Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen (ER) and progesterone (PR) receptor levels were assayed in 2,284 primary breast cancer patients who either smoked (350) or suffered diabetes mellitus type 2 (1997-2003). In a group of 1010, 95 patients had diabetes mellitus type 2 whereas 393--such signs of cardiovascular pathology as atherosclerosis, arterial hypertension and ischemic heart disease (2000-2003). Among the premenopausal smokers, the ER+PR-phenotype predominated (t = 2.18, p < 0.05) as well as among the diabetics (t = 2.01, p < 0.05). In reproductive diabetics, the share of PR- tumors was significantly higher than in diabetes-free patients (t = 2.17, p < 0.05). There was no correlation between diabetes and the tumor receptor phenotype in the menopausal group, while ER + tumors--occurred more frequently in smokers (t = 2.33, p = 0.02). There was no link between cardiovascular pathology and receptor status in either of the age groups. Hence, the increasing proportion of ER + PR--tumors in smokers and diabetes mellitus patients occurs in a random manner in menstruating women, which is associated with elevated estrogenemia. This indicates the phenomenon of switching of estrogen effects involving disturbed transduction of estrogen signals.
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PMID:[Breast cancer receptor status in smoking and diabetic patients]. 1622 98

In July 2002, data from the Women's Health Initiative (WHI) trial provided strong evidence for an increased risk of cardiovascular disease with use of combined estrogen plus progestogen in postmenopausal women. These unexpected results triggered a large and ongoing discussion about the role of hormone replacement therapy (HRT). We investigated the frequency of HRT before and after the publications of the WHI trial and the Heart and Estrogen/Progestin Replacement Study II (HERS II) in a population-based random sample of German women aged 45 - 65 years. A total of 8380 women completed a questionnaire on menopausal status, hysterectomy and HRT. 75 % were postmenopausal. Mean age was 56.1 years; mean age of natural menopause 49.9 years; mean duration of postmenopause was 11 years; 27 % of the women had undergone hysterectomy. The percentage of current HRT users dropped by 16 % (35.4 % to 29.8 %, p = 0.004), past users increased from 19.8 % to 23.5 % (p = 0.03). Among current HRT users, the share of combined conjugated estrogen/progestogen decreased by 41 % (p = 0.008). We observed a decreased prevalence of HRT among German women 7 months after publication of the HERS II and WHI results. The decline was, however less pronounced than reported from other countries. The use of conjugated estrogen/gestagen combinations declined disproportionately compared to other formulations.
Exp Clin Endocrinol Diabetes 2005 Oct
PMID:Patterns of hormone replacement therapy in a population-based cohort of postmenopausal German women. Changes after HERS II and WHI. 1623 55

This review presents a comprehensive, evenhanded evaluation of the evidence from experimental, in vitro and human studies associating environmental and therapeutic factors with risk of colorectal cancer. Life styles correlated with the greatest increase in colorectal cancer risk are the ones that typify a diet rich in fat and calories, alcohol drinking and tobacco smoking, and low intake of vegetable, fruits and fibers, referred to as a "western diet," as well as sedentary style (i.e., no- or low-exercise). This kind of life style has also been associated with other chronic diseases (other cancers, obesity, dyslipedemia, diabetes, hypertension cardiovascular, and hypertension). The evidence does not implicated red meat as a risk factor, and fiber has been shown to protect against colorectal adenomas and carcinomas. Calcium, vitamin D, folate, and some antioxidant vitamins and minerals (gamma-tocopherol and selenium) have protective effects, and daily exercise for > or =30 min results in a significant decrease in risk. Estrogen use (hormone replacement therapy) substantially reduces colorectal cancer risk in postmenopausal women. Nonsteroidal anti-inflammatory drugs (e.g., aspirin) in excessive doses is protective, especially in high risk populations, but the side effects of its use and cost incurred due to its continued intake over long periods must be carefully scrutinized before any recommendations are made for the general public.
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PMID:Effect of diet, life style, and other environmental/chemopreventive factors on colorectal cancer development, and assessment of the risks. 1629 19

The cerebral vasculature is a target tissue for sex steroid hormones. Estrogens, androgens, and progestins all influence the function and pathophysiology of the cerebral circulation. Estrogen decreases cerebral vascular tone and increases cerebral blood flow by enhancing endothelial-derived nitric oxide and prostacyclin pathways. Testosterone has opposite effects, increasing cerebral artery tone. Cerebrovascular inflammation is suppressed by estrogen but increased by testosterone and progesterone. Evidence suggests that sex steroids also modulate blood-brain barrier permeability. Estrogen has important protective effects on cerebral endothelial cells by increasing mitochondrial efficiency, decreasing free radical production, promoting cell survival, and stimulating angiogenesis. Although much has been learned regarding hormonal effects on brain blood vessels, most studies involve young, healthy animals. It is becoming apparent that hormonal effects may be modified by aging or disease states such as diabetes. Furthermore, effects of testosterone are complicated because this steroid is also converted to estrogen, systemically and possibly within the vessels themselves. Elucidating the impact of sex steroids on the cerebral vasculature is important for understanding male-female differences in stroke and conditions such as menstrual migraine and preeclampsia-related cerebral edema in pregnancy. Cerebrovascular effects of sex steroids also need to be considered in untangling current controversies regarding consequences of hormone replacement therapies and steroid abuse.
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PMID:Influence of sex steroid hormones on cerebrovascular function. 1679 20

Metabolic control is central to positive clinical outcome in patients with diabetes. Empowerment has been linked to metabolic control in this clinical group. The current study sought to determine key psychometric properties of the Chinese version of the Diabetes Empowerment Scale (C-DES) and to explore the relationship of the C-DES sub-scales to metabolic control in 189 patients with a diagnosis of diabetes. Confirmatory factor analysis established that the five sub-scales of the C-DES offered a highly satisfactory fit to the data. Furthermore, C-DES sub-scales were found to have generally acceptable internal consistency and divergent reliability. However, convergent reliability of C-DES sub-scales could not be established against metabolic control. It is concluded that future research needs to address ambiguities in the relationship between empowerment and metabolic control in order to afford patients an evidenced-based treatment package to assure optimal metabolic control.
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PMID:Psychometric properties of the Chinese version of the diabetes empowerment scale. 1712 8

Heart failure with normal ejection fraction (HF-NEF) is frequently believed to be more common in women than in men. However, the interaction of gender and age has rarely been analyzed in detail, and knowledge of the distinction between pre- and postmenopausal women is lacking. Some of the studies that have described a higher prevalence of HF-NEF in women relied on clinical diagnoses of HF together with normal systolic function and did not measure diastolic function. This applies to the analysis of patients hospitalized for HF and some epidemiological investigations that agree on the greater prevalence of HF-NEF in women. Population-based studies with echocardiographic determination of diastolic function have suggested equal or greater prevalence of diastolic dysfunction in men. Major risk factors for HF-NEF include hypertension, aging, obesity, diabetes, and ischemia. Hypertension is more frequent in women and can contribute to left ventricular and arterial stiffening in a gender-specific way. Aging, obesity, and diabetes affect myocardial and vascular stiffness differently and lead to different forms of myocardial hypertrophy in women and men. In contrast, ischemia may play a greater role in men. Gender differences in ventricular diastolic distensibility, in vascular stiffness and ventricular/vascular coupling, in skeletal muscle adaptation to HF, and in the perception of symptoms may contribute to a greater rate of HF-NEF in women. The underlying molecular mechanisms include gender differences in calcium handling, in the NO system, and in natriuretic peptides. Estrogen affects collagen synthesis and degradation and inhibits the renin-angiotensin system. Effects of estrogen may provide benefit to premenopausal women, and the loss of its protective mechanisms may render the heart of postmenopausal women more vulnerable. Thus, a number of molecular mechanisms can contribute to the gender differences in HF-NEF.
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PMID:Role of gender in heart failure with normal left ventricular ejection fraction. 1718 12

Estrogens are essential for fertility and also have important effects on regulation of adiposity and the euglycemic state. We report here that lipin1, a candidate gene for lipodystrophy and obesity that is a phosphatidic acid phosphatase critical in regulation of cellular levels of diacylglycerol and triacylglycerol and a key regulator of lipid utilization, is rapidly and robustly down-regulated in the uterus by estradiol via the estrogen receptor. Lipin1 is expressed predominantly in the uterine luminal and glandular epithelium, and during the estrous cycle, lipin1 is lowest when blood levels of estrogen are highest. Lipin1 is expressed throughout all cells in the liver of ovariectomized female mice, and a sustained down-regulation is observed at the mRNA, protein and immunohistochemical levels after estrogen administration. Because the coupling of proper energy use and availability is central to reproduction, we also investigated expression of lipin1 in the uterus and liver of several mouse models of diabetes. Nonobese diabetic (NOD) mice, which have high blood levels of estrogen and impaired fertility, were severely deficient in lipin1 in the uterus and liver, which, interestingly, could be restored by insulin treatment. By contrast, nonobese diabetic/severe combined immunodeficient (NOD-SCID) mice, which do not develop diabetes, showed normal levels of lipin1. Our findings of lipin1 regulation by estrogen in two key target organs suggest a new role for this lipid-regulating phosphatase not only in central metabolic regulation but also in uterine function and reproductive biology. Estrogen regulation of lipin1 may provide a mechanistic link between estrogens, lipid metabolism, and lipid signaling.
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PMID:Lipin1 regulation by estrogen in uterus and liver: implications for diabetes and fertility. 1746 59

The purpose of the present study was to determine the relationships between atherosclerotic calcified plaque (CP) and bone mineral density (BMD) in subjects with type 2 diabetes mellitus (DM2). CP in the coronary arteries, carotid bifurcation, and abdominal aorta was measured using computed tomography (CT) in 1023 diabetic subjects from 453 families. Trabecular volumetric BMD in thoracic (T-vBMD) and lumbar (L-vBMD) spine was measured with quantitative CT (QCT), while areal BMD (aBMD) in the lumbar spine and hip was measured by dual X-ray absorptiometry (DXA). Correlation coefficients were computed to assess the magnitude of associations and generalized estimating equations (GEE1) were used to make statistical inferences while accounting for familial correlation. Subjects were 53.8% female, 85% European American (EA) and 15% African American (AA). After adjustment for age, significant inverse associations between CP and vBMD persisted in EA men (correlations between -0.11 and -0.16, all p<0.05 with the exception of carotid CP vs. T-vBMD, p=0.076) and in AA women, excluding aortic CP (correlations between -0.16 and -0.25, all p<0.05). Estrogen use in AA but not EA women was consistently associated with an inverse relation between CP and vBMD. Significant inverse relationships between CP and vBMD were observed in EA men and AA women with DM2 after adjusting for age and other covariates. QCT determined vBMD was more strongly related to CP than aBMD by DXA. The relation between CP and BMD in diabetes is influenced by age, sex, and ethnicity, with further effect modification by hormone replacement therapy.
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PMID:Calcified atherosclerotic plaque and bone mineral density in type 2 diabetes: the diabetes heart study. 1796 37

Estrogen is known to affect vascular function and diabetes development, but the relative contribution of estrogen receptor (ER) isoforms is unclear. The aim of this study was to determine how individual ER isoforms modulate inflammatory enzymes in the vascular wall of control and streptozotocin (STZ)-injected rodents. Primary cultures of rat aortic smooth muscle cells (SMCs) were stimulated with inflammatory agents in the presence or absence of increasing concentrations of the ER alpha and ER beta-selective agonists 4,4',4''-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT) and diarylpropionitrile (DPN), respectively. The production of inducible nitric-oxide synthase (iNOS), a classical indicator of vascular inflammation, was significantly reduced by PPT in control but not diabetic SMCs, whereas it was further enhanced by DPN treatment in both groups. This distinct action profile was not related to changes in ER transcriptional activity. However, extracellular signal-regulated kinase 1/2 signaling was activated by DPN but not by PPT in cytokine-treated SMCs. In cultured aortic rings from both normoglycemic and STZ-diabetic mice, pharmacological activation of ER alpha attenuated cytokine-driven iNOS induction by 30 to 50%. Vascular iNOS levels were decreased consistently when adding 1 nM 17beta-estradiol to aortic tissues from ER beta- but not ER alpha-knockout mice. These findings suggest a possible role for ER alpha-selective ligands in reducing vascular inflammatory responses under normo- and hyperglycemic conditions.
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PMID:Distinct roles of estrogen receptor-alpha and beta in the modulation of vascular inducible nitric-oxide synthase in diabetes. 1883 49

Estrogen and progesterone affect endothelial function, coagulation factors, platelet function, lipids, and inflammation and have neuroprotective effects in experimental animals. Oral contraceptives containing low-dose estrogen increase the risk of ischemic stroke, but the absolute risk is low. Risk factors further increasing the risk of stroke in users of oral contraceptives include smoking, hypertension, diabetes, hyperlipidemia, migraine with aura, and thrombophilia. Progestin-only contraceptives do not increase the risk of stroke and are preferable in women with cerebrovascular disease or risk factors. Hormone replacement therapy (HRT) with estrogen alone or combined with progesterone increases the risk of ischemic stroke by 40% with no effect on hemorrhagic stroke. Stroke risk increases with the dose of estrogen. The time between menopause and the initiation of HRT does not influence ischemic stroke risk. The only indication for HRT is the treatment of vasomotor symptoms; if needed for this purpose, the lowest dose of estrogen should be used for the shortest possible duration.
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PMID:Use of oral contraceptives and postmenopausal hormone replacement: evidence on risk of stroke. 1899 Mar 15


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