34 research outputs found

    The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function In Vivo and Induces Insulin Resistance

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    The function of the pancreatic β-cell is the storage and release of insulin, the main hormone involved in blood glucose homeostasis. The results in this article show that the widespread environmental contaminant bisphenol-A (BPA) imitates 17β-estradiol (E(2)) effects in vivo on blood glucose homeostasis through genomic and nongenomic pathways. The exposure of adult mice to a single low dose (10 μg/kg) of either E(2) or BPA induces a rapid decrease in glycemia that correlates with a rise of plasma insulin. Longer exposures to E(2) and BPA induce an increase in pancreatic β-cell insulin content in an estrogen-receptor–dependent manner. This effect is visible after 2 days of treatment and starting at doses as low as 10 μg/kg/day. After 4 days of treatment with either E(2) or BPA, these mice developed chronic hyperinsulinemia, and their glucose and insulin tolerance tests were altered. These experiments unveil the link between environmental estrogens and insulin resistance. Therefore, either abnormal levels of endogenous estrogens or environmental estrogen exposure enhances the risk of developing type 2 diabetes mellitus, hypertension, and dyslipidemia

    An epidemiologically rare case of Vibrio vulnificus infection that occurred in October in an inland city of Japan

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     A 68-year-old man with alcohol addiction, who lived in the suburbs of Tsuyama, an inland city located in northeast Okayama prefecture, was transported to the emergency unit of the Tsuyama Central Hospital in a state of cardiopulmonary arrest (CPA). Despite rigorous systemic investigation and treatment, the patient died 2 hours after arrival. After his death, Vibrio vulnificus was isolated from his blood culture.  Vibrio vulnificus causes fatal infection in humans, usually only in areas located close to the sea where appropriate temperature and suitable salt concentration for its growth are available. Therefore, its occurrence is epidemiologically restricted ; in Japan, the western coastal areas, especially in summers, are reported to be the high-risk regions. This is a rare case because it occurred in a city approximately 50 kilometers from both the Sea of Japan and the Pacific coast of Okayama, and at the end of October in 2011. Economic development and distribution systems have made it possible to transport various food products from coastal areas or abroad to any place in a short time, such that these infections can potentially develop in areas other than expected. We should be aware of the increasing risk of Vibrio vulnificus infection during any season and at any place, especially in patients with abnormal liver function

    2ガタ トウニョウビョウ カンジャ ニオケル ケットウ シヒョウ ト ゲンエン ガ モタラス ケツアツ テイカ トノ レンカン

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    Background : The majority of patients with type2diabetes mellitus(T2DM)have hypertension, leading to serious cardiovascular events, including acute myocardial infarction, heart failure and stroke. Therefore, blood pressure(BP)control is a critical issue in patients with T2DM. Although sodium restriction is known to reduce BP, it is unclear what factors are associated with sodium restriction-induced BP reduction in T2DM patients. Subjects and Methods : A retrospective analysis was performed in hospitalized patients with T2DM(66males and61females, mean age :58.1±14.2years, mean HbA1c :9.5±2.0%). They received diet therapy including sodium restriction as NaCl of5to8g/day during admission. The relationship between changes in systolic BP(SBP)during admission and clinical parameters at the time of admission was statistically analyzed. Results : Mean SBP in the sodium-restricted patients was significantly reduced during admission( from 130.2±16.1 to 122.7±13.9 mmHg, p<0.01). Multiple regression analysis showed that serum creatinine levels and presence of hypertension were inversely associated with and that initial SBP value was positively associated with the change in SBP. On the other hand, no glycemic parameters, including fasting plasma glucose levels, HbA1c, M values calculated from daily blood glucose profile, duration of T2DM and duration of hospitalization, were associated with the change in SBP. Conclusion : Sodium restriction-induced BP reduction in T2DM patients was associated with presence of hypertension, serum creatinine levels and initial SBP values. Sodium restriction is a useful treatment for T2DM patients regardless of their glycemic condition

    Treatment algorithm of ACTH deficiency

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    Objective : To examine diagnostic performance of corticotropin-releasing hormone (CRH) test combined with baseline dehydroepiandrosterone sulfate (DHEA-S) in patients with a suspect of central adrenal insufficiency. Methods : Patients (n=215) requiring daily or intermittent hydrocortisone replacement, or no replacement were retrospectively checked with their peak cortisol after CRH test and baseline DHEA-S. Results : None of 106 patients with the peak cortisol ≥ 17.5 μg / dL after CRH test required replacement, and all 64 patients with the peak cortisol < 10.0 μg / dL required daily replacement. Among 8 patients with 10.0 μg / dL ≤ the peak cortisol < 17.5 μg / dL and baseline DHEA-S below the reference range, 6 patients required daily replacement and 1 patient was under intermittent replacement. Among 37 patients with 10.0 μg / dL ≤ the peak cortisol < 17.5 μg / dL and baseline DHEA-S within the reference range, 10 and 6 patients were under intermittent and daily replacement, respectively. Conclusions : No patients with the peak cortisol ≥ 17.5 μg / dL required hydrocortisone replacement, and all patients with the peak cortisol below 10.0 μg / dL required daily replacement. Careful clinical evaluation was required to determine requirement for replacement in patients with 10.0 μg / dL ≤ the peak cortisol < 17.5 μg / dL even in combination with baseline DHEA-S

    Suppression of the Hypothalamic-pituitary-adrenal Axis by Maximum Androgen Blockade in a Patient with Prostate Cancer

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    A 78-year-old Japanese man showed suppression of the hypothalamic-pituitary-adrenal axis during maximum androgen blockade (MAB) therapy including chlormadinone acetate (CMA) for prostate cancer. After stopping the MAB therapy, both the basal ACTH level and the response to CRH recovered. While no reports have indicated that CMA suppresses the hypothalamic-pituitary-adrenal axis in patients with prostate cancer, CMA has been shown to inhibit this axis in animals. These observations suggest that we must monitor the hypothalamic-pituitary-adrenal axis in patients treated with CMA, especially under stressful conditions

    Remarkable Shrinkage of a Growth Hormone (GH)-secreting Macroadenoma Induced by Somatostatin Analogue Administration : A Case Report and Literature Review

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    Acromegaly is caused by excessive growth hormone secretion, usually from pituitary adenomas. Somoatostatin analogues are widely used as primary or adjunctive therapy in the management of acromegaly. In this report, we present a case with remarkable shrinkage of a tumor after relatively short-term octreotide long-acting release (LAR) administration. During the 30-month follow-up after starting octreotide LAR, there was no recurrence of acromegaly with remarkable shrinkage of the tumor on pituitary magnetic resonance imaging. A literature review of the predictors for tumor shrinkage after the administration of somatostatin analogues in patients with acromegaly is also discussed in relation to this case

    The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function and Induces Insulin Resistance-1

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    <p><b>Copyright information:</b></p><p>Taken from "The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function and Induces Insulin Resistance"</p><p>Environmental Health Perspectives 2005;114(1):106-112.</p><p>Published online 20 Sep 2005</p><p>PMCID:PMC1332664.</p><p>This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.</p
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