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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

Brain Res Bull. 1978 Sep-Oct;3(5):549-53.
Similar effects of estrogen and lateral hypothalamic lesions on feeding behavior of female rats.

Nance DM, Gorski RA.

Department of Anatomy, College of Medicine, University of South Florida, Tampa 33612.

Many similarities exist between the inhibitory influence of estrogen on food intake (FI) and body weight (BWt) in female rats and the effect of lateral hypothalamic (LH) lesions on energy balance. Thus, a possible interaction of small electrolytic LH lesions (0.8 mA/10 sec) with hormone-dependent changes in FI, BWt and feeding patterns of female rats was examined. Relative to sham operated controls, rats with LH lesions showed a transitory period of anorexia and initial loss of BWt. Subsequently, FI and BWt gains of lesioned rats returned to control levels although a small chronic reduction in mean BWt was observed relative to sham animals. Daily changes in FI and BWt during 4-day estrous cycles as well as post-ovariectomy increases in FI and BWt were comparable for lesion and sham animals. Also, both groups showed a similar decrease in FI and BWt following a SC injection of estradiol benzoate (EB). Possible effects of LH lesions were further examined by analyzing feeding patterns. Feeding behavior was continuously monitored with photodetectors and recorded on an Esterline Angus event marker before and after a single SC injection of 6 micrograms of EB. Relative to shams, LH animals showed an exaggerated diurnal distribution of meals, ate smaller meals of shorter duration and had larger intervals between meals during the light period. EB was found to shift the feeding patterns of sham animals towards the meal patterns shown by the lesioned rats (exaggerated diurnal distribution of meals, etc.). However, the lesioned rats also showed a normal change in feeding patterns following EB, albeit these changes occurred from a markedly different baseline level.(ABSTRACT TRUNCATED AT 250 WORDS)

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=122720&dopt=Abstract

Cancer Causes Control. 2003 Feb;14(1):75-84.
Body mass index and colon cancer: an evaluation of the modifying effects of estrogen (United States).

Slattery ML, Ballard-Barbash R, Edwards S, Caan BJ, Potter JD.

Health Research Center, Department of Family and Preventive Medicine, 375 Chipeta Way, Suite A, University of Utah, Salt Lake City, UT 84108, USA.

OBJECTIVE: The association between body mass index (BMI) and colon cancer has been reported to be different for men and women. No prior literature has examined if estrogen influences these differences. METHODS: Using data from an incident population-based case (n = 1,972) and control (n = 2386) study of colon cancer we evaluated if estrogen modifies the association between BMI and risk of colon cancer. RESULTS: Women who were estrogen-negative (postmenopausal women not taking hormone replacement therapy, HRT) were at increased risk of colon cancer regardless of indicator of estrogen status used (i.e. estrogen-negative compared to estrogen-positive women defined as either being premenopausal or postmenopausal women using HRT, OR 1.54, 95% CI 1.23-1.93; no recent exposure to estrogens compared to current or HRT use within the past 2 years, OR 1.58, 95% CI 1.24-2.00; postmenopausal women not currently using HRT compared to postmenopausal women taking HRT, OR 1.65, 95% CI 1.29-2.12). BMI (kg/m2) was not associated with an increased risk of colon cancer among women who were estrogen-negative. However, women who were estrogen-positive experienced a greater than two-fold increase in colon cancer risk if they had a BMI of > 30 relative to those who had a BMI of <23 (for estrogen-positive, OR, 2.50, 95% CI 1.51-4.13; premenopausal, OR 2.19, 95% CI 0.94-5.07; postmenopausal using HRT, OR 3.36, 95% CI 1.58-7.13). Among men the colon cancer risk associated with BMI decreased with advancing age. Physical activity modified the increased colon cancer risk associated with a large BMI. CONCLUSIONS: These data suggest the importance of estrogen in colon cancer etiology. Being estrogen-negative resulted in a significant increased risk of colon cancer. However, BMI significantly increased the risk of colon cancer among women who were estrogen-positive. We hypothesize that estrogen up-regulates IGF-I receptors and IRS-I levels in the colon, which in turn increases susceptibility to obesity-induced increased levels of insulin. We further hypothesize that androgens may have similar effects in men given the decline in colon cancer risk associated with BMI with advancing age.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12708728&dopt=Abstract

Acta Endocrinol (Copenh). 1975 Jan;78(1):180-91.
Urinary gonadotrophins in the Sertoli-Cell-only syndrome.

Christiansen P.

In order to study the hypophyseal-testicular axis in males with complete absence of germinal epithelium, the urinary total hypophyseal gonadotrophins (HG), urinary follicle stimulating hormone (FSH) and urinary luteinizing hormone (LH) were measured by specific bioassays in 12 males with classical Sertoli-cell-only syndrome and compared with HG, FSH, and LH in normal and castrated men. HG and FSH were significantly higher than HG and FSH in normal men (P smaller than 0.0025, P smaller than 0.0005, respectively), but significantly lower than in castrated men (P less than 0.001, P less than 0.01, respectively). LH was not different from LH of normal men, but significantly lower than in castrated men (P less than 0.0005). All patients had normal excretion of androgen metabolites (androsterone plus aetiocholanolone) but a dexamethasone suppression test, performed in 8 subjects, revealed that in 2 cases of testicular origin, the values were below the normal range. The excretion of oestrogens was within the normal range. The presented data support the concept that the germinal epithelium produces a substance capable of inhibiting FSH secretion from the hypophyses, the Sertoli cell itself, however, having a basal production of this inhibitor. The finding of low excretion of testicular androgen metabolites in some of the patients and normal urinary LH, indicates that disturbances in the LH-testosterone feedback mechanism in such patients may occur and that the previous concept of isolated defects of spermatogenesis in all such patients was erroneous.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=123110&dopt=Abstract

Brain Res. 1975 Mar 28;86(3):353-71.
Effect of pinealectomy, gonadectomy, pCPA and pineal extracts on the rat parvocellular neurosecretory hypothalamic system; a fluorescence histochemical investigation.

Smith AR, Kappers JA.

Using the fluorescence histochemical technique, yellow autofluorescent granules were observed in neurones of the arcuate and ventromedial hypothalamic nuclei of the rat (type I cells). In the same nuclei, neurones could be demonstrated showing a formaldehyde-induced yellow fluorescence (type II cells). Microelectrophoresis and special staining methods applied to the pineal gland revealed the autofluorescent compound to be a protein containing a relatively high content of tryptophan. It is probable that the formaldehyde-induced yellow fluorescence is due to the presence of serotonin. In view of investigating a possible functional relationship between the pineal gland and the parvocellular hypothalamic nuclei mentioned, hypothalamic type I and type II cells, as well as autofluorescent and serotonin-containing pinealocytes, if present, were quantified under the following experimental conditions: (1) p-chlorophenylalanine (pCPA) administration, (2) castration, (3) pinealectomy, and (4) pinealectomy followed by substitution using rat and sheep pineal extract. Administration of pCPA caused a decrease in the number of type II and an increase in the number of type I cells, both in the pineal gland and the hypothalamic nuclei. Castration, in contrast, was followed by an increase in the number of autofluorescent pinealocytes, but a decrease of autofluorescent neurones in the hypothalamic nuclei (type I cells) while the number of serotonin-containing pinealocytes increased; decreasing in both hypothalamic nuclei. After pinealectomy the hypothalamic nuclei showed an increase of type I neurones, but a decrease of type II nerve cells. Pinealectomy followed by substitution using pineal extracts restored the number of type I and type II neurones to that normally found in the arcuate and ventromedial hypothalamic nuclei of control animals. The present investigation brings histological evidence of an influence exerted by the rat pineal gland on nuclei forming part of the hypothalamic hypophyseotropic area. The data obtained and some of the literature strongly suggest that the type II neurones, which probably contain serotonin, inhibit, in the same hypothalamic nuclei, the production of luteinizing hormone-releasing factor (LH-RF). As yet, the function of the autofluorescent compound present in the type I neurones is not known.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=123166&dopt=Abstract

Cancer Res. 1975 Mar;35(3):560-7.
Influence of insulin on estrogen-induced responses in the r3230ac mammary carcinoma.

Cohen ND, Hilf R.

The R3230AC mammary adenocarcinoma was not dependent on insulin; tumor growth was equal to or greater in diabetic rats than in intact animals. However, tumor growth was reduced when daily doses of insulin were administered. Treatment with estrogen inhibited growth of the R3230AC carcinoma, either in diabetic rats or in intact animals simultaneously treated with insulin. The effects of insulin plus estrogen treatment appeared to be additive in causing inhibition of tumor growth. Tumors from diabetic rats showed few metabolic alterations as reflected by little or no changes in the activities of selected glycolytic enzymes, pyruvate kinase, phosphofructokinase, and hexokinase, nor any striking changes in the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, representing the pentose phosphate pathway. A modest reduction in the ratio of utilization of (1-14C)glucose: (6-14C)glucose was seen in vitro by tumors from diabetic rats. It was concluded that insulin, along with estrogen and prolactin, should be considered as a hormonal factor that influences growth of this automonous, hormone-responsive adenocarcinoma.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=123168&dopt=Abstract

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