Juvenile hormone-induced biosynthesis of vitellogenin in Leucophaea maderae.
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Adipose Tissue↗
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Results for “hormone biosynthesis”
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The biosynthesis and hormonal regulation of surfactant formation.
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Adult↗
The biosynthesis of hormones by non-endocrine tumours--a review.
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Adrenocorticotropic Hormone↗
[Role of aspartic acid in the biosynthesis of hormones and the nitrogen metabolism of the thyroid].
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Animals↗
Studies on rat pituitary homografts. II. Effects of thyrotropin-releasing hormone on in vitro biosynthesis and release of growth hormone and prolactin.
A study was made of the effect of TRH, administered in vivo by iv infusion or added in vitro to the incubation fluid, on tissue fragments prepared from rat normotopic and ectopic pituitaries. The latter were 30-day-old pituitary grafts transplanted under the kidney capsule in hypophysectomized animals. No detectable effect of TRH was found with normotopic glands. In contrast, the neurohormone produced a large increase in GH and PRL biosynthesis in the grafts, as revealed by the rise in hormone content as well as increased incorporation of L-[3H]leucine into the two hormones. These effects of TRH 1) are dose related; 2) appear after a latent period of at least 15 min; and 3) persist, although attenuated, for some time after removing the neurohormone. In vitro release of GH and PRL by tissue fragments prelabeled with L-[3H]leucine was studied by following the appearance of the radioactive hormones in the incubation fluid. Exposure to TRH produced a prompt, 2-fold or greater increase in hormone release from grafts but not from normotopic gland fragments. The possible mechanisms whereby pituitary somatotrophs and mammotrophs removed from the influence of the central nervous system increase their responsiveness to TRH stimulation are considered.
Animals↗
Responsiveness of neoplastic and hyperplastic parathyroid tissues to calcium in vitro.
Secretory and biosynthetic responses of adenomatous, carcinomatous, and hyperplastic parathyroid tissues to variable concentrations of extracellular calcium were assessed in vitro. Tissues, obtained at the time of parathyroidectomy, were incubated for 4 h in media containing radioactive amino acids and varying (0.5-5.0 mM) concentrations of calcium. Amounts of newly synthesized and total parathyroid hormone and proparathyroid hormone in extracts of tissues and media were measured by polyacrylamide gel electrophoresis and by radioimmunoassay, respectively. All tissues studied (six adenomas, two specimens of chief-cell hyperplasia, one carcinoma, and normal bovine and human glands) responded to changes in calcium concentrations; decreasing concentrations of calcium stimulated release and decreased tissue storage of hormone. Six of the abnormal tissues required greater than normal concentrations of calcium (1.8-2.4 mM for 50% of effect) to elicit secretory responses comparable with those of normal glands (1.4 mM). Maximum effects of calcium on release of hormone varied from 2- to 10-fold among different tissues. Release of some hormone persisted even in concentrations of calcium as high as 5.0 mM. Relative amounts of hormone released from and retained in the tissues varied greatly among the tissues, as did the absolute amounts of hormone produced; newly synthesized, labeled hormone ranged between 0.6 and 12% of total labeled protein, and immunoreactive hormone ranged between 0.015 and 0.9% of total tissue protein. Effects of calcium on hormone biosynthesis, as determined by analyses of amounts of proparathyroid hormone in the tissues, were variable among tissues and in many cases were negligible. These results indicate that neoplastic and hyperplastic parathyroid tissues retain secretory responsiveness to changes in extracellular concentrations of calcium. Responses, however, are highly variable among different tissues, and in many instances are abnormal, inasmuch as greater than normal concentrations of calcium are required to alter release and synthesis of hormone. A combination of both increased mass of glandular tissue and abnormal regulations of hormone secretion appear to contribute to the hypersecretion of hyperparathyroidism.
Adenoma↗
Biosynthesis of polypeptide hormones.
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Adrenocorticotropic Hormone↗
[Virilizing granulosa-cell tumors of the ovaries].
On the basis of the results of morphological and histochemical study of two malignant granulosa cell tumours removed in women with the virile syndrome the author came to the conclusion that theca-tissue was a necessary structural component of such tumours. Theca cell component can be expressed to a different extent, but its cells, in contrary to the cells of the prevailing ganulosa cell component of such tumours, possessed a high enzymatic activity providing the processes of the steroid hormone biosynthesis, and contained lipids intimately connected with these processes. These data permit to regard the theca cell component of malignant granulosa cell tumours as the main source of hormones produced by such tumours.
Aged↗
[Activity of adrenal cytoplasmic dehydrogenase following prolonged ACTH administration].
The activity of cytoplasmic dehydrogenases of the adrenal cells was examined during the prolonged injections of ACTH to Wistar rats. The indices of specific steroid synthesis function of the glands remained relatively high in the course of the whole experiment. Changes in the rats of corticosterone synthesis and dehydrogenase activities were phasic in character; they included an initial synchronic activation the first two days with its subsequent decrease (7 days of ACTH injections). The prevalence of activities of NADP-dependent dehydrogenases in combination with reactivation of steroidogenesis was marked during the concluding phase (13 days) of the experiment. A possibility of the adaptive role of selective activation of NADP-dependent enzymes in the maintenance of a high level of hormone biosynthesis under conditions of prolonged ACTH stimulation is discussed.
11-Hydroxycorticosteroids↗
From beta-lipotropin to beta-endorphin and 'pro-opio-melanocortin'.
Studies on the biosynthesis of beta-LPH on the one hand, and of ACTH on the other, have produced a new concept, that of a single precursor form which contains three active molecules. Thus, it is proper to name such a precursor 'pro-opio-melanocortin.' The concept that beta-LPH was a precursor molecule was first put forward in 1967 and was based on both structural forms and biological activities. The discovery that morphine-like substances are part of the C-terminal fragment of beta-LPH brought an additional important biological side product. That, together with the recent demonstration of ACTH as part of a still larger precursor, constitutes an exciting model for the study of peptide hormone biosynthesis. We have shown unambiguously that beta-endorphin is the result of a maturation process from the large precursor, while beta-LPH is an important and transient intermediary. Since it is also present in the brain, our recent results using pars intermedia cells can be applied to study the fabrication and degradation of these molecules in the brain. We expect to see it established that all other neuropeptides are also biosynthesized as larger precursor molecules whose structure at the site of cleavage could well be constituted of two basic amino acids like in the pro-opio-melanocortin.
Adrenocorticotropic Hormone↗
Androgen biosynthesis in experimental cryptorchidism.
This study was conducted to investigate the effects of unilateral cryptorchidism on androgen production and testicular maturation. Experimental cryptorchidism was produced in small and large prepuberal guinea pigs by forcing the testis to remain in the abdomen for a period of 30 days. Small prepuberal animals, which did not reach sexual maturity, showed discrete reductions in the size and weight of the ectopic testes when compared with the scrotal testes. Immaturity of germinal line, tubular size, and intertubular spaces were more pronounced in the ectopic tissue. Both glands produced 4-androstenedione as a primary metabolic product of pregnenolone. Large prepuberal animals, puberal at the time of operation, showed tubular size, spermatic line, and interstitial tissue completely developed in the scrotal gland. Testosterone production was quite similar to that produced in postpuberal testes. The ectopic organ showed only Sertolic cells, some vacuolated, and a few spermatogonia in the tubules. The spaces contained Leydig cells. A significant accumulation of 4-adrenostenedione and a lower testosterone production, compared with that found in the scrotal gland, were observed. The histologic immaturity and the hormonal biosynthesis of the puberal cryptorchid testis parallel findings in scrotal glands from sexually immature guinea pigs.
17-alpha-Hydroxypregnenolone↗
Maternal high-fat diet modulates lupus nephritis through fetal Wnt-steroid hormone and epigenetic reprogramming in MRL/lpr mouse offspring.
We previously investigated whether maternal high-fat diet (HFD) exposure alters lupus nephritis (LN) progression in MRL/lpr offspring. Contrary to expectation, maternally HFD-exposed offspring showed delayed and attenuated nephritic progression compared with control diet offspring. The maternal HFD developmental impact on LN remains unclear. Here, integrated amniotic fluid metabolomics and fetal liver transcriptomics revealed that maternal HFD reshaped the intrauterine molecular environment, particularly involving steroid hormone biosynthesis and Wnt/β-catenin-associated regulatory networks. Methylome profiling further demonstrated broad CpG hypomethylation, immune-related differentially methylated region enrichment, and an inverse association between global CpG methylation and oxidative genomic DNA damage. Among candidate regulatory nodes, Axin2, a canonical Wnt/β-catenin target and feedback regulator, emerged as a potential link between fetal nutritional exposure, epigenetic remodeling, and persistent pathway modulation. Although whole-locus and gene body methylation of Axin2 were not markedly altered, promoter-region methylation showed an increasing tendency under maternal HFD exposure. In adult offspring, maternal HFD was associated with reduced Axin2 protein expression, decreased Wnt-responsive transcripts, increased peripheral corticosterone levels, and attenuation of LN progression. The inverse association between Axin2 expression and corticosterone further suggested coupling between suppressed Wnt pathway output and steroid hormone remodeling. Together, these findings support a developmental model in which maternal HFD reshapes the fetal intrauterine environment and establishes a persistent Wnt-steroid hormone-epigenetic regulatory axis that unexpectedly attenuates LN progression in genetically susceptible offspring.
Axin2↗
Male pseudohermaphroditism: genetics and clinical delineation.
The genetics and clinical delineation of male pseudohermaphroditism are reviewed. These disorders are categorized initially by their genetic etiology--cytogenetic, Mendelian, or teratogenic. It is especially important to distinguish cytogenetic forms, usually associated with 45,X/46,XY mosaicism, from Mendelian (genetic) forms because in the former the prevalence of gonadoblastomas or dysgerminomas is about 15--20%. Genetic forms include (1) those associated with a multiple malformation pattern, (2) those due to an error in adrenal or testicular hormonal biosynthesis, (3) complete testicular feminization, (4) incomplete testicular feminization, (5) Reifenstein syndrome, (6) pseudovaginal perineoscrotal hypospadias, and (7) agondia, and possibly other conditions. Incomplete testicular feminization and the Reifenstein syndrome may or may not represent varied expressivity of the same trait. The designation pseudovaginal perineoscrotal hypospadias is appropriate only if constellations of clinical features are present and if no metabolic abnormalities are demonstrable. Etiology and available genetic data are reviewed for each of these disorders.
Abnormalities, Multiple↗
Mitochondria from human term placenta. II. Characterization of respiratory pathways and coupling mechanisms.
Pathways of electron transport utilized for respiration in human term placental mitochondrial preparations were differentiated and characterized through the use of classical respiratory chain inhibitors and multiple sources of reducing equivalents. Mechanisms of associated energy conservation and utilization were examined in the preparations with uncouplers and inhibitors of phosphorylation. Inhibition by rotenone, antimycin A and cyanide established the classical electron transport chain as the major pathway of respiration with glutamate and succinate as substrates. Approximately 20% of glutamate-supported respiration was insensitive to inhibitors and may proceed by the cytochrome P-450 linked pathway of electron transport. Approximately 50% of ascorbate-N,N,N',N'-tetramethyl-p-phenylenediamine supported respiration was insensitive to 10-3 M cycanide and must utilize an undefined by-pass of cytochrome oxidase. A rotenone- and antimycin-insensitive, exterior pathway for NADH oxidation was demonstrated which could be artificially linked by exogenous cytochrome c to the cytochrome oxidase region of the classical electron transport system. Glycerol 3-phosphate also supported oxidative phosphorylation yielding ADP/O ratios of 2. Respiration of placental mitochondria was stimulated by 2,4-dinitrophenol and gramicidin. With succinate, dinitrophenol-stimulated respiration exceeded that obtained in the presence of ADP. Oligomycin and atractyloside prevented the stimulation of respiration by ADP. Thus, respiration appeared coupled through normal mechanisms to ATP formation and ion transport. A preferential coupling of respiration to the energy-utilizing processes of steroid hormone biosynthesis may exist.
Antimycin A↗
Ovarian H3K27ac remodeling is associated with impaired follicular development in laying hens with fatty liver hemorrhagic syndrome.
Fatty liver hemorrhagic syndrome (FLHS) is a metabolic disease of laying hens that reduces egg production and is accompanied by reproductive impairment, but the ovarian regulatory mechanisms that connect nutritional stress to follicular dysfunction remain unclear. This study examined whether active chromatin remodeling in the ovary is associated with FLHS induced by a high-energy, low-protein (HELP) diet. Hy-Line Brown hens were assigned to a basal diet or HELP diet, and ovarian tissue was collected for histone H3 lysine 27 acetylation (H3K27ac) chromatin immunoprecipitation sequencing and RNA sequencing. The HELP diet reduced laying performance and the numbers of small yellow and hierarchical follicles, indicating compromised follicular development. Genome-wide H3K27ac profiling identified 2,111 regions with lower acetylation and 1,707 regions with higher acetylation in FLHS ovaries. Genes linked to differential H3K27ac regions were enriched in pathways related to oocyte meiosis, cell cycle control, FoxO signaling, gonadotropin-releasing hormone signaling, and steroid hormone biosynthesis. RNA sequencing identified 341 differentially expressed genes, with a predominance of downregulated genes. Integration of chromatin and transcriptome data highlighted folliculogenesis-related genes, including FGF1, FGF9, and MMP10, that showed reduced H3K27ac enrichment together with decreased expression. Super-enhancer analysis further identified 131 regions with reduced H3K27ac signal in FLHS ovaries, including regions located near PCNA and RAP1A, two genes involved in cellular proliferation and survival signaling. Motif enrichment of differential H3K27ac regions implicated Fos, SF-1/NR5A1, and GATA-4 as candidate transcriptional regulators. These findings indicate that HELP diet-induced FLHS is associated with broad attenuation of active ovarian regulatory elements and reduced expression of genes required for follicle growth, tissue remodeling, and steroidogenic function. The study provides an ovarian epigenomic framework for understanding reproductive decline in FLHS-affected laying hens.
Fatty liver hemorrhagic syndrome↗
Multi-omics integration uncovers adaptive responses of stomach and pyloric ceca to artificial feed in mandarin fish (Siniperca chuatsi).
The mandarin fish, as an obligate piscivore, is highly dependent on live bait, which restricts its intensive aquaculture. Although domestication has enabled it to partially accept formulated diets, the tissue-specific molecular adaptation mechanisms of its digestive tract to artificial feed remain unclear. In this study, we conducted an integrated analysis of mandarin fish fed with live bait or artificial diet for three weeks, combining growth performance evaluation, gastric histology, and paired transcriptomic and metabolomic analyses of the stomach and pyloric ceca. AD feeding significantly improved growth performance, while histological examination revealed marked hyperplasia of the gastric mucosa and disorganized fold structures. Transcriptomic analysis identified 5065 and 3381 differentially expressed genes in the stomach and pyloric ceca, respectively. In the stomach, the artificial diet induced a glutathione-dependent antioxidant response, accompanied by glycolytic reprogramming and coordinated upregulation of genes in the extracellular matrix (ECM)-receptor interaction signaling pathway, including those encoding collagen, laminin, and integrin. In the pyloric ceca, the tricarboxylic acid (TCA) cycle and oxidative phosphorylation were broadly suppressed, whereas glycosaminoglycan degradation and lysosomal pathways were activated. Metabolomic analysis showed that gastric metabolites were enriched in vascular and inflammatory mediator pathways, while metabolites in the pyloric ceca were enriched in peroxisome proliferator-activated receptor (PPAR) signaling, sphingolipid signaling, and steroid hormone biosynthesis pathways. Following artificial diet feeding, integrated multi-omics analysis of the stomach revealed significant enrichment of pathways such as phospholipase D signaling, sphingolipid signaling, and arachidonic acid metabolism, accompanied by the accumulation of key metabolites including sphingosine-1-phosphate, 20-hydroxyeicosatetraenoic acid, and cellobiose. Integrated analysis of the pyloric ceca identified significantly altered pathways, including sphingolipid metabolism, alpha-linolenic acid metabolism, and glutathione metabolism, along with elevated levels of sphingosine-1-phosphate, sphingosine galactoside, and 9-hydroxy-12-oxo-10,15-octadecadienoic acid, as well as decreased glutathionylspermidine. These findings systematically unveil the tissue-specific molecular adaptation characteristics of the mandarin fish digestive tract in response to artificial feed, providing an important basis for understanding the molecular mechanisms of dietary adaptation in carnivorous fish and for optimizing artificial feed formulations.
Animals↗
Mode of action of carbimazole in Graves' disease.
In a series of hyperthyroid subjects treated with a high dose 'block-replace' regime, mean thyroidal technetium uptake was shown to fall progressively over an 18 month period. Furthermore, sub-total inhibition of hormone biosynthesis could be demonstrated, without evidence of proportionate inhibition of organification, the regression of radio-iodine on technetium thyroid uptake showing similar slopes in euthyroid, treated and untreated hyperthyroid subjects. Together with the reported differential in remission rates between propranolol and anti-thyroid drugs, it is concluded that carbimazole does not act solely by inhibiting intrathyroid hormono-genesis, but more definitively by affecting thyroid hyperstimulation at a pre-biosynthetic level. The inability to demonstrate normal suppressibility of trapping in any subject in the present series despite extended therapy with a 'block-replace' regime, further suggests that current concepts of 'suppressibility' are invalid, the progressive fall in technetium uptake being unlikely to represent spontaneous restoration of a normal pituitary-thyroid axis, but rather a direct influence or prolonged therapy with anti-thyroid drugs on the natural history of the disease.
Adolescent↗
Comprehensive identification and analysis of clusters of tandemly duplicated genes reveal their contributions to adaptive evolution of green plants.
Tandem gene duplication occurred more frequently compared with the episodic whole-genome duplication (WGD), providing a continuous supply of genetic material for evolutionary innovation and adaptation to changing environments. The rising roles of clusters of tandemly duplicated genes (CTDGs) in the evolution of phenotypic diversity have been unraveled in mammals. However, the content and biological roles of CTDGs remain largely unknown in plants. Here, we comprehensively identified CTDGs in 220 published plant genomes representing major lineages of green plants. The number of CTDGs showed great variation across taxa, ranging from 0 to 6028. The size of CTDGs varied from 2 to 47 genes, with small clusters containing two members predominating. Interestingly, significant expansion of CTDGs was found in early-diverging land plants and is closely associated with the evolution of key traits (e.g., ABA response, plant cuticle, UV-B resistance) required for plants to conquer terrestrial environments. Functional enrichment analysis revealed conserved and specialized functional profiles among different sizes of CTDGs in both Arabidopsis thaliana and the bryophyte Physcomitrium patens. Small CTDGs were enriched in fundamental stress responses, including protein modification, signal transduction, and responses to diverse stress stimuli, while large CTDGs were enriched in more sophisticated processes such as plant hormone biosynthesis and signaling, plant-microbe interactions, and reproductive processes. Expression pattern analyses of CTDGs under different stress conditions in A. thaliana and P. patens revealed that the highest number of CTDGs showed differential expression under drought stress, suggesting important roles of CTDGs in the evolution of desiccation tolerance in early land plants. The results of this study provide new additions to our knowledge about the abundance of CTDGs across green plants and reveal their important contributions to enable plants to overcome stressful environments on land.
Gene Duplication↗