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Hormone Metabolism (hormone + metabolism)

Distribution by Scientific Domains
Medical Sciences42%
Chemistry42%

Kinds of Hormone Metabolism

  • steroid hormone metabolism
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    Selected Abstracts

    An evolutionary concept for altered steroid hormone metabolism in patients with rheumatoid arthritis

    EXPERIMENTAL DERMATOLOGY, Issue 2 2005
    Rainer H. Straub
    The pathogenesis of chronic disabling inflammatory diseases (CDIDs) is partly understood. The presently used concepts focus mainly on abnormalities of the immune system but this view is incomplete. The presented concept is a new framework for the pathogenesis of CDIDs. It integrates evolutionary theories with the classical immunological standpoint, which is further linked with a neuroendocrine immune view of erroneous homeostatic adaptation of the other supersystems (nervous system, endocrine system, reproductive system): 1. In CDIDs, the loss of tolerance against self and harmless foreign antigens leads to continuous immune aggression which is dependent on a multifactorial genetically polymorph background (the initiation). 2. However, advantageous or disadvantageous adaptation to CDIDs were not evolutionary conserved because CDIDs severely impaired reproduction or appeared after the reproductive phase and, thus, imply a strong negative selection pressure. 3. Reactions of all supersystems are evolutionary conserved for transient inflammatory reactions such as the elimination of infectious agents, wound healing, foreign body reaction and many others. 4. The sum of the false reactions of all supersystems , conserved for transient inflammation , provide the pathogenetic background for the chronification of CDIDs because a continuous aggressive situation is created (the chronification). The human disease of rheumatoid arthritis is used as a prototypic CDID to illustrate the integrated view point. The synovial tissue innervation is in the focus of this concept. [source]

    Effect of lindane on CYP-mediated steroid hormone metabolism in male mice following in utero exposure

    JOURNAL OF APPLIED TOXICOLOGY, Issue 8 2009
    Emma Di Consiglio
    Abstract A wide number of pesticides, including highly persistent organochlorinated compounds, such as lindane (LIN), may induce reproductive and developmental alterations by directly binding to the estrogen/androgen receptors or altering steroid hormone metabolism. In the present work, we have investigated whether LIN in utero exposure of CD1 mice affects the reproductive system in male offspring by causing an impairment of the CYP-dependent steroid hormone metabolism. Dam exposure to 25 mg kg,1 b.w. LIN occurred during critical developmental periods, from gestational days 9 to 16. Effects on hepatic CYP-mediated testosterone (TST) hydroxylase, aromatase activities and testicular parameters were tested at postnatal days (PND 50, 65,69, 100) that are critical for sexual maturation in CD1 mice. In the adult F1 mice significant changes of male reproductive endpoints (testis weight, spermatid number) as well as dramatic effects on CYP-mediated TST metabolism were observed on PND 65,69, in the absence of any of systemic toxicity. The levels of TST 6, - and 2, -hydroxylation and dehydrogenation showed the highest level of reduction, suggesting CYP 3A and 2C families as the major target of LIN induced effects. All changes were almost recovered on PND 100. No effects on aromatase activity were evidenced. Overall, these findings provide useful information for a better characterization of the LIN mode of action. They suggest that LIN-induced toxicity in males is linked to an impairment of steroid hormone homeostasis, due to CYP-mediated TST catabolism modulation and differs from LIN receptor-mediated mechanism previously reported in females. Copyright © 2009 John Wiley & Sons, Ltd. [source]

    Cover Picture , Mol.

    MOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 11 2008
    Nutr.
    Recent events have seen the focus shift from toxicity to the benefits of adequate or supplemented levels of selenium in the diet because it is likely to influence cancer incidence and also affects hormone metabolism and immunity. This Special Issue is intended to serve as a useful primer for both those interested in using nutrition to minimize disease and those directly involved in the study of selenium biology. [source]

    Abiotic stress and plant responses from the whole vine to the genes

    AUSTRALIAN JOURNAL OF GRAPE AND WINE RESEARCH, Issue 2010
    G.R. CRAMER
    Abstract Drought, salinity and extreme temperatures significantly limit the distribution of grapes around the world. In this review, the literature of grape responses to abiotic stress with particular reference to whole plant and molecular responses observed in recent studies is discussed. A number of short-term and long-term studies on grapevine shoots and berries have been conducted using a systems biology approach. Transcripts, proteins and metabolites were profiled. Water deficit, salinity and chilling altered the steady-state abundance of a large number of transcripts. Common responses to these stresses included changes in hormone metabolism, particularly abscisic acid (ABA), photosynthesis, growth, transcription, protein synthesis, signalling and cellular defences. Some of the transcriptional changes induced by stress were confirmed by proteomic and metabolomic analyses. More than 2000 genes were identified whose transcript abundance was altered by both water deficit and ABA. Different gene sets were used to map molecular pathways regulated by ABA, water deficit, salinity and chilling in grapevine. This work supports the hypothesis that ABA is a central regulator of abiotic stress tolerance mechanisms. ABA affects signalling pathways that trigger important molecular activities involving metabolism, transcription, protein synthesis, and cellular defence and also regulates important physiological responses such as stomatal conductance, photoprotection and growth. Systems biology approaches are providing more comprehensive understanding of the complex plant responses to abiotic stress. The molecular sets generated from mapping the ABA-inducible stress responses provide numerous targets for genetic and cultural manipulation for improved plant protection and grape quality. [source]

    Obesity and polycystic ovary syndrome

    CLINICAL ENDOCRINOLOGY, Issue 2 2006
    T. M. Barber
    Summary The aetiology of Polycystic Ovary Syndrome (PCOS) is complex and multifactorial. There is much evidence, however, to suggest that adipose tissue plays an important role in the development and maintenance of PCOS pathology. There is a close correlation between adiposity and symptom severity in women with PCOS, and even modest reductions in weight generally translate into significant improvements in menstrual regularity, fertility and hyperandrogenic features. This review article considers the various mechanisms that might underlie this link between excess adiposity and PCOS , including the effects of differential insulin sensitivity, abnormal steroid hormone metabolism and adipocytokine secretion. Greater attention to the therapeutic options available to reduce the impact of excess adiposity on ovarian and metabolic function is essential to the management of PCOS. [source]

    Recombinant hGH replacement therapy and the hypothalamus,pituitary,thyroid axis in children with GH deficiency: when should we be concerned about the occurrence of central hypothyroidism?

    CLINICAL ENDOCRINOLOGY, Issue 6 2003
    Claudia Giavoli
    Summary objective, Recombinant hGH treatment may alter thyroid hormone metabolism and we have recently reported that 50% of patients with GH deficiency (GHD) due to organic lesions, previously not treated with thyroxine, developed hypothyroidism during treatment with recombinant human GH (rhGH). These results prompted us to evaluate the impact of rhGH treatment on thyroid function in children with GHD. design, Open study of GH treatment up to 12 months. Investigations were performed at baseline, and after 6 and 12 months of GH therapy. measurement and study subjects, Serum TSH, FT4, FT3, AbTg and AbTPO, IGF-I, height and weight, were evaluated in 20 euthyroid children (group A) with idiopathic isolated GHD and in six children (group B) with multiple pituitary hormone deficiencies (MPHD) due to organic lesions. Among the latter, four already had central hypothyroidism and were on adequate LT4 replacement therapy, while two were euthyroid at the beginning of the study. results, Serum IGF-I levels normalized in all patients. In both groups, a significant reduction in FT4 levels (P < 0·01) occurred during rhGH therapy. No patient in group A had FT4 values into the hypothyroid range, while in four of six patients in group B, fell FT4 levels into the hypothyroid range during rhGH. In particular, the two euthyroid children developed central hypothyroidism during rhGH treatment, and their height velocities did not normalize until the achievement of euthyroidism through appropriate LT4 substitution. No variation in serum FT3 and TSH levels was recorded in either groups. conclusion, Contrary to that observed in patients with MPHD, rhGH replacement therapy does not induce central hypothyroidism in children with idiopathic isolated GHD, further supporting the view that in children with MPHD, as in adults, GHD masks the presence of central hypothyroidism. Slow growth (in spite of adequate rhGH substitution and normal IGF-I levels) is an important clinical marker of central hypothyroidism, therefore a strict monitoring of thyroid function is mandatory in treated children with MPHD. [source]