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Volume 37 / No. 4 / 2003
Original articles
Review
Author Index, Vol. 37
Subject Index, Vol. 37
Endocrine Regulations (since 1967 to 1990 Endocrinologia Experimentalis) is an international journal on experimental and clinical endocrinology edited quarterly in English by care of the Institute of Experimental Endocrinology, Slovak Academy of Sciences (Bratislava, Slovakia) and published by the Slovak Academic Press (Bratislava, Slovakia).
This journal aims to publish original manuscripts or minireviews on experimental and clinical endocrinology and diabetes.
The submission of a manuscript to Endocrine Regulations implies that it has not been previously published or is not being submitted for publication elsewhere and that the manuscript has been approved by all authors who are ready to take public responsibility for the content.
All materials relating to human investigation will be published upon the understanding that design of the work has been approved by the local Ethical Committee or that it conforms to ethical guidelines of the Declaration of Helsinki. The animal experiments should state the conformance to guidelines on animal care.
MANUSCRIPT SUBMISSION
Manuscripts in triplicate with three sets of illustrations (of which one is an original) should be sent to:
Richard Kvetnansky, Ph.D., Dr.Sc., Chief Editor,
Institute of Experimental Endocrinology,
Vlárska 3, 833 06 Bratislava, Slovakia
All text must be printed on one side of the sheet only with appropriate margins and double spacing to give adequate space for editorial notes. The corresponding author should indicate his/her full mailing address including phone and fax numbers and the e-mail address.
Manuscripts on disc. The submissions of manuscripts prepared on 3.5 inch discs on IBM compatible computers is encouraged, the preferred word processors being Microsoft Word. However, also in this case the disc must be accompanied by three hard copies of the manuscript. The disk should be labelled by the name of the first author, type of word processor, its version and file name and must also accompany the final version of the manuscript.MANUSCRIPT PREPARATION
Title page should give * the title of the article (main key words should be preferably included into the title to give sufficient information to allow the reader to judge the relevance of a paper to his field), * full names of authors, * institute of origin, * short title (running head), * name and full address of corresponding author including phone and fax numbers and e-mail naddress as well.
Abstract should clearly indicate the purpose of the study (Objective), basic procedures (Methods), main findings (Results) and principal conclusions (Conclusions). New and original findings should be emphasized, clearly defined and defended. The abstract must be easily understood indepenently of the full text of the paperReferences. Begin this section on a new page. References should be assembled in alphabetical order according to the first author. More than one paper from the same author(s) in the same year must be identified by the letters a, b, c etc. placed after the year of publication. All listed references must be cited in the text by the first author et al. and the year (in a case of two authors only cite both). Following possibilities are recommended: (1) Brown and White (1993) found that ...; (2) ... as observed by Black et al. (1992); (3) ... as previously reported by several authors (Black et al. 1992; Brown and White 1993; Green et al. 1995).
The names of authors in the text and in references should be typed in small letters and underlined (e.g. White and Brown). The volume should be typed in bold.
The style for the list of references is as follows:A.Journal Articles:
Itoh M, Okugawa T, Shiratori N, Ohashi H: Treatment with triiodothyronine (T3) against multinodular goiter fails to prevent the onset of Graves disease. Endocrine Regul 29, 151-156, 1995B. Book Chapters:
Mornex R, Orgiazzi JJ: Hyperthyroidism. In: The Thyroid Gland (Ed. M de Visscher), pp. 279-362, Raven Press, New York 1980C. Books:
Podoba J: Endemic goiter in Slovakia. VEDA, Bratislava, 1962The statement “in press” may be used only for a paper accepted for publication in the indicated journal. Unpublished data or Personal communication may be used in the text, but must not be listed in References.
Tables should be constructed as simply as possible, typed on separate sheets and numbered consecutively with Arabic numeral. There should be a short and descriptive heading and appropriate footnotes. Not more than 4 vertical rows should be used in a table planned to occupy one column and not more than 8-10 rows for that designed for two columns of a page.There are no page charges. Reprints order forms are sent to the corresponding author together with galley proofs. Color illustrations may be published for extra charges.
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Ladislav Macho, Stefan Zorad, Zofia Radikova, 1 Patricia Patterson-Buckedahl, Richard Kvetnansky
Institute of Experimental Endocrinology, Slovak Academy of
Sciences, 833 06 Bratislava, Slovakia;
1 Center of Alcohol Studies, Rutgers University, Pistacaway, N.J., USA, e-mail: ueenlaco@savba.sk
Summary:
Objective. The mechanisms of harmful effect of excessive chronic ethanol intake on cardiovascular and neuronal systems, metabolic processes and protective effects of low ethanol intake on cerebrovascular and cardiovascular disturbances are not yet known. The aim of present study was to investigate the effect of short-term and long-term ethanol consumption on food intake, plasma levels of corticosterone (CS), glucose (G) and insulin (INS) in intact rats and in animals exposed to immobilization stress (IMO) or restrain stress (RESTR). The insulin binding to specific membrane receptors in adipocytes, muscle and liver was also determined.
Methods. Adult male rats were fed liquid diet without and with ethanol (5 % per weight) for 9-12 days (short-term intake) and at the end the animals were exposed to acute IMO stress. The second group of rats was fed solid diet and without or with ethanol in drinking water (6 % per volume) for 52 days (long-term ethanol intake). A part of these animals was exposed to repeated restrain stress during 42 days. The groups of pair fed rats with the same food intake as in ethanol diet fed animals were in both experiments. The food intake, plasma glucose, insulin and corticosterone levels were determined. Plasma cell membranes were isolated from adipose, liver and skeletal muscle tissues and insulin binding to specific receptors was determined.
Results. Decreased food consumption was observed after ethanol intake. Increased plasma G and CS were noted in rats fed ethanol diet for a short time. Plasma insulin levels were not affected by ethanol intake. Exposure to IMO stress resulted in increase of plasma G levels in controls and pair fed groups. A higher increase of CS plasma levels after IMO stress was noted in rats with ethanol intake for a short-time, however, no changes of plasma CS were noted after repeated exposure to restrain stress. Plasma levels of insulin were decreased after IMO and restrain stresses, while in rats fed ethanol diet for a short-time insulin decrease was deeper as compared to controls. The binding capacity of insulin receptors in adipose tissue was elevated in rats fed ethanol diet and deep decrease of insulin binding was noted in rats exposed to stress. In liver insulin binding was elevated after short-term ethanol intake and stress exposure resulted in decrease of insulin binding in ethanol fed rats. The binding capacity of insulin receptors in skeletal muscle was not changed in rats fed ethanol diet.
Conclusions. The results showed 1. differences in short term and long term ethanol intake on basal glucose, insulin and corticosterone levels, 2. effects of ethanol intake on changes of insulin plasma levels and insulin binding in adipose and liver tissues after exposure to stress, 3. effects of short term ethanol intake on the response of plasma hormones to immobilization stress.
Key words: Ethanol intake - Stress response - Glycemia - Insulinemia -
Insulin biding - Rats
ENDOCRINE REGULATIONS, Vol. 37, 195–202, 2003
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Lucia Medvedova 1, Jan Knopp , Robert Farkas
Institute of Experimental Endocrinology, Slovak Academy of
Sciences, 833 06 Bratislava, Slovakia;
1 Department of Genetics, Graduate Programme, Faculty of Science,
Comenius University, Bratislava, Slovakia
Summary:
Objective. Terminal glycosylations such as
fucosylation and especially sialylation are crucial in maturation of proteins
for their particular function. In cells and tissues where their function is
under hormonal control, often terminal processes including glycosylations are
tightly regulated by hormones. Therefore, it is not surprising that two key
enzyme families involved in these steps, fucosyltransferases and
sialyltransferases, are directly controlled by steroid hormones.
Methods. Gene structure and protein sequences have been analyzed by set of Unix-based complex sequence analysis programs of the Wisconsin GCG package, and from some other resources. Protein secondary structure predictions were based on several independent programs and applications complementing each other depending on the algorithm used, all running on Unix platforms.
Results. Comparison of these two types of enzymes from organisms where
they are known to be under direct hormonal regulation has revealed that although
sialyltransferases are broad family of proteins, the only known enzymes to be
under hormonal control are a-2,6-sialyltransferases and in the case of fucosyl
moieties transferring enzymes these are a-1,2/6-fucosyltransferases.
Interestingly, hormonally regulated sialyltransferases from as evolutionary
distant organisms as human and fruitfly share several important features
including secondary structure characteristics encompassing sialyl L and S motifs
in which they differ from other sialyltransferases. Analogous organizational and
structural similarities were found also in hormonally regulated
fucosyltransferases.
Conclusions. Data indicate that hormonal control of these classes of enzymes as a regulatory mechanism could be attained relatively early during the evolution in order to obtain selective control over specific protein modification process which plays an important role during ontogenic development.
Key words: Steroid hormones - Sialyltransferase - Fucosyltransferase -
Gene structure and expression - Protein sequence and secondary structure
ENDOCRINE REGULATIONS, Vol. 37, 203–210, 2003
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Z. Ostrowska, B. Kos-Kudla 1, M. Nowak 1, E. Swietochowska, B. Marek 1, J. Gorski, D. Kajdaniuk 1, K. Wolkowska
Department of Clinical Biochemistry,
1 Department of Pathophysiology and Endocrinology, The Medical University of Silesia, Zabrze, Poland, E-mail: ozdrasiek@poczta.onet.pl
Summary:
Objective. The influence of pinealectomy and long-term melatonin (MEL) administration on circadian oscillations of selected biochemical markers of bone metabolism [serum alkaline phosphatase (ALP) activity, carboxyterminal propeptide type I procollagen (PICP) and carboxyterminal telopeptide type I collagen (ICTP) concentrations as well as urinary excretion of hydroxyproline (HYP) and Ca] and possible involvement of circadian secretion of IGF-I, parathyroid, thyroid, adrenal cortex and gonads function in this mechanism was evaluated.
Methods. Studies were performed in 192 adult male Wistar rats weighing 145±9 g which were subjected to pinealectomy or sham operation. In half of the animals from each group MEL (Sigma, USA) in a dose of 50 mg/100 g b.w. was administered intraperitonealy (daily between 17.00 and 18.00 h for a 4-week period). Material for studies (blood and urine) was collected every 3 hours during a day. Hormones, PICP and ICTP concentrations were determined with the use of RIA methods, whereas ALP, HYP and Ca values - spectrophotometrically.
Results. The study has shown that pinealectomy had an inducing, while exogenous MEL a suppressing effect upon the level of investigated biochemical markers of bone metabolism. Furthermore, substantial changes in the values of amplitude and phase of their circadian oscillations were shown. Distinct, dependent on the time of day disturbances in circadian fluctuations of PICP, ICTP, HYP and Ca showing generally negative correlation with changes in endogenous MEL concentrations and positive with IGF-I and corticosterone (B) levels were found. In addition, changes in circadian oscillations of ALP and PICP correlated negatively with daily oscillations of calciotropic hormones and B. However, ICTP, HYP and Ca concentrations correlated positively with circadian fluctuations of B and FT3 (the latter only in sham operated rats receiving MEL).
Conclusions. This study showed that both pinealectomy and long-term MEL administration influence the circadian rhythm of bone metabolism and that an important role in the mechanism of this dependence is played by the changes of endogenous MEL levels. Secondary changes in circadian oscillations of calciotropic hormones, IGF-I and corticosterone concentrations, caused by pinealectomy and long-term MEL administration result in altered bone metabolism rhythm.
Key words: Pinealectomy - Melatonin - Bone metabolism - Hormones -
Circadian rhythm - Male rats
ENDOCRINE REGULATIONS, Vol. 37, 211–224, 2003
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J. J. Stepan, 1 F. Alenfeld, 2 G. Boivin, 3 J. H. M. Feyen, 4 P. Lakatos
Charles University School of Medicine, Prague, Czech
Republic,
1 Zentrum für Muskel- und Knochenforschung, Klinikum Benjamin
Franklin, Berlin, B.R.D
2 INSERM Unité 403, Faculté de Médecine R. Laennec, 69372
Lyon Cedex 08, France,
3 Bristol-Myers Squibb, Princeton NJ, USA,
41st Department of Medicine, Semmelweis University Medical School, Budapest, Hungary, E-mail: jstepan@vol.cz
Summary:
In the treatment of osteoporosis, the aim of the
antiresorptive therapy is to restore bone density by decreasing bone remodeling.
The process of bone remodeling plays a role in plasma calcium homeostasis
and serves to modify bone architecture in order to meet changing mechanical
needs, to maintain osteocyte viability, and to repair microdamage in bone
matrix. Estrogen deficiency results in a number of detrimental effects on
bone, including suppression of osteocyte survival as well as impairment of
osteoblast response to mechanical stimuli and repair of ageing bone. In this
review, effects of available antiresorptive therapies on endocrine regulations
of bone metabolism in postmenopausal osteoporosis are compared.
The aim of antiresorptive treatment is to ensure adequate bone remodeling,
reparation of microdamage of bone, and increased bone strength. Ideally, this
effect should be maintained long-term. Several agents are approved for the
treatment of osteoporosis. Calcitonin transiently inhibits osteoclast activity
without decreasing osteoblast collagen synthesis. Aminobisphosphonates decrease
bone remodeling by decreasing osteoclast activity and by inducing osteoclast
apoptosis. This allows more time for secondary mineralization to proceed to
completion in the existing bone tissue mass, so increasing the mechanical
resistance of bone to loading. Estrogens and raloxifene (a selective estrogen
receptor modulator that acts as an estrogen agonist in bone) suppress bone
remodeling to the premenopausal range, maintaining the function of osteoblasts
and osteocytes. In the placebo-controlled osteoporosis treatment trials, all the
above treatments reduced the risk of fractures. Raloxifene therapy was also
associated with a favorable or neutral effect in the cardiovascular system,
and a reduced incidence of breast cancer. Selection of appropriate drug for
treatment of postmenopausal osteoporosis should take into account the long-term
effect of the antiresorptive agent on bone. Moreover, the effects on other
tissues ++should also be considered, and this encompasses both safety concerns,
as well as the potentially beneficial effects on other tissues. Further
investigation is needed to evaluate the different modes of action of these
agents, and their long-term effects on bone and other tissues.
Key Words: Apoptosis - Bisphosphonates - Calcitonin - Cytokines -
Estrogen - Osteoblasts -Osteoclasts - SERM - Raloxifene
ENDOCRINE REGULATIONS, Vol. 37, 227–240, 2003
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