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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

Zhonghua Nei Ke Za Zhi. 2003 Mar;42(3):177-80.
[The effects of continuous stimulation with different doses of parathyroid hormone 1-34 fragment on human SaoS-2 cells]

[Article in Chinese]

Li M, Meng XW, Zhou XY, Xing XP, Liu HC.

Department of Endocrinology, Peking Union Medical College Hospital, Peking Unoin Medical College, Chinese Academy of Medical Science, Beijing 100730, China. limeilzahoo.com

OBJECTIVE: To observe the effects of different doses of human parathyroid hormone fragment (hPTH)1-34 on SaoS cells and to explore the signal pathway and mechanism. METHODS: 5 x 10(4) cells/ml SaoS cells were seeded. Doses of 5, 50, 500 and 5 000 micro g/L hPTH1-34 were supplemented respectively. Total RNA was extracted by Trizol kit. Alkaline phosphatase (ALP), osteocalcin (BGP) and cAMP concentrations were measured by chemical, radioimmunoassay and competitive protein binding methods. c-fos gene expression level was semi-quantified by reverse transcriptase (RT)-PCR. RESULTS: ALP activity was higher in 500 micro g/L dose (P < 0.05 vs. control). BGP level was inhibited in 5 000 micro g/L dose (P < 0.05 vs. control and pretreatment). 50 and 500 micro g/L hPTH1-34 enhanced cAMP level significantly (P < 0.05 vs. control). No obvious increase of cAMP level was found in 5 000 micro g/L and 5 micro g/L dose groups (P > 0.05 vs. control and pretreatment). c-fos expression was higher in 50 and 500 micro g/L group. CONCLUSION: Different doses of hPTH1-34 exert distinct effects on osteoblasts. hPTH1-34 affects ALP and c-fos depending on protein kinase A signal pathway. hPTH1-34 exerts its action via regulation of osteoblasts by c-fos.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12816700&dopt=Abstract [PubMed - in process]

Am J Physiol Regul Integr Comp Physiol. 2003 Jun 19 [Epub ahead of print].
c-Kit Mutant Mouse Behavioral Phenotype: Altered Meal Patterns and CCK Sensitivity but Normal Daily Food Intake and Body Weight.

Chi MM, Powley TL.

Department of Psychological Sciences, Purdue University, West Lafayette, IN, USA.

The mouse W/W(v) mutation of the c-Kit receptor causes extensive loss of gastrointestinal interstitial cells of Cajal and vagal intramuscular arrays (IMAs; one of the two putative mechanoreceptors in gastrointestinal smooth muscle). To characterize the behavioral phenotype of the c-Kit mouse and to evaluate the roles of these mechanoreceptors in controlling food intake, meal patterns and daily intakes of W/W(v) mice and controls were examined using solid (20 mg pellets) and liquid (Isocal) maintenance diets. After the meal pattern experiments, CCK (0.5, 1, 2, 4, 8 and 16 micro g/kg i.p.) was administered to examine the role of the interstitial cells and vagal IMA mechanoreceptors in relaying peripheral signals of satiety activated by CCK-A receptors, while the specificity of the response was assessed with the antagonist Devazepide (300 micro g/kg i.p.). On both diets, the W/W(v) mice ate smaller meals for shorter durations, with a compensatory increase in meal number, resulting in daily intakes and body weights similar to the controls. After CCK injections, the mutant mice consistently suppressed intake more (~2X) in 30-minute tests, regardless of the test diet (12.5% glucose, chow, pellets, and Isocal). The increased sensitivity of W/W(v) mice to CCK reflected an increased potency of the hormone (c-Kit mouse ED50 = 2.4 micro g/kg; control ED50 = 6.4 micro g/kg) and a shift of the dose-response curve to the left. Devazepide blocked the CCK suppression of ingestion. These results indicate that the selective loss of the interstitial cells and IMAs disrupts short-term feeding of the W/W(v) mice by inducing an earlier satiety, possibly by altering gastric accommodation and/or emptying, without affecting the long-term mechanisms controlling overall intake or body weight. The results also suggest that the reduction of interstitial cells and IMAs augments the sensitivity to or increases the efficiency of exogenous CCK.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12816741&dopt=Abstract [PubMed - as supplied by publisher]

Am J Physiol Regul Integr Comp Physiol. 2003 Oct;285(4):R791-9. Epub 2003 Jun 19.
Stress facilitates body weight gain in genetically predisposed rats on medium-fat diet.

Michel C, Levin BE, Dunn-Meynell AA.

Neurology Service (127C VA Medical Center, 385 Tremont Ave., E. Orange, NJ 07018-1095. levimdnj.edu

To assess the interaction between stress and energy homeostasis, we immobilized male Sprague-Dawley rats prone to diet-induced obesity (DIO) or diet resistance (DR) once for 20 min and then fed them either low-fat (4.5%) chow or a medium-fat (31%), high-energy (HE) diet for 9 days. Stressed, chow-fed DIO rats gained less, while stressed DIO rats on HE diet gained more body weight and had higher feed efficiency and plasma leptin levels than unstressed controls. Neither stress nor diet affected DR body weight gain. While stress-induced plasma corticosterone levels did not differ between phenotypes, DIO rats were initially more active in an open field and had higher hippocampal dentate gyrus and CA1 glucocorticoid receptor (GR) mRNA than DR rats, regardless of prior stress or diet. HE diet intake was associated with raised dentate gyrus and CA1 GR and amygdalar central nucleus (CeA) corticotropin-releasing hormone (CRH) mRNA expression, while stress was associated with reduced hypothalamic dorsomedial nucleus Ob-R mRNA and CeA CRH specifically in DIO rats fed HE diet. Thus a single stress triggers a complex interaction among weight gain phenotype, diet, and stress responsivity, which determines the body weight and adiposity of a given individual.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12816743&dopt=Abstract [PubMed - in process]

Endocrinology. 1999 May;140(5):1984-9.
Evidence that insulin-like growth factor I and growth hormone are required for prostate gland development.

Ruan W, Powell-Braxton L, Kopchick JJ, Kleinberg DL.

Department of Medicine, New York University School of Medicine, and the Department of Veterans Affairs Medical Center, New York 10016, USA.

Insulin-like growth factor I (IGF-I) has been implicated as a factor that may predispose one to prostate cancer. However, no specific relationship between IGF-I and prostate development or cancer in vivo has been established. To determine whether IGF-I was important in prostate development, we examined prostate architecture in IGF-I(-/-) null mice and wild-type littermates. Glands from 44-day-old IGF-I-deficient animals were not only smaller than those from wild-type mice, but also had fewer terminal duct tips and branch points and deficits in tertiary and quaternary branching (P < 0.0001), indicating a specific impairment in gland structure. Administration of des(1-3)-IGF-I for 7 days partially reversed the deficit by increasing those parameters of prostate development (P < 0.006). That IGF-I production probably mediates an effect of GH in this process was indicated by the observations that GH antagonist transgenic mice also had significantly impaired prostate development (P < 0.0002) and that bovine GH had no independent effect on stimulating prostate development in IGF-I null animals. The data indicate that IGF-I deficiency is the proximate cause of impaired prostate development and give credence to the idea that, like testosterone, GH and IGF-I may be involved in prostate cancer growth as an extension of a normal process.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10218945&dopt=Abstract

Clin Chem. 2003 Jul;49(7):1139-48.
Urinary estrone conjugate and pregnanediol 3-glucuronide enzyme immunoassays for population research.

O'Connor KA, Brindle E, Holman DJ, Klein NA, Soules MR, Campbell KL, Kohen F, Munro CJ, Shofer JB, Lasley BL, Wood JW.

Department of Anthropology and Center for Studies in Demography and Ecology, University of Washington, Seattle WA 98195, USA. oconnor.washington.edu

BACKGROUND: Monitoring of reproductive steroid hormones at the population level requires frequent measurements, hormones or metabolites that remain stable under less than ideal collection and storage conditions, a long-term supply of antibodies, and assays useful for a range of populations. We developed enzyme immunoassays for urinary pregnanediol 3-glucuronide (PDG) and estrone conjugates (E1Cs) that meet these criteria. METHODS: Enzyme immunoassays based on monoclonal antibodies were evaluated for specificity, detection limit, parallelism, recovery, and imprecision. Paired urine and serum specimens were analyzed throughout menstrual cycles of 30 US women. Assay application in different populations was examined with 23 US and 42 Bangladeshi specimens. Metabolite stability in urine was evaluated for 0-8 days at room temperature and for 0-10 freeze-thaw cycles. RESULTS: Recoveries were 108% for the PDG assay and 105% for the E1C assay. Serially diluted specimens exhibited parallelism with calibration curves in both assays. Inter- and intraassay CVs were <11%. Urinary and serum concentrations were highly correlated: r = 0.93 for E1C-estradiol; r = 0.98 for PDG-progesterone. All Bangladeshi and US specimens were above detection limits (PDG, 21 nmol/L; E1C, 0.27 nmol/L). Bangladeshi women had lower follicular phase PDG and lower luteal phase PDG and E1Cs than US women. Stability experiments showed a maximum decrease in concentration for each metabolite of <4% per day at room temperature and no significant decrease associated with number of freeze-thaw cycles. CONCLUSIONS: These enzyme immunoassays can be used for the field conditions and population variation in hormone metabolite concentrations encountered in cross-cultural research.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12816911&dopt=Abstract

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