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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Toxicol Ind Health. 1999 Jan-Mar;15(1-2):65-79.
Peripubertal exposure to the antiandrogenic fungicide, vinclozolin, delays puberty, inhibits the development of androgen-dependent tissues, and alters androgen receptor function in the male rat.

Monosson E, Kelce WR, Lambright C, Ostby J, Gray LE Jr.

University of North Carolina Chapel Hill, USA.

Vinclozolin is a well-characterized antiandrogenic fungicide. It produces adverse effects when administered during sexual differentiation, and it alters reproductive function in adult male rats by acting as an androgen-antagonist. Two active metabolites of vinclozolin, M1 and M2, compete with natural androgens for the rat and human androgen receptors (ARs), an effect that blocks androgen-induced gene expression in vivo and in vitro. In addition to their effects during perinatal life, androgens play a key role in pubertal maturation in young males. In this regard, the present study was designed to examine the effects of peripubertal oral administration of vinclozolin (0, 10, 30, or 100 mg kg-1 day-1) on morphological landmarks of puberty, hormone levels, and sex accessory gland development in male rats. In addition, as binding of the M1 and M2 to AR alter the subcellular distribution of AR by inhibiting AR-DNA binding, we examined the effects of vinclozolin on AR distribution in the target cells after in vivo treatment. We also examined serum levels of vinclozolin, M1, and M2 in the treated males so that these could be related to the effects on the reproductive tract and AR distribution. Vinclozolin treatment delayed pubertal maturation (at 30 and 100 mg kg-1 day-1) and retarded sex accessory gland and epididymal growth. Serum luteinizing hormone (LH; significant at all dosage levels) and testosterone and 5 alpha-androstane, 3 alpha, 17 beta-diol (at 100 mg kg-1 day-1) levels were increased. Testis size and sperm production, however, were unaffected. It was apparent that these effects were concurrent with subtle alterations in the subcellular distribution of AR. In control animals, most AR were in the high salt cell fraction, apparently bound to the natural ligand and DNA. Vinclozolin treatment reduced the amount of AR in the high salt (bound to DNA) fraction and it increased AR levels in the low salt (inactive, not bound to DNA) fraction. M1 and M2 were found in the serum of animals from the two highest dosage groups, but they were present at levels well below their K1 values. In summary, these results suggest that when the vinclozolin metabolites occupy a small percentage of AR in the cell, this prevents maximal AR-DNA binding and alters in vivo androgen-dependent gene expression and protein synthesis, which in turn results in obvious alterations of morphological development and serum hormone levels. It is noteworthy that similar exposures during prenatal life result in a high incidence of malformations in male rats.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10188192&dopt=Abstract

Turk J Pediatr. 2002 Jul-Sep;44(3):211-4.
Leptin levels in children with insulin dependent diabetes mellitus.

Bideci A, Cinaz P, Ezgu FS.

Department of Pediatrics, Gazi University, Faculty of Medicine, Ankara, Turkey.

Leptin, a product of the ob gene, is a polypeptide hormone produced in adipose tissue that informs the brain about the amount of energy storage of body fat. It has very important effects on neuroendocrine functions and energy expenditure. The aim of our study was to determine leptin levels of children with insulin dependent diabetes mellitus (IDDM), which is known to affect body metabolism, and to investigate the relationship between duration of the disease, insulin dosage, HbA1c levels, body mass index (BMI), serum lipids and IGF-1 levels. Sixteen patients with IDDM (chronological age 13.8 +/- 2.6 years) whose HbAlc levels were 10.2 +/- 1.9 %, BMI 21.2. +/- 2.7 kg/m2, insulin dosage 0.9 +/- 0.4 U/kg/day and duration of the disease 6.7 +/- 2.6 years, and 12 healthy controls (13.4 +/- 2.6 years) were included in the study. Fasting plasma leptin levels were measured by radioimmunoassay method. The mean plasma leptin levels of the patient and the control groups were 19.1 +/- 7.6 ng/ml and 6.1 +/- 2.9 ng/ml, respectively, and significant difference was found between the two groups (p < 0.05). No correlation was found between leptin values and IGF-1, cholesterol, HDL-cholesterol, LDL-cholesterol, triglyceride levels, atherogenic index, insulin dosage or HbA1c levels in the patient group. A weak statistical correlation was determined between BMI and leptin levels in the IDDM group (r = 0.28, p < 0.05). A positive correlation was also found between leptin levels and the duration of the disease (r = 49, p < 0.05). As a result, it seems that leptin levels of children with IDDM differed from the levels of the control group significantly, and that the duration of insulin therapy was responsible for this difference.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12405431&dopt=Abstract

Turk J Pediatr. 2002 Jul-Sep;44(3):215-8.
Serum insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 levels in severe iodine deficiency.

Alikasifoglu A, Ozon A, Yordam N.

Division of Pediatric Endocrinology, Hacettepe University, Faculty of Medicine, Ankara, Turkey.

Iodine deficiency is an important public health problem worldwide. It is well known that it has severe consequences such as brain damage, developmental delay, deficits in hearing and learning and lower intellectual attainment. It also has a negative impact on growth. In this study, we aimed to address this issue and we assessed height standard deviation scores of children living in an area of severe iodine deficiency in comparison to those living in a mild iodine deficiency area. Serum levels of insulin-like growth factor-I (IGF-I), IGF-binding protein-3 (IGFBP-3), thyroxine (T4), and thyroid stimulating hormone (TSH) were also analyzed to investigate the mechanisms by which iodine depletion leads to growth failure. Pubertal children in a severe iodine deficient SID area had lower height standard deviation scores (HSDS), IGF-I and IGFBP-3 levels than those living in mild iodine deficient MID area. Similar findings could not be elucidated in the prepubertal age group. The major determinants of HSDS were age, IGF-I, IGFBP-3 and TSH. IGF-I and IGFBP-3 were negatively correlated with T4. These findings suggest that iodine deficiency has a negative impact on growth, as well as IGF-I and IGFBP-3 levels. This effect seems to be due to the derangements in thyroid hormone economy arising from iodine depletion. The degree of this impact may be related to the duration of iodine depletion or may be dependent on the developmental stage of the organism at the time of iodine depletion.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12405432&dopt=Abstract

Reprod Nutr Dev. 2002 May-Jun;42(3):275-80.
In vitro maturation and fertilisation of bovine oocytes in relation to GH gene polymorphism (Leu/Val).

Lechniak D, Adamowicz T, Stanislawski D, Kaczmarek D.

August Cieszkowski, Agricultural University of Poznan, Department of Genetics and Animal Breeding, Poland. lechniaay.au.poznan.pl

The present study describes the analysis of the associations between the growth hormone gene polymorphism (Leu/Val) and oocyte maturation and in vitro fertilisation in cattle. Two independent experiments were carried out. In the first one, oocytes were collected from 49 single ovaries, matured in vitro, measured and cytogenetically analysed. One ovary was considered as a donor. The procedure of the donor's genotyping at the GH locus was based on DNA extracted from the granulosa cells. The GH genotype did not influence the oocyte diameter nor the number of oocytes collected, which were selected for maturation and matured. An unreduced chromosome number was found in 8.8% of the cells at the second metaphase stage and 42.9% of the donors. This anomaly was observed in all genotype groups with a higher frequency in the VV cows (P < 0.01). In the second experiment, the oocytes collected from 72 single ovaries were matured and fertilised in vitro. The GH genotype of a donor did not influence the number of zygotes cleaved on day-2. It has to be mentioned, that due to the low frequency of the VV genotype (0.03), the results of the present study should be treated as preliminary and need further analysis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12405455&dopt=Abstract

Equine Vet J Suppl. 2002 Sep;(34):22-8.
Training-induced alterations in glucose metabolism during moderate-intensity exercise.

Geor RJ, McCutcheon LJ, Hinchcliff KW, Sams RA.

Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus 43210, USA.

In several species, physical conditioning (training) provokes a large shift in substrate utilisation during submaximal exercise. Few studies in horses have quantitatively examined these effects. Therefore, the effects of exercise training on plasma glucose kinetics during submaximal exercise were examined in 7 horses (5 Thoroughbred, 2 Standardbred; age 3-9 years) that had been paddock-rested for at least 6 months. Two days after determination of maximum aerobic capacity (VO2max), horses ran on a treadmill (4 degree incline) at 55% of VO2max (UT) for 60 min or until fatigue and then completed 6 weeks of moderate-intensity training on a treadmill (5 days/week). Following training and a second VO2max test, the horses completed exercise trials at the same absolute (ABS) and relative (REL) workload in random order, with at least 3 days between tests. After training, VO2max had increased (P<0.05) by 14.9% (mean +/- s.e. pretraining 118.4 +/- 7.4 ml/kg bwt/min; post-training 136.1 +/- 7.8 ml/kg bwt/min). Mean exercise duration was longer (P<0.05) in the ABS trial (57 +/- 1.9 min) than in the UT (46 +/- 3.9 min) and REL (49 +/- 4.6 min) trials. Plasma glucose concentration increased during exercise, and was lower (P<0.05) in ABS than in UT and REL at the end of exercise. Mean glucose rate of appearance (Ra) and disappearance (Rd) were 22 and 21% lower (P<0.05), respectively, in ABS than in UT, but mean glucose Ra and Rd did not differ between the UT and REL trials. Exercise-induced changes in glucagon, epinephrine and norepinephrine were blunted (P<0.05) in ABS, but not REL, when compared to UT. It is concluded that 6 weeks of moderate-intensity training results in a decrease in glucose flux during submaximal exercise at the same absolute, but not relative, workload. The training-induced decrease in glucose flux may, in part, be due to altered plasma concentrations of the major glucoregulatory hormones.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12405654&dopt=Abstract

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