferation.

Animals↗

PubMed1998

Effect of lutein on beta-carotene absorption and cleavage.

Carotenoid interactions during absorption and in postabsorptive metabolism have been observed in both human and animal studies. We reviewed the mutual interactions reported between lutein and beta-carotene and report new data on the postprandial beta-carotene and retinyl ester response in the triglyceride-rich plasma lipoprotein (TRL) fraction in volunteers after a single test meal with beta-carotene alone, or beta-carotene combined with lutein or lycopene. Results indicate an inhibitory effect of lutein on beta-carotene absorption, but apparently not on beta-carotene cleavage. In a comparative study with two beta-carotene/lutein ratios (2:1 and 1:2, respectively), this inhibitory effect of lutein was found to be most marked when lutein was the predominant carotenoid. In studies on plasma (serum) response also an inhibitory effect of beta-carotene on lutein response was observed.

Absorption↗

PubMed1989

Effect of D-tryptophan-6-luteinizing hormone-releasing hormone on the tumoral growth and plasma sex steroid levels in cirrhotic patients with hepatocellular carcinoma.

Certain evidence suggests androgen dependence of hepatocellular carcinoma in cirrhotic patients. Consequently, it was postulated that antiandrogen therapy might be effective in the treatment of hepatocellular carcinoma. D-Tryptophan-6-luteinizing hormone-releasing hormone is a potent agonist analog of luteinizing hormone-releasing hormone which, when chronically administered, inhibits the pituitary gonadal axis and testicular androgen secretion in man. We studied the effects of D-tryptophan-6-luteinizing hormone-releasing hormone on tumoral growth in 17 male cirrhotic patients with hepatocellular carcinoma. After 3 to 6 months of therapy, no tumoral response was observed. Furthermore, measurements of plasma levels of testosterone, dihydrotestosterone, androstenedione, estradiol, estrone and sex hormone-binding globulin were performed before and 3 months after initiation of the antiandrogenic treatment. Before treatment, hypoandrogenism and hyperestrogenism were present; D-tryptophan-6-luteinizing hormone-releasing hormone induced a fall in plasma testosterone and dihydrotestosterone levels. Only a moderate decrease in estradiol and no modification of plasma estrone and sex hormone-binding globulin were found, indicating that the hyperestrogenemia of cirrhotic patients could be attributed to an increase in peripheral aromatization of androgens of adrenal origin. The inability of D-tryptophan-6-luteinizing hormone-releasing hormone to reduce the growth of hepatocellular carcinoma is not totally in disagreement with the concept of androgen dependence of hepatocellular carcinoma since D-tryptophan-6-luteinizing hormone-releasing hormone does not inhibit the production of androgens of adrenal origin.

Aged↗

PubMed1992

Intracellular calcium and the signaling mechanism of luteinizing hormone-releasing hormone in rat granulosa cells.

OBJECTIVE: The purpose of these studies was to determine the source(s) of the increase in intracellular free calcium in response to luteinizing hormone-releasing hormone in ovarian granulosa cells. STUDY DESIGN: Rat granulosa cells were cultured and loaded with fura-2-acetoxy-methyl ester, a fluorescent calcium indicator dye, and intracellular free calcium measured by microspectrofluorometry. The source of the luteinizing hormone-releasing hormone induced increase in intracellular Ca++ was investigated with various calcium channel blockers (verapamil, diltiazem, and nifedipine), high K+ buffer, and perifusion with media lacking Ca++. RESULTS: All three voltage-sensitive calcium channel blockers (10(-5) mol/L) tested were ineffective in blocking the luteinizing hormone-releasing hormone induced intracellular Ca++ increase. Treatment with high K+ buffer also had no effect. Perifusion with media lacking calcium resulted in a gradual loss of the luteinizing hormone-releasing hormone response, an effect that was accelerated by repeated stimulation with hormone. Transient replacement of extracellular Ca++ failed to restore the response but continued perifusion with Ca(++)-replete media allowed a luteinizing hormone-releasing hormone response 10 minutes later. CONCLUSIONS: The luteinizing hormone-releasing hormone induced intracellular Ca++ increase does not appear to result from the opening of voltage-sensitive or K(+)-dependent Ca++ channels. To the contrary, this response likely results from the release of Ca++, primarily from intracellular stores.

Animals↗