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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

J Virol. 2002 Sep;76(17):8572-81.
Mechanisms of inhibition of nuclear hormone receptor-dependent hepatitis B virus replication by hepatocyte nuclear factor 3beta.

Tang H, McLachlan A.

Department of Cell Biology, The Scripps Research Institute, La Jolla, California 92037, USA.

The nuclear hormone receptors hepatocyte nuclear factor 4 (HNF4) and the retinoid X alpha (RXRalpha) plus the peroxisome proliferator-activated receptor alpha (PPARalpha) heterodimer support hepatitis B virus (HBV) replication in nonhepatoma cells. Hepatocyte nuclear factor 3 (HNF3) inhibits nuclear hormone receptor-mediated viral replication. Inhibition of HBV replication by HNF3beta is associated with the preferential reduction in the level of the pregenomic RNA compared with that of precore RNA. Hepatitis B e antigen (HBeAg), encoded by the precore RNA, mediates part of the inhibition of viral replication by HNF3beta. The amino-terminal transcriptional activation domain of HNF3beta is essential for the inhibition of HBV replication. The activation of transcription by HNF3 from HBV promoters downstream from the nucleocapsid promoter appears to contribute indirectly to the reduction in the steady-state level of 3.5-kb HBV RNA, possibly by interfering with the elongation rate of these transcripts. Therefore, transcriptional interference mediated by HNF3 may also regulate HBV RNA synthesis and viral replication.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163577&dopt=Abstract

J Nutr. 2002 Aug;132(8):2183-7.
Pregnancy and lactation affect markers of calcium and bone metabolism differently in adolescent and adult women with low calcium intakes.

Bezerra FF, Laboissiere FP, King JC, Donangelo CM.

Laboratorio de Bioquimica Nutricional e de Alimentos, Departamento de Bioquimica, Instituto de Quimica, Universidade Federal do Rio de Janeiro, Brazil.

Physiologic adaptation to the high calcium demand during pregnancy and lactation may be different in adolescents than in adults, particularly at low calcium intake. The aim of this cross-sectional study was to compare biochemical markers of calcium and bone metabolism between adolescent (14-19 y) and adult (21-35 y) women with calcium intake approximately 500 mg/d, in three different physiologic states, i.e., control (nonpregnant, nonlactating; NPNL), pregnant and lactating. Markers of calcium metabolism [serum Ca, P and intact parathyroid hormone (iPTH); urinary Ca and P] and of bone turnover [urinary deoxypyridinoline (D-Pyr) and plasma bone alkaline phosphatase (BAP)] were measured in NPNL (adolescents, n = 12 and adults, n = 25), pregnant (adolescents, n = 30 and adults, n = 36) and lactating (adolescents, n = 19 and adults, n = 26) women. In the NPNL women, iPTH, D-Pyr and BAP were higher (P < 0.001) and urinary Ca was lower (P < 0.001) in adolescents than in adults. Serum iPTH was higher (P < 0.001) and urinary Ca was lower (P < 0.01) in adolescents than in adults also in pregnancy and lactation. Compared with NPNL women, serum Ca decreased (P < 0.001) with pregnancy in adolescents but not in adults. The increase in D-Pyr with pregnancy and lactation was very pronounced in adults ( approximately 130%, P < 0.001) but less in adolescents (<25%, P < 0.01). BAP increased (P < 0.001) with pregnancy and lactation in adults ( approximately 60%) but decreased (P < 0.001) with pregnancy in adolescents ( approximately 13%). Pregnancy and lactation appear to affect bone turnover in adolescent and adult women with low calcium intake differently.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163659&dopt=Abstract

J Nutr. 2002 Aug;132(8):2246-50.
Body weight and food intake profiles are modulated by sex hormones and tamoxifen in chronically hypertensive rats.

Wallen WJ, Belanger MP, Wittnich C.

Department of Physiology, University of Toronto, Canada M5S 1A8.

Sex hormones and the selective estrogen receptor modulator tamoxifen affect food consumption and body weight in normotensive rats. This study investigated the effects of hormone manipulation and tamoxifen on weight gain and food intake in the presence of chronic systemic hypertension. Male and female spontaneously hypertensive rats (SHR) were either neutered or sham operated before puberty, and subgroups of neutered females received either estrogen replacement therapy (ERT) or tamoxifen at the age of 12 wk. Weekly body weight and food consumption were assessed, and food consumption was normalized to metabolic weight (g body(2/3)). Neutering reduced weight gain in males (P = 0.0001), but increased it in females (P < 0.0001). Both ERT and tamoxifen treatment prevented this increase in weight, with body weight dropping to levels of sham-operated rats for ERT, whereas rats given tamoxifen maintained greater body weights than sham-operated rats (P < 0.0001). This contrasts with previous work in normotensive females in which sham-operated and tamoxifen-treated females did not differ. Neutering reduced normalized food consumption relative to sham-operated rats in both males and females (P < 0.05). Although ERT returned it to normalized intakes of sham-operated rats, tamoxifen reduced normalized food consumption relative to that of both sham-operated and ERT groups. In hypertensive rats, body weight is modulated by sex hormones in both males and females, but in opposite directions. Both estrogen and tamoxifen exert immediate effects in females. Interestingly, the effect of tamoxifen on body weight appears to be greater in hypertensive than in normotensive rats.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163670&dopt=Abstract

Pharmacopsychiatry. 2002 Jul;35(4):127-34.
Relationship between cortisol and serotonin metabolites and transporters in alcoholism [correction of alcolholism].

Heinz A, Jones DW, Bissette G, Hommer D, Ragan P, Knable M, Wellek S, Linnoila M, Weinberger DR.

Intramural Research Program, Clinical Brain Disorders Branch/NIMH, Bethesda, MD, USA. andreas.heinharite.de

BACKGROUND: Stress hormone activation may induce clinical depression via an interference with central serotonergic neurotransmission. In alcoholics, a reduction in serotonin transporters was associated with clinical depression, and an activation of cortisol secretion is frequently found during detoxification. We assessed the interaction between stress hormone activation, serotonin transporters, monoamine metabolites in the cerebrospinal fluid (CSF), and mood states in male and female alcoholics and healthy control subjects. METHODS: The availability of serotonin transporters was measured with [I-123]beta-CIT and SPECT in the raphe area of the brainstem in 31 alcoholics after four weeks of abstinence and in 25 age-matched healthy volunteers. Concentrations of plasma cortisol were measured on the day of the SPECT scan. Within one week after the SPECT scan, we assessed monoamine metabolites and corticotropin-releasing factor (CRF) in the CSF. RESULTS: Clinical depression was associated with a reduction in serotonin transporter availability among male alcoholics. Among male alcoholics and healthy volunteers, CSF 5-HIAA and plasma cortisol concentrations were inversely correlated with the availability of raphe serotonin transporters and positively correlated with the severity of clinical depression. No significant correlations were observed between raphe serotonin transporters and HVA, MHPG and CRF concentrations in the CSF. CONCLUSION: Our findings support the hypothesis of an interaction between reduced serotonin transporters, stress hormone activation and clinical depression. They confirm the hypothesis that serotonergic neurotransmission dysfunction in alcoholism is limited to male alcoholics. The observed interactions between high cortisol concentrations and reduced serotonin transporter availability warrant further studies in major depression and other neuropsychiatric diseases with implied cortisol activation and serotonergic dysfunction.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12163982&dopt=Abstract

Clin Nephrol. 2002 Dec;58(6):431-7.
Relationship between body composition, sex hormones and leptinemia in hemodialyzed patients with chronic renal failure.

Chudek J, Adamczak M, Kokot F, Karkoszka H, Ignacy W, Klimek D, Wiecek A.

Department of Nephrology, Endocrinology and Metabolic Diseases, Silesian University Medical School, Katowice, Poland.

BACKGROUND: Females are characterized by significantly higher plasma leptin concentration than males. It seems likely that sex hormones influence leptinemia independently from differences in body composition. The aim of the present study was to analyze the contribution of plasma concentrations of testosterone and estradiol on leptinemia in hemodialyzed patients. METHODS: 110 hemodialyzed patients--HD (60 M, 50 F) and 70 healthy subjects (HS) (30 M, 40 F) were enrolled in this study. Plasma leptin, testosterone or estradiol and CRP concentrations and body composition by dual-energy X-ray absorptiometry (DEXA) were assessed. RESULTS: Total body fat was significantly higher in females than in males (27.5 +/- 1.5% vs. 17.2 +/- 1.0% of body weight in HD and 36.0 +/- 1.0% vs. 18.2 +/- 1.4% in HS, respectively). Plasma leptin concentrations were markedly higher in females than in males both in HD (27.9 +/- 5.4 ng/ml vs. 9.6 +/- 1.9 ng/ml) and HS (16.5 +/- 1.7 ng/ml vs.3.1 +/- 0.4 ng/ml). A highly significant, strong positive correlation was found between total fat mass (TFM) and leptinemia in all studied groups. No significant univaried correlation between plasma leptin and testosterone or estradiol concentrations respectively was found both in HD and HS. Multiple regression analyses showed that the main determinant of leptinemia is TFM (beta = 0.623 and 0.798 in HS females and males respectively, and beta = 1.058 and 0.797 in HD females and males respectively). Plasma concentration of testosterone (beta = -0.139 and beta = -0.075 in male HD and HS respectively) and estradiol (beta = 0.199 and beta = 0.046 in females HD and HS, respectively) contributed to leptinemia only in a minor degree. CONCLUSION: Both testosterone and estradiol are minor contributors to leptinemia both in HS and HD patients. The main determinant of leptinemia in these subjects is total body fat mass.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12508965&dopt=Abstract

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