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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Findings are presented from the 1993 European Society of Contraception Oral Contraceptive Survey conducted in 12 member countries among 102 physicians. Findings are considered suggestive because of the low response rate of 25% to the mailed questionnaire to 400 physicians. The aim is to determine the prescribing practices of oral contraceptives. Over 50% of physicians prescribed the following modern, low-dose combined formulations: Marvelon, Mercilon, Minulet, Gynera, Cilest, and Femodene. 66% of physicians prescribed monophasic pills containing 20-30 mcg of ethinyl estradiol and low doses of desogestrel, gestodene, levonorgestrel, or norgestimate. 58% preferred oral pills because of their tolerability. Other desirable features were the cost, hormonal content, and other factors. 94% prescribed oral pills for women aged over 40 years who were healthy and did not smoke. 75% would not prescribe oral pills to women who were over the age of 35 years and who smoked. Over 50% of physicians recommended mammograms for women aged over 35 years who used oral pills. 45% routinely performed lipoprotein screening of oral pill users. 8% did so only for patients aged over 30 years. 42 physicians out of the 102 responding had a protocol based on the total cholesterol level. 61% prescribed oral pills for women with non-insulin-dependent diabetes. The majority prescribed oral pills for women with insulin-dependent diabetes. 38% of physicians who prescribed oral pills for women with diabetes prescribed very-low-dose monophasic oral contraceptives. 85% prescribed oral pills for women with gestational diabetes. 42% were concerned about patient risk of cardiovascular disease. The study revealed a range of practices among physicians.
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PMID:European Society of Contraception oral contraceptives survey update: birth control methods in "Europe of the 12". 857 53

The aim of the present experiments was to demonstrate the release of insulin-like growth factor-I (IGF-I) by human granulosa cells, and to examine the role of growth hormone (GH), oxytocin, steroids and cAMP-dependent intracellular mechanism in its control. A significant accumulation of IGF-I in a serum-supplemented medium in which the human granulosa cells were cultured for 4 days was observed. The concentration of IGF-I in the medium was particularly high at 3 and 4 days of culture. The addition of GH (1-10,000 ng/ml) to the medium increased IGF-I secretion by the cells. A higher GH dose (100,000 ng/ml) was inhibitory. Oxytocin stimulated IGF-I release at doses of 10-10,000 ng/ml. Dibutyryl-cAMP, isobutyl-methyl-xanthine (inhibitor of cAMP catabolism) or forskolin (stimulator of cAMP production) inhibited IGF-I output at these doses. Additions of progesterone (1-1,000 ng/ml) did not affect IGF-I release, whilst adrostenedione and estradiol were stimulatory at doses of 1, 10, 100, 1,000 ng/ml and 10, 100 and 1,000 ng/ml respectively. Testosterone inhibited IGF-I at a dose of 1,000 ng/ml but not at lower doses (1, 10 or 100 ng/ml). Blockade of estradiol (but not of testosterone) in the medium by specific antisera (1 or 10%) significantly reduced IGF-I output. The same effect was observed with an antiserum to progesterone when added at 0.1%, whilst higher doses (1 or 10%) stimulated IGF-I secretion. The present observations demonstrate the involvement of peptide, steroid hormones and cAMP in the regulation of IGF-I secretion by luteinized human granulosa cells. In particular, both GH and oxytocin are stimulators of IGF-I release. Estradiol and androstenedione, but not testosterone, may also be stimulators of IGF-I output. The involvement of progesterone in this process can also not be excluded. A cAMP-dependent intracellular mechanism appears to play an inhibitory role in the regulation of IGF-I secretion by luteinized human granulosa cells.
Exp Clin Endocrinol Diabetes 1995
PMID:The release of insulin-like growth factor-I by luteinized human granulosa cells in vitro: regulation by growth hormone, oxytocin, steroids and cAMP-dependent intracellular mechanisms. 878 8

The influence of the acute withdrawal of insulin therapy in streptozocin-diabetic female swine was examined for changes in 1) the in vivo pulsatile secretion of luteinizing hormone (LH), 2) the preovulatory-like gonadotropin patterns after exogenous estradiol, and 3) the in vitro LH secretion by cultured pituitary cells. In Experiment 1, ovariectomized diabetic pigs (n = 4) were maintained with insulin therapy until 4 d before estradiol benzoate (EB; 7 micrograms/kg body weight; subcutaneous) was administered. Four normal ovariectomized pigs, matched for age and weight, served as controls. The diabetic state was confirmed by the measurement of glucose and insulin concentrations during a glucose tolerance test. Pulsatile LH secretion was not influenced by experimental diabetes mellitus. However, the expected surge in LH was not induced by EB in diabetic gilts. In contrast, three of four normal gilts had a preovulatory-type surge in LH. Concentrations of follicle-stimulating hormone in serum were not affected by diabetes mellitus. Estradiol concentrations in serum after ER were influenced by diabetes mellitus (treatment by time interaction; P < 0.001). In individual estradiol profiles, maximum concentrations were similar (104 +/- 10.4 and 91 +/- 12.0 ng/ml for normal and diabetic pigs, respectively), but the interval to maximum concentration was delayed in diabetic pigs (27.5 vs. 9.0 h; SE = 3.0; P < 0.05). However, the duration of standing estrus (2.2 +/- .3 d) and the interval from EB to estrus (3.6 +/- 0.3 d) were not influenced by diabetes mellitus. In Experiment 2, LH secretion by cultured cells and residual cellular LH content were greater in the pituitaries of normal than diabetic pigs (P < 0.05), and only cells from normal pigs responded to gonadotropin-releasing hormone (GnRH), with increased production of LH (P < 0.05). In conclusion, diabetes mellitus did not affect pulsatile LH secretion but did lower the ability of exogenous estradiol to stimulate a surge in vivo and of GnRH to increase LH in vitro, suggesting that the pituitary response to estradiol and GnRH is more severely affected by diabetes than is the GnRH pulse generator.
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PMID:Depressed luteinizing hormone response to estradiol in vivo and gonadotropin-releasing hormone in vitro in experimentally diabetic swine. 888 98

Hyperandrogenicity in women is closely associated with insulin resistance and a risk factor for cardiovascular disease and noninsulin-dependent diabetes mellitus (NIDDM). Therefore, 25 postmenopausal women with NIDDM and sex hormone-binding globulin values less than 60 nmol/L, as an indicator of a moderate hyperandrogenicity, were treated with 2 mg 17-beta-estradiol orally for 3 months in a double-blind, cross-over, placebo-controlled trial. During the last 16 days of active treatment, 1 mg norethisterone acetate was added for 10 days for endometrial protection. Blood glucose, glycosylated hemoglobin, insulin, c-peptide, lipoprotein profile, sex steroid hormones, GH, and insulin-like growth factor I (IGF-I) were measured, and insulin sensitivity was determined by the euglycemic hyperinsulinemic clamp method. All metabolic measurements were taken at baseline and after 68 days of active or placebo treatment. Estradiol treatment, compared with the placebo period, was followed by a marked increase of sex hormone-binding globulin and a decrease of free testosterone. Blood glucose, glycosylated hemoglobin, c-peptide, total cholesterol, low-density lipoprotein cholesterol, and IGF-I decreased significantly (P < 0.01-P < 0.001), whereas high-density lipoprotein cholesterol rose (P < 0.001). In conclusion, estrogen replacement therapy in postmenopausal women with NIDDM ameliorated hyperandrogenicity, and this was accompanied by marked improvements in glucose homeostasis and lipoprotein profile.
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PMID:Estrogen replacement therapy decreases hyperandrogenicity and improves glucose homeostasis and plasma lipids in postmenopausal women with noninsulin-dependent diabetes mellitus. 902 68

These studies determined whether diabetes and estradiol treatment altered norepinephrine (NE) release from hypothalamus, preoptic area (POA), and cortical slices from ovariectomized (OVX) female rats. Animals were sacrificed 12 days after the onset of streptozotocin-induced diabetes and 48 h following vehicle or estradiol injection. Brain slices were preloaded with 3H-NE, and release was evoked twice (S and S2) by electrical stimulation. Diabetes increased hypothalamic NE release during S1 regardless of the administration of vehicle or estradiol. Neither estradiol treatment nor diabetes alone affected NE release during S2 in the hypothalamus or POA. Estradiol treatment elevated NE release in the POA during S2 but only in diabetic animals. Moreover, estradiol elevated cortical NE release during S2 regardless of the presence or absence of disease. We also examined whether alpha2-adrenoceptor regulation of NE release was influenced by diabetes or hormone treatment. Enhancement of NE release by alpha2-adrenoceptor antagonism was evident in all 3 brain regions. However, alpha2-adrenoceptor regulation of NE release was unaffected by diabetes and hormone treatment. These findings suggest that diabetes alters NE release in the hypothalamus/POA of female rats. Additionally, this work identifies a novel action of estradiol to enhance stimulated NE release in the cortex of female rats.
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PMID:Effects of diabetes and estradiol on norepinephrine release in female rat hypothalamus, preoptic area and cortex. 969 36

The effects of progesterone and RU 486 on cellular proliferation and differentiation in long term cultures of mixed human endometrial cells were studied. The endometrial tissue was obtained from women with normal menstrual cycles who were undergoing hysterectomy for benign growths. Estradiol supplemented cultures were treated with progesterone and/or RU 486 for 27 days. Cell number was measured by crystal violet assay, and prolactin secretion was used as a marker of differentiation. Progesterone doubled the rate of proliferation, but the addition of RU 486 reduced it to baseline again. The gestagen increased prolactin secretion up to 30 times, while the addition of RU 486 suppressed it to baseline levels. When administered to cells that were pretreated with progesterone for 15 days RU 486 abolished the progesterone effects. RU 486 alone was without any effect. Our results indicate that (1) in vitro progesterone is essential for the initiation and maintenance of proliferation and differentiation of endometrial cells and (2) RU 486 acts as a pure progesterone antagonist in our culture model.
Exp Clin Endocrinol Diabetes 2000
PMID:Inhibition of proliferation and differentiation by RU 486 in human endometrial stromal and epithelial cells in vitro. 1096 58

The effects of RU 486 together with estradiol and progesterone on estrogen receptor alpha and progesterone receptor (isoforms A and B) expression were studied in human endometrial long term cultures at the mRNA and protein level. We asked whether ligand induced receptor regulation, found in mammals in vivo, is also found in human cultured endometrial cells with special regard to the progesterone isoforms A and B. Endometrial cultures were maintained for 27 days. Media were supplemented with progesterone and/or estradiol alone or in combination with RU 486. Receptor expression (estrogen receptor alpha and progesterone receptor isoform A and B) was examined at the mRNA level by RT-PCR and at the protein level by western blot analysis. All receptor types examined were expressed in our culture model. Estradiol led to a general increase of receptor expression whereas treatment with estradiol in combination with progesterone down regulated receptor expression. The receptor down regulation was not found when RU 486 was additionally supplemented into the medium. Activation or inhibition of expression due to these treatments was similar for both PR isoforms. Our results (1) show that in our culture system estradiol induced up regulation of estrogen receptor and progesterone receptor A and B and suggest that the estrogen induced up regulation is prevented by progesterone (2) a clear cut antigestagenic effect of RU 486 and (3) suggest that both progesterone isoforms are analogously regulated in our culture model. We conclude that human endometrial cell cultures are suitable for the study of the dynamics of steroid receptor expression.
Exp Clin Endocrinol Diabetes 2001
PMID:Regulation of estrogen receptor alpha and progesterone receptor (isoform A and B) expression in cultured human endometrial cells. 1145 36

Steroids act on the follicle through autocrine and paracrine mechanisms to regulate follicular growth and steroidogenesis. Estradiol plays a significant role in determining the fate of the developing follicle and acts via specific receptors which are nuclear transcription factors. It has been established that besides classical estrogen receptor-alpha (ER alpha) novel forms termed ER beta exist. In species studied to date these two types of ERs exhibit different tissue localisation patterns and levels of expression. The present study was performed to determine whether ER alpha and ER beta are differentially expressed in the porcine ovary. Immunohistochemical studies using antibodies to ER alpha and ER beta, established the predominance of ER beta over ER alpha in the porcine ovary. Cyclical changes in estrogen receptor-beta expression were observed. The immunostaining was present in all types of follicles, and decreased in corpus luteum while it regressed. In the contrary estrogen receptor-alpha staining was seen only in large preovulatory follicle and in early corpora lutea.
Exp Clin Endocrinol Diabetes 2001
PMID:Differential distribution of estrogen receptor-beta and estrogen receptor-alpha in the porcine ovary. 1145 37

The main advantage of the triphasic oral contraceptive (OC) is its reduced corticosteroid content, which is accompanied by a reduction in metabolic impact. Triphasic pills differ according to their components and according to whether or not their estrogen dose is constant. The Triella pill has a constant dose of 35 mcg ethinyl estradiol (EE) and a dose of norethisterone that increases from .50 to 1 mg, while Triquilar-Trinordiol mimics the preovulatory estrogen peak while also varying the progestin content. In a study of 22,728 cycles, the Pearl index was only .06/100 woman years for triphasic pills. Comparisons with existing monophasic pills indicate that triphasics may offer improved cycle control, but the fact should be emphasized to patients that cycle control is an inappropriate criterion for choice of pills. Metabolic effects or possible carcinogenic effects are more important qualities. Triphasic pills have been found to improve acne, not to affect weight or blood pressure, and to reduce the frequency of headaches, nervousness, and breast tenderness. Studies have shown that triphasics containing levonorgestrel produce minimal effects on lipid metabolism, while less rigorous studies on triphasics containing norethisterone have also yielded favorable results. It is true however that knowledge of the relationship between alterations in plasma cholesterol caused by Triella use and the etiology of certain diseases remains incomplete. Low dose triphasic pills appear to have fewer deleterious effects on glucose metabolism than higher dose pills, but they are not entirely without effect and should not be prescribed for women at risk of developing diabetes. Studies examining modifications of the intima and coagulation factors have given reassuring results, and neither triphasics with levonorgestrel nor those with norethisterone modify the blood pressure. Triphasics entail a reduction in the levels of estradiol and testosterone and a slight increase of plasma renin activity but no modification in plasma aldosterone. The subtle effects on the gonodotropic axis are considered especially fitting for young women in whom post-pill ovulatory function is preserved. Endometrial biopsies show that the state of the endometrium with OC use is not well understood and highly variable. The triphasic pill approaches as closely as possible the normal physiology of the endometrium while still suppressing ovulation.
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PMID:[The triphasic pill]. 1228 Feb 9

Serum glucose and serum insulin levels were measured during oral glucose tolerance tests in 100 women, 20-39 years of age, who used the OC (oral contraceptive) preparation Stediril and in a control group of 96 women of the same age group. Significantly lower fasting serum glucose levels were observed after 6 months of OC use. Significant decreases in glucose tolerance were observed among OC users who had taken OCs for longer than 6 months. The blood glucose levels were elevated significantly in this group 60 and 120 minutes after the beginning of the test. No correlation could be found between age and changes in glucose tolerance. No significant differences in fasting serum insulin levels were found in either group. A significant increase in serum insulin levels was observed among women who had used OCs longer than 6 months; this increase was apparent only 120 minutes after the beginning of the test. These changes in glucose tolerance were found to be reversible. Glucose tolerance tests should be preformed once a year on OC users, more often if an abnormality in glucose metabolism, e.g. latent diabetes, is present.
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PMID:[Influence of oral contraceptives on changes of the carbohydrate metabolism]. 1230 58


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