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1
Nurullina, G. I. "Glucocorticoid pulse therapy аnd carbohydrate metabolism in rheumatic diseases." Kazan medical journal 94, no. 6 (December 15, 2013): 920–23. http://dx.doi.org/10.17816/kmj1820.
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Glucocorticoids are used in clinical practice for more than 50 years and are a great advance in the treatment of systemic inflammatory diseases. High doses of intravenous glucocorticoids (pulse therapy) are effective in conditions requiring rapid immunosuppression and antiinflammatory effect, such as systemic lupus erythematosus, rheumatoid arthritis, glomerulonephritis and systemic vasculitides. The advantage of this method are increased efficacy and lower rate of complications associated with prolonged administration of glucocorticoids. At the same time, glucocorticoid pulse therapy is associated with increased risk of hyperglycemia or even can be a cause of steroid-induced diabetes in patients without known hyperglycemia, as well as worsen glycemia control in patients with diabetes. Increased hepatic gluconeogenesis, inhibition of glucose uptake and metabolism in peripheral tissues and altered both receptor and post-receptor insulin action can lead to an increased serum glucose levels. In patients with inadequate compensatory reserves of pancreas, a clinical picture of diabetus mellitus can develop while treated with glucocorticoids. Blood glucose levels begin to rise 6-12 hours after the infusion of high doses of glucocorticoids. Risk factors for developing glucose intolerance and diabetes include advanced age, obesity, family history of diabetes and high cumulative doses of glucocorticoids. Glucocorticoid-induced diabetes is a common complication of pulse therapy, but exact causes are still not elucidated yet, current literature data on glucocorticoid-induced hyperglycemia are scarce.
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Wardani, Indah Sapta. "Steroid Induced Diabetes Mellitus: An Overview." JURNAL SAINS TEKNOLOGI & LINGKUNGAN 9, no. 1 (March 30, 2023): 206–13. http://dx.doi.org/10.29303/jstl.v9i1.441.
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Glucocorticoids are often used as immunosuppressant and anti-inflammatory therapy in various medical conditions. In addition to providing clinical benefits, glucocorticoids have various side effects, one of which is related to steroid-induced diabetes mellitus (SIDM). Steroid-induced diabetes mellitus can be a new onset or an exacerbation of hyperglycemia in patients who have previously been diagnosed with DM. Acute and chronic hyperglycemia due to steroids can have an impact on lengthening hospitalization, infectious complications, decreased response to therapy and increased mortality. The challenges of managing steroid-induced diabetes mellitus vary widely. Understanding of pathophysiology, risk factors, diagnosis and therapy can add insight regarding the comprehensive management of steroid-induced DM
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Nykytiuk, L. A. "Diabetes Mellitus Induced by Exogenous Administration of Glucocorticoids." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY, no. 8.80 (January 12, 2017): 17–19. http://dx.doi.org/10.22141/2224-0721.8.80.2016.89532.
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Rana, M. Asim, Mujtaba H. Siddiqui, Sitara Raza, Kinza Tehreem, M. F. Ullah Mahmood, Muhammad Javed, M. Ahad Qayyum, and M. M. Hafeez. "Incidence of Steroid-induced Diabetes in COVID-19 patients." Pakistan Journal of Medical and Health Sciences 15, no. 10 (October 30, 2021): 2595–96. http://dx.doi.org/10.53350/pjmhs2115102595.
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Background: Since the COVID-19 pandemic has started, glucocorticoids have been proved to be one of the most effective lifesaving treatments for respiratory complications associated with SARS CoV-2. Aim: To review the incidence of steroid induced diabetes and the associated risk factors in COVID-19 patients. Study Design: Retrospective cohort study Place and duration of the study: Bahria International Hospital Lahore from 15th April 2020 to 31st December 2020 Methodology: Two hundred and thirty patients of COVID-19 cases treated with glucocorticoids (Dexamethasone 4mg BID) were enrolled. All known cases of pre-existing diabetes mellitus and with initial (admission) random blood glucose levels of more than 200 mg/dl were excluded. Patients labelled as glucocorticoid induced diabetes mellitus (GI-DM)met the following criteria, fasting blood glucose level of more than 126 mg/dl or a random glucose level of more than200 mg/dlon two occasions after starting these patients on steroids. Results: The glucocorticoid induced diabetes mellitus was 36 (15.65%). Multivariate logistic regression analysis revealed that older age (odds ratio 1.19, 95% confidence interval (1.02-1.36) was found to be the most profound risk factor for GI-DM. Conclusion: Glucocorticoid induced diabetes mellitus found to be associated with glucocorticoid used among COVID-19 patients especially in older ages. So, it is recommended that the treating physicians should consider this side effect of steroids especially when dealing with geriatric cases. Keywords: Hyperglycaemia, COVID-19, Steroids, SARS-CoV-2, Diabetes mellitus, Steroids induced diabetes, Glucocorticoids
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Oğuz, Seda Hanife. "Management of glucocorticoid-induced diabetes." Acta Medica 55 (December 3, 2024): 17–21. https://doi.org/10.32552/2024.actamedica.1097.
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Glucocorticoid-induced diabetes (GID) is a frequent metabolic complication of glucocorticoid therapy. It results from both insulin resistance and impaired insulin secretion, exacerbated by glucocorticoid use. Despite its prevalence, consensus guidelines on screening and management remain limited. GID affects approximately one in five patients receiving long-term glucocorticoid therapy. Risk factors include older age, high BMI, prediabetes, ethnicity, and high-dose systemic glucocorticoids. All patients initiated on moderate to high doses of glucocorticoids should be assessed for GID risk factors and closely monitored for the development of hyperglycemia and diabetes. In addition, glucocorticoid therapy can significantly exacerbate hyperglycemia in individuals with pre-existing diabetes, and stringent glucose monitoring is crucial. Treatment should be tailored to individual patient. Oral anti-diabetics such as metformin and sulfonylureas might be used in selected patients with mild GID. However, insulin is the primary treatment for severe hyperglycemia. Early detection and individualized management strategies are critical to mitigate GID’s impact. Further research is needed to develop consensus guidelines and optimize treatment approaches.
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Schakman, O., H. Gilson, and J. P. Thissen. "Mechanisms of glucocorticoid-induced myopathy." Journal of Endocrinology 197, no. 1 (January 31, 2008): 1–10. http://dx.doi.org/10.1677/joe-07-0606.
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Glucocorticoid-induced muscle atrophy is characterized by fast-twitch or type II muscle fiber atrophy illustrated by decreased fiber cross-sectional area and reduced myofibrillar protein content. Muscle proteolysis, in particular through the ubiquitin– proteasome system (UPS), is considered to play a major role in the catabolic action of glucocorticoids. The stimulation by glucocorticoids of the UPS is mediated through the increased expression of several atrogenes (‘genes involved in atrophy’), such as atrogin-1 and MuRF-1, two ubiquitin ligases involved in the targeting of protein to be degraded by the proteasome machinery. Glucocorticoids also exert an anti-anabolic action by blunting muscle protein synthesis. These changes in protein turnover may result from changes in the production of two growth factors which control muscle mass, namely IGF-I and myostatin respectively anabolic and catabolic toward the skeletal muscle. The decreased production of IGF-I as well as the increased production of myostatin have been both demonstrated to contribute to the muscle atrophy caused by glucocorticoids. At the molecular level, IGF-I antagonizes the catabolic action of glucocorticoids by inhibiting, through the PI3-kinase/Akt pathway, the activity of the transcription factor FOXO, a major switch for the stimulation of several atrogenes. These recent progress in the understanding of the glucocorticoid-induced muscle atrophy should allow to define new therapies aiming to minimize this myopathy. Promising new therapeutic approaches for treating glucocorticoid-induced muscle atrophy are also presented in this review.
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Schultz, Helga, Birthe Krogh Rasmussen, Peter Lommer Kristensen, Andreas Kryger Jensen, and Ulrik Pedersen-Bjergaard. "Early incidence of glucocorticoid-induced diabetes in patients with brain tumors: a retrospective study of the first 7 days of treatment." Neuro-Oncology Practice 5, no. 3 (October 25, 2017): 170–75. http://dx.doi.org/10.1093/nop/npx027.
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Abstract Background Hyperglycemia or diabetes is a well-known side effect of treatment with glucocorticoids. In patients with brain tumors, glucocorticoids are widely used to treat symptoms of peritumoral edema. We conducted a retrospective study of patients with suspected brain tumor to determine the incidence of and risk factors for glucocorticoid-induced diabetes. Methods This was a retrospective study of patients referred with suspected brain tumor to a neurological department, using data from a clinical database, electronic medical records, the laboratory system, and the pathology information bank. . Nondiabetic patients with a neuroimaging-verified brain tumor treated with high-dose glucocorticoid and monitored with glucose measurements were included in the study. Results Among 809 patients referred with suspected brain tumor, 171 were eligible for the study. Thirty-eight (22%) patients developed glucocorticoid-induced diabetes, defined as 2 glucose measurements ≥200 mg/dl (11.1 mmol/l) within the first week of treatment, and 4 of the patients were treated with insulin. The majority of patients with glucocorticoid-induced diabetes were identified on days 2, 3, and 4, and glucose levels were highest in the afternoon and evening. We were not able to identify any risk factors for glucocorticoid-induced diabetes and glucocorticoid-induced diabetes had no influence on survival in our cohort. Conclusions Glucocorticoid-induced diabetes is frequent in the first 7 days of treatment in patients with brain tumors. The results emphasize the need for screening for glucocorticoid-induced diabetes in this group of patients to avoid comorbidity expected to arise from hyperglycemia.
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Aberer, Felix, Daniel A. Hochfellner, Harald Sourij, and Julia K. Mader. "A Practical Guide for the Management of Steroid Induced Hyperglycaemia in the Hospital." Journal of Clinical Medicine 10, no. 10 (May 16, 2021): 2154. http://dx.doi.org/10.3390/jcm10102154.
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Glucocorticoids represent frequently recommended and often indispensable immunosuppressant and anti-inflammatory agents prescribed in various medical conditions. Despite their proven efficacy, glucocorticoids bear a wide variety of side effects among which steroid induced hyperglycaemia (SIHG) is among the most important ones. SIHG, potentially causes new-onset hyperglycaemia or exacerbation of glucose control in patients with previously known diabetes. Retrospective data showed that similar to general hyperglycaemia in diabetes, SIHG in the hospital and in outpatient settings detrimentally impacts patient outcomes, including mortality. However, recommendations for treatment targets and guidelines for in-hospital as well as outpatient therapeutic management are lacking, partially due to missing evidence from clinical studies. Still, SIHG caused by various types of glucocorticoids is a common challenge in daily routine and clinical guidance is needed. In this review, we aimed to summarize clinical evidence of SIHG in inpatient care impacting clinical outcome, establishment of diagnosis, diagnostic procedures and therapeutic recommendations.
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Nangalama, A. W., and G. P. Moberg. "Interaction between cortisol and arachidonic acid on the secretion of LH from ovine pituitary tissue." Journal of Endocrinology 131, no. 1 (October 1991): 87–94. http://dx.doi.org/10.1677/joe.0.1310087.
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ABSTRACT In several species, glucocorticoids act directly on the pituitary gonadotroph to suppress the gonadotrophin-releasing hormone (GnRH)-induced secretion of the gonadotrophins, especially LH. A mechanism for this action of these adrenal steroids has not been established, but it appears that the glucocorticoids influence LH release by acting on one or more post-receptor sites. This study investigated whether glucocorticoids disrupt GnRH-induced LH release by altering the liberation of arachidonic acid from plasma membrane phospholipids, a component of GnRH-induced LH release. Using perifused ovine pituitary tissue, it was established that exposure of gonadotrophs to 1–1000 nmol cortisol/l for 4 h or longer significantly reduced GnRH-stimulated LH release with the maximal inhibitory effect being observed after 6 h of exposure to cortisol. This suppressive effect of cortisol could be reversed by administration of arachidonic acid, which in its own right could stimulate LH release from ovine pituitary tissue. Furthermore, the inhibitory effect of cortisol on GnRH-stimulated LH release could be directly correlated with decreased pituitary responsiveness to GnRH-stimulated arachidonic acid liberation, consistent with our hypothesis that glucocorticoids can suppress GnRH-induced secretion of LH by reducing the amount of arachidonic acid available for the exocytotic response of GnRH. Journal of Endocrinology (1991) 131, 87–94
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Thompson, E. Brad. "Mechanisms of T-cell Apoptosis Induced by Glucocorticoids." Trends in Endocrinology & Metabolism 10, no. 9 (November 1999): 353–58. http://dx.doi.org/10.1016/s1043-2760(99)00187-3.
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Fruchter, Oren, Tomoshige Kino, Emmanouil Zoumakis, Salvatore Alesci, Massimo De Martino, George Chrousos, and Ze’ev Hochberg. "The Human Glucocorticoid Receptor (GR) Isoform β Differentially Suppresses GRα-Induced Transactivation Stimulated by Synthetic Glucocorticoids." Journal of Clinical Endocrinology & Metabolism 90, no. 6 (June 1, 2005): 3505–9. http://dx.doi.org/10.1210/jc.2004-1646.
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The β-isoform of human glucocorticoid receptor β (hGRβ) acts as a natural dominant negative inhibitor of hGRα-induced transactivation of glucocorticoid-responsive genes. We determined hGRβ ability to suppress hGRα transactivation that was induced by commonly used synthetic glucocorticoids. HepG2/C3A cells were transiently cotransfected with GR cDNA and a glucocorticoid-responsive promoter, luciferase (MMTV-luc). Transfected cells were incubated for 16 h with glucocorticoid and luciferase. For each compound, a dose-response curve was constructed, and half-maximal effective concentrations and maximal transcriptional activities were compared. hGRβ, at a 1:1 ratio to hGRα, differentially suppressed hGRα-induced maximal transcriptional activity stimulated by triamcinolone, dexamethasone, hydrocortisone, and betamethasone (by 96, 68, 62, and 49%, respectively) but not by methylprednisolone. The suppressive effect of hGRβ on hGRα-induced transactivation was stronger at lower concentrations of all tested glucocorticoids, whereas it was blunted at higher concentrations. We conclude that the potency of the dominant negative effect of hGRβ on hGRα-induced transactivation depends on both the type and the dose of the synthetic glucocorticoids in use. These results may provide helpful information concerning the selection of synthetic glucocorticoids for treatment of pathological conditions in which hGRβ modulates the sensitivity of tissues to glucocorticoids.
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Rosas, Alejandro L., Anna A. Kasperlik-Zaluska, Lucyna Papierska, Barbara Lee Bass, Karel Pacak, and Graeme Eisenhofer. "Pheochromocytoma crisis induced by glucocorticoids: a report of four cases and review of the literature." European Journal of Endocrinology 158, no. 3 (March 2008): 423–29. http://dx.doi.org/10.1530/eje-07-0778.
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ContextPheochromocytoma crisis (PC) is a rare life-threatening endocrine emergency that may present spontaneously or can be unmasked by ‘triggers’, including certain medications that provoke the release of catecholamines by tumors. Several isolated cases of PC have been reported after administration of exogenous glucocorticoids; evidence that these drugs cause adverse events in patients with pheochromocytoma is mainly anecdotal.PatientsWe report four cases of PC most likely induced by glucocorticoids and review seven previous reports in the literature linking steroid administration to the development of PC.ResultsIn four new cases reported here, glucocorticoid administration was associated with a fatal outcome in one case, a pheochromocytoma multisystem crisis in another, and serious hypertensive crises in two others. Two patients had incidental adrenal masses and were undergoing high-dose dexamethasone suppression tests (DST).ConclusionsExogenous glucocorticoids may unpredictably trigger PC. Pheochromocytoma should be included in the differential diagnosis of any patient who develops a hypertensive crisis, cardiac failure, tachycardia, headache, and abdominal or chest pain after receiving exogenous glucocorticoids. Glucocorticoid induced PC is frequently associated with hemorrhagic pheochromocytoma. Although exogenous glucocorticoids cause serious complications unpredictably, they should be avoided or administered only if necessary and with caution in patients with known or suspected pheochromocytoma. During the investigation of incidental adrenal masses, pheochromocytoma should ideally be ruled out before administering glucocorticoids. However, no cases have been reported with 1 mg of dexamethasone when given as a DST in patients with pheochromocytoma; larger doses, as low as 2 mg of dexamethasone, may trigger a PC. A patient with pheochromocytoma presenting as an adrenal incidentaloma may also be at risk if exposed to glucocorticoids given as pre-treatment in case of allergy to contrast media.
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Kashino, Chiaki, Toru Hasegawa, Yasuhiro Nakano, Nahoko Iwata, Koichiro Yamamoto, Yasuhiko Kamada, Hisashi Masuyama, and Fumio Otsuka. "Involvement of BMP-15 in Glucocorticoid Actions on Ovarian Steroidogenesis by Rat Granulosa Cells." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A767—A768. http://dx.doi.org/10.1210/jendso/bvab048.1561.
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Abstract Glucocorticoid receptor (GR) are known to be expressed in the ovary and glucocorticoids are shown to exert direct effects on granulosa cell functions. In the clinical setting, menstrual abnormality, amenorrhea and hypermenorrhea can be shown in patients with glucocorticoid excess. On the other hand, glucocorticoids can also be used for the treatment of PCOS with hyperandrogenism. However, the effects of glucocorticoids on the reproductive system have not been fully elucidated. In the present study, we investigated the influence of glucocorticoids on follicular steroidogenesis using primary culture of rat granulosa cells, by focusing on the ovarian bone morphogenetic proteins (BMPs) acting as a luteinizing inhibitor. Granulosa cells isolated from female immature rats were treated with follicle-stimulating hormone (FSH) in the presence of dexamethasone (Dex) in serum-free conditions. After treatment with Dex for 48 h, the changes of estradiol (E2) and progesterone (P4) production and cAMP synthesis induced by FSH treatments were measured by ELISA. Total RNAs of granulosa cells treated with FSH, Dex and BMPs were extracted and mRNA levels of steroidogenetic factors and enzymes, BMP receptors and Id-1 were quantified by real-time RT-PCR. Phosphorylation of Smad1/5/9 induced by BMPs was evaluated by Western blotting using cell lysates in the presence or absence of Dex. As a result, it was revealed that Dex treatment decreased FSH-induced E2 production by granulosa cells. In accordance with the steroid results, Dex suppressed FSH-induced P450arom mRNA expression as well as FSH-induced cAMP synthesis by granulosa cells. By contrast, Dex treatment augmented FSH-induced P4 production by granulosa cells in a concentration-dependent manner. Dex treatment was found to enhance basal and FSH-induced mRNA levels of P4-synthetic enzymes including P450scc and 3βHSD. Of note, Dex treatment activated the BMP target gene Id-1 transcription and Smad1/5/9 phosphorylation, in particular, induced by BMP-15 among various BMP ligands including BMP-2, -4, -6, -7, -9 and -15. It was also revealed that Dex treatment increased mRNA levels of ALK-6, a type-I receptor for BMP-15, and that BMP-15 treatment in turn upregulated GR mRNA levels expressed by granulosa cells. Given that BMP-15 acts as an inhibitor for P4 production by suppressing FSH-receptor actions, it was suggested that glucocorticoid is functionally linked to the enhancement of endogenous BMP-15, leading to the negative feedback toward the P4 overproduction induced by FSH and Dex in granulosa cells. Collectively, it was revealed that glucocorticoids elicit differential effects on the ovarian steroidogenesis of E2 and P4, in which GR and BMP-15 actions are mutually enhanced in granulosa cells.
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Loghin-Oprea, Natalia, Virginia Salaru, Silvia Stratulat, Lucia Mazur Nicorici, and Minodora Mazur. "Management in multimorbidity: glucocorticoid-induced hyperglycemia and diabetes in rheumatic diseases." Public Health, Economy and Management in Medicine, no. 5(102) (November 2024): 39–45. https://doi.org/10.52556/2587-3873.2024.5(102).06.
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Glucocorticoids (GC) are drugs with an important antiinflammatory and immunosuppressive effect, being recommended in treating autoimmune diseases, but which have a series of metabolic side effects, including diabetes. The purpose of the research is to highlight the possibilities of monitoring and treating hyperglycemia and diabetes mellitus (DM) induced by glucocorticoids in patients with rheumatic diseases to optimize the management of these patients. A literature review on the management of glucocorticoid-induced hyperglycemia and diabetes was performed. The databases searched were PubMed, Medline, Web of Science. The MeSh terms were „corticosteroid-induced hyperglycemia” OR „corticosteroidinduced diabetes” AND (rheumatic diseases). 26 sources were identified and analyzed. American and British Diabetic Society guidelines for the diagnosis and management of glucocorticoid-induced hyperglycemia and diabetes aim largely at hospitalized patients, and subsequent outpatient follow-up is inconclusive. At the initiation of GC therapy, it is recommended to assess the basal blood glucose in hospitalized people with DM, four times a day postprandial, and in patients who are not known to have diabetes - once a day. With the development of steroid-induced DM, oral antidiabetics will be recommended, and in cases when patients present significant hyperglycemia in association with signs of diabetic ketoacidosis or hyperosmolar hyperglycemic state, the recommendations of the international guidelines are to initiate insulin. After stopping the administration of GC, the blood sugar will be constantly and repeatedly monitored, together with the review of the hypoglycemic therapy and the achievement of normoglycemia during 3 months, and if it persists, the blood sugar will be monitored after 3 months, together with the performance of the oral glucose tolerance test or HbA1c.
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Akshaya, N., Ravi Krishna, and N. Venkateswaramurthy. "Steroids Induced Hyperglycemia: Its Effects and Management." Journal of Drug Delivery and Therapeutics 13, no. 6 (June 15, 2023): 166–71. http://dx.doi.org/10.22270/jddt.v13i6.6074.
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Steroids are medications that have been widely utilized for a number of ailments, both acute and chronic. The action of endogenous steroids, nuclear hormones that penetrate cell membranes to bind to certain glucocorticoid receptors in the cytoplasm of target cells to form glucocorticoid-receptor (GR) complexes, is mimicked by synthetic glucocorticoids. The translocated activated GR complex regulates DNA transcription in the cell nucleus. The main factor for drug-induced hyperglycemia is steroids. They not only worsen hyperglycemia in those who already have diabetes mellitus (DM), but they can also lead to DM in people who've not previously experienced it. Their incidence can reach up to 46% of patients, and their glucose levels can rise by up to 68% over baseline. Steroid effects are often narrow and reversible. Drug-induced diabetes is supposed to go away as steroid doses are decreased because their impact on endocrine metabolism returns to normal; however, this is often not the case. The synthesis of lipolysis, proteolysis, and hepatic glucose is increased by glucocorticoids (GCs) because they act as a substrate for oxidative stress metabolism. A wide range of medical conditions has been treated with GCs. Although steroid-induced hyperglycemia has been proven to be medically effective, it is still a widespread and potentially dangerous issue that must be taken into consideration when administering any GC dose. The most common scenario requires the use of insulin, particularly when the serum glucose level is greater than 200 mg/dL.
Keywords: Steroids, Glucocorticoids, Hyperglycemia, Resistance, Insulin
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Vagnerová, K., M. Kverka, P. Klusoňová, P. Ergang, I. Mikšík, H. Tlaskalová-Hogenová, and J. Pácha. "Intestinal inflammation modulates expression of 11β-hydroxysteroid dehydrogenase in murine gut." Journal of Endocrinology 191, no. 2 (November 2006): 497–503. http://dx.doi.org/10.1677/joe.1.06732.
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The effect of glucocorticoids is controlled at the pre-receptor level by the activity of 11β-hydroxysteroid dehydrogenase (11HSD). The isoform 11HSD1 is an NADP+-dependent oxidoreductase, usually reductase, that amplifies the action of glucocorticoids due to reduction of the biologically inactive 11-oxo derivatives cortisone and 11-dehydrocorticosterone to cortisol and corticosterone. The NAD+-dependent isoform (11HSD2) is an oxidase that restrains the effect of hormones due to 11β-oxidation of cortisol and corticosterone to their 11-oxo derivatives. Although the immunosuppressive and anti-inflammatory effects of glucocorticoids are well known, the relationship between inflammation and local metabolism of glucocorticoids is not well understood. In this study, we demonstrated that colitis induced by dextran sulfate sodium modulates colonic 11HSD1. Experimentally induced intestinal inflammation stimulated colonic NADP+-dependent but not NAD+-dependent 11HSD activity. Colonic 11HSD1 mRNA was increased, whereas 11HSD2 mRNA was not changed. Additional parallel studies revealed a similar pattern of 11HSD1 mRNA induction in mesenteric lymph nodes and intestinal intraepithelial lymphocytes, but not in spleen and peritoneal macrophages. These data suggest that inflammation modulates local metabolism of glucocorticoid and support the notion that pre-receptor regulation of endogenous corticosteroids might play a role in inflammatory processes.
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Horváth, Katalin M., Zsuzsanna Bánky, Béla E. Tóth, György M. Nagy, and Béla Halász. "Dual Role of Glucocorticoids in Suckling-Induced Prolactin Secretion." Endocrine 15, no. 3 (2001): 287–90. http://dx.doi.org/10.1385/endo:15:3:287.
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Mazziotti, Gherardo, Andrea Giustina, Ernesto Canalis, and John P. Bilezikian. "Glucocorticoid-Induced osteoporosis: clinical and therapeutic aspects." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 8 (November 2007): 1404–12. http://dx.doi.org/10.1590/s0004-27302007000800028.
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Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Fractures, which are often asymptomatic, may occur in as many as 30_50% of patients receiving chronic glucocorticoid therapy. Vertebral fractures occur early after exposure to glucocorticoids, at a time when bone mineral density (BMD) declines rapidly. Fractures tend to occur at higher BMD levels than in women with postmenopausal osteoporosis. Glucocorticoids have direct and indirect effects on the skeleton. They impair the replication, differentiation, and function of osteoblasts and induce the apoptosis of mature osteoblasts and osteocytes. These effects lead to a suppression of bone formation, a central feature in the pathogenesis of GIO. Glucocorticoids also favor osteoclastogenesis and as a consequence increase bone resorption. Bisphosphonates are the most effective of the various therapies that have been assessed for the management of GIO. Anabolic therapeutic strategies are under investigation. Teriparatide seems to be also efficacious for the treatment of patients with GIO.
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Gregório, Luiz Henrique de, Paulo G. Sampaio Lacativa, Ana Cláudia C. Melazzi, and Luis Augusto Tavares Russo. "Glucocorticoid-induced osteoporosis." Arquivos Brasileiros de Endocrinologia & Metabologia 50, no. 4 (August 2006): 793–801. http://dx.doi.org/10.1590/s0004-27302006000400024.
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Glucocorticoid-induced osteoporosis is the most frequent cause of secondary osteoporosis. Glucocorticoids cause a rapid bone loss in the first few months of use, but the most important effect of the drug is suppression of bone formation. The administration of oral glucocorticoid is associated with an increased risk of fractures at the spine and hip. The risk is related to the dose, but even small doses can increase the risk. Patients on glucocorticoid therapy lose more trabecular than cortical bone and the fractures are more frequent at the spine than at the hip. Calcium, vitamin D and activated forms of vitamin D can prevent bone loss and antiresorptive agents are effective for prevention and treatment of bone loss and to decrease fracture risk. Despite the known effects of glucocorticoids on bone, only a few patients are advised to take preventive measures and treat glucocorticoid-induced osteoporosis.
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Kaleda, Maria I., Irina P. Nikishina, and Alesya V. Firsa. "Belimumab in a Patient with Systemic Lupus Erythematosus with Juvenile Onset and Steroid-induced Diabetes: Clinical Case." Current Pediatrics 22, no. 6 (January 12, 2024): 546–53. http://dx.doi.org/10.15690/vsp.v22i6.2649.
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Background. The management of children with systemic lupus erythematosus (SLE) is usually associated with lifelong systemic glucocorticoids administration and, thereby, high risk of serious side effects, including steroid-induced diabetes. The belimumab (B-lymphocyte stimulator inhibitor) administration significantly reduces the glucocorticoids dose, the risk and severity of steroid therapy complications. Clinical case description. The patient was diagnosed with SLE at the age of 16 years. Therapy with hydroxychloroquine and oral glucocorticoid at a high dose (methylprednisolone 56 mg per day) was initiated. Steroid-induced diabetes was diagnosed 1 month after the therapy start; avascular necrosis sites were revealed in 2 months. Mycophenolate mofetil made it possible to achieve the disease activity control. However, the belimumab was prescribed 5 months after diagnosis verification due to continuous insulin requirement and avascular necrosis progression. Conclusion. Belimumab is the only genetically engineered biologic drug approved for the treatment of children with SLE. As a result of its use, it was possible to stabilize the patient's condition quickly (within 3 months), to reduce significantly the dose of oral glucocorticoid, methylprednisolone (from 24 to 8 mg/day), to achieve remission of steroidinduced diabetes with further insulin withdrawal, and also to relieve avascular necrosis clinical symptoms.
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Wang, Zeng, Yi Qian Qu, Yang Zhang, Xing Yu Zhu, Xiao Wei Gong, and Hong Yu Chen. "Efficacy of Glucocorticoids and Glucocorticoid-Induced Hyperglycaemia in Renal Disease: A Meta-Analysis of Randomized Controlled Trials." Computational and Mathematical Methods in Medicine 2022 (March 7, 2022): 1–8. http://dx.doi.org/10.1155/2022/2484626.
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Background. Glucocorticoids are the most effective anti-inflammatory and immunosuppressive drugs used to treat patients with renal disease. This study pooled the current evidence of the efficacy of Glucocorticoids and Glucocorticoid-induced hyperglycaemia in renal disease. Methods. We conducted a systematic literature search on PubMed, Cochrane Central, and Web of Science for relevant randomized controlled trials (RCTs) up to September 1, 2021. The meta-analysis, sensitivity analysis and bias analysis were performed using Review Manager 5. 3. Results. In this study, seven RCTs with 797 patients were included in our analysis. The analysis revealed that glucocorticoids had a certain alleviating effect on the reduction of renal function. (risk ratio [RR] 0.49 95% confidence interval [Cl] 0. 28 to 0.85, p =0.01) and reduction of proteinuria (weight mean difference [WMD] -0.43; 95% CI -0.57 to-0.28) when compared with the control group. Patients receiving glucocorticoids therapy did not have an increased risk of developing new-onset diabetes mellitus or impaired glucose tolerance. (RR 3.76 95% CI 0.54 to 26.10, p =0.18). For other safety outcomes, glucocorticoids therapy did not increase risk of respiratory infections (RR 1.63, 95% CI 0. 69to3. 89, p =0.27) and Gastrointestinal SAEs is relatively controversial (RR 1.10, 95% CI 0.32 to 3.79, p =0.88). Discussion. In conclusion, current clinical evidence indicates that glucocorticoids is efficacious and safe to renal disease compared with control. Further research comparing long-term glucocorticoids use is needed.
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Ermolaeva, A. S., and V. V. Fadeev. "Type 2 amiodarone-induced thyrotoxicosis: efficacy of glucocorticoid therapy, a retrospective analysis." Problems of Endocrinology 69, no. 6 (January 24, 2024): 17–27. http://dx.doi.org/10.14341/probl13267.
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BACKGROUND: Type 2 amiodarone-induced thyrotoxicosis remains a significant problem of endocrinology and cardiology. Due to the increase a life expectancy of the population, the prevalence of cardiac arrhythmias and prescribing of amiodarone are increasing. Thyrotoxicosis aggravates the existing cardiovascular disease in patients, leads to the progression of left ventricular dysfunction, relapses of arrhythmias, increasing the risk of adverse outcomes. The tactic of further management of patients is complicated: it is necessary to resolve the issue of canceling or continuing the use of antiarrhythmic drugs necessary for a patient with a history of cardiac arrhythmia, as well as competent therapy of the thyroid pathology that has arisen. Oral glucocorticoids are the first-line drugs for the treatment of patients with moderate and severe type 2 amiodarone-induced thyrotoxicosis. Despite the appearance of clinical recommendations, opinions on the management of patients are differ, both among cardiologists and among endocrinologists. Often thyrostatics are prescribed to patients simultaneously with glucocorticoids, although it doesn’t have pathogenetic basis.AIM: To evaluate the efficacy of various therapy options in patients with type 2 amiodarone-induced thyrotoxicosis.MATERIALS AND METHODS: The retrospective study included 38 patients (20 men and 18 women aged 35 to 85 years) with type 2 amiodarone-induced thyrotoxicosis. All patients underwent an analysis of anamnestic, anthropometric data, complex laboratory and instrumental diagnostics. According to the treatment options, 3 groups were retrospectively formed: without therapy (n=19), taking glucocorticoids (n=11) and combination of glucocorticoids and thyrostatics (n=8). The follow-up period was 6–18 months, including the treatment. The efficacy of treatment in the groups was evaluated by the time of reaching euthyroidism on the background of glucocorticoid therapy and duration of thyrotoxicosis; the search was conducted for potential predictors of delayed response to glucocorticoid therapy and long-term course of thyrotoxicosis.RESULTS: The average age was 62.0 [52.9; 66.3] years. The level of free thyroxine was significantly decreased after 1 month from the start of therapy in both groups: from 38.1 [32.1; 58.4] to 23.4 [19.6; 29.3] pmol/l (p<0.001) in the group taking glucocorticoids; from 73.9 [42.2; 75.6] to 39.3 [22.4; 47.2] pmol/l (p<0.001) in the combination therapy group. The time of reaching euthyroidism was longer in the combination therapy group (p=0.047), didn’t depend on the dose (p=0.338) and duration of taking thiamazole (p=0.911), the delayed response to therapy correlated with age (p=-0.857; p=0.007) and time interval from the appearance of clinical symptoms of thyrotoxicosis to the start of glucocorticoid therapy (p=0.881; p<0.001).CONCLUSION: The results demonstrate the dependence of glucocorticoid response on the age of the patient and start time of therapy relative to the duration of thyrotoxicosis, inexpediency of additional prescribing thyrostatics in type 2 amiodarone-induced thyrotoxicosis.
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Feilleux-Duche, S., M. Garlatti, R. Burcelin, M. Aggerbeck, J. Bouguet, J. Girard, J. Hanoune, and R. Barouki. "Acinar zonation of the hormonal regulation of cytosolic aspartate aminotransferase in the liver." American Journal of Physiology-Cell Physiology 266, no. 4 (April 1, 1994): C911—C918. http://dx.doi.org/10.1152/ajpcell.1994.266.4.c911.
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The zonation of the expression and regulation of the cytosolic aspartate aminotransferase (cAspAT) mRNAs in the liver acinus was investigated in diabetic and/or adrenalectomized rats. Dexamethasone increased cAspAT activity two- to threefold alone and up to sixfold in combination with streptozotocin-induced diabetes. Northern blot analysis showed that the cAspAT mRNAs were increased by those treatments; the effect of streptozotocin was reversed by the administration of insulin. In situ hybridization experiments showed that basal cAspAT mRNAs were uniformly distributed within the liver acinus. However, cAspAT mRNAs were induced by glucocorticoids specifically in the periportal zone and by streptozotocin in a larger area including the periportal and intermediary zone. The alpha 2u-globulin mRNAs which are specifically expressed in the perivenous hepatocytes are also induced by glucocorticoids in this zone, suggesting that the specific regulation of the cAspAT gene by glucocorticoids in the periportal zone is not due to the absence of functional glucocorticoid receptors in the other zones. We conclude that the regulation of the cAspAT housekeeping gene is zone specific in the liver. Furthermore, this zonation depends on the gene and on the type of hormonal or pharmacological treatment.
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Strack, A. M., R. J. Sebastian, M. W. Schwartz, and M. F. Dallman. "Glucocorticoids and insulin: reciprocal signals for energy balance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 1 (January 1, 1995): R142—R149. http://dx.doi.org/10.1152/ajpregu.1995.268.1.r142.
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Signals that regulate long-term energy balance have been difficult to identify. Increasingly strong evidence indicates that insulin, acting on the central nervous system in part through its effect on neuropeptide Y (NPY), inhibits food intake. We hypothesized that corticosteroids and insulin might serve as interacting, reciprocal signals for energy balance, acting on energy acquisition, in part through their effects on hypothalamic NPY, as well as on energy stores. Because glucocorticoids also stimulate insulin secretion, their role is normally obscured. Glucocorticoids and insulin were clamped in adrenalectomized rats with steroid replacement and streptozotocin-induced diabetes. Glucocorticoids stimulated and insulin inhibited NPY mRNA and food intake. Glucocorticoids inhibited and insulin increased energy gain as determined by the change in body weight. When adrenalectomized diabetic rats were treated, corticosterone stimulated and insulin inhibited food intake, and, respectively, inhibited and increased overall energy gain. More than 50% of the variance was explained by regression analysis of the two hormones on food intake and body weight. Thus glucocorticoids and insulin are major, antagonistic, long-term regulators of energy balance. The effects of corticosterone and insulin on food intake may be mediated, in part, through regulation of hypothalamic NPY synthesis and secretion.
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Gunin, AG, IN Mashin, and DA Zakharov. "Proliferation, mitosis orientation and morphogenetic changes in the uterus of mice following chronic treatment with both estrogen and glucocorticoid hormones." Journal of Endocrinology 169, no. 1 (April 1, 2001): 23–31. http://dx.doi.org/10.1677/joe.0.1690023.
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Glucocorticoids have been known to be involved in the regulation of some aspects of estrogen action on the uterus. However, the effect of glucocorticoids on changes in uterine morphogens produced by chronic estrogen exposure is not known. Therefore, the aim of this work was to examine the role of glucocorticoids on proliferative and morphogenetic uterine reactions induced by continuous estrogen treatment. Ovariectomized mice received subcutaneous injections of estradiol dipropionate in olive oil (2 microg per 100 g body weight once a week) or vehicle and drank water with or without dexamethasone (2 mg/l) for 30, 60 and 90 days. Treatment with dexamethasone caused a marked reduction in estradiol-induced changes in uterine weight, in proliferation (estimated from the proportion of mitotic and BrdU-labeled cells in all uterine tissues), and in changes in estradiol-dependent morphogenesis, which was redirected from the formation of atypical hyperplasia in animals receiving only estradiol to the appearance of simple or cystic endometrial hyperplasia in animals receiving both estradiol and dexamethasone. Estradiol alone increased dramatically the number of perpendicular oriented mitoses in luminal and glandular epithelia, and administration of dexamethasone inhibited this effect. In the absence of estradiol, chronic treatment with dexamethasone has no effect on all uterine parameters tested. Thus, chronic glucocorticoid treatment produces a complex antiestrogenic effect in the uterus of mice. Estradiol-induced changes in mitosis orientation are probably responsible for changes in the shape of glands and development of endometrial hyperplasia.
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Paredes, Sílvia, and Marta Alves. "Abordagem e Tratamento da Hiperglicemia Induzida por Glicocorticóides." Acta Médica Portuguesa 29, no. 9 (September 30, 2016): 556. http://dx.doi.org/10.20344/amp.7758.
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Introduction: Glucocorticoids have been associated to several side effects, specially a diabetogenic action, the most common and representative effect. Glucocorticoid-induced hyperglycemia is a common medical condition, with general associated morbidity andmortality.Material and Methods: It was performed a literature review about the management and treatment of glucocorticoid-induced hyperglycemia.Results: Through numerous not quite fully understood mechanics, glucocorticoids promote hyperglycemia in non-diabetic patients andworsen diabetes control in diabetic individuals. Glucocorticoid-induced hyperglycemia presents key patterns, enhanced in the postprandial period and scheduled-dependent. Despite the existence of guidelines for hyperglycemia treatment in non-critic hospitalized and non-hospitalized patients, there are no guidelines respecting glucocorticoid-induced hyperglycemia. Nevertheless, it is known that glucocorticoid-induced hyperglycemia is complex and demanding, requiring a specific approach. Indeed, glucocorticoid-induced hyperglycemia treatment depends on the glucocorticoid used, its dose, frequency and schedule. Furthermore, the scheme of treatment previously used by diabetic individuals also influences the choice of the new scheme.Discussion and Conclusion: The authors reviewed the glucocorticoid induced-hyperglycemia thematic and propose strategies to approach and treat glucocorticoid induced-hyperglycemia in diabetic and non-diabetic individuals. This review is expected to be useful in different settings and crosswise to all medical specialties.
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Antoni, F. A., J. Hoyland, M. D. Woods, and W. T. Mason. "Glucocorticoid inhibition of stimulus-evoked adrenocorticotrophin release caused by suppression of intracellular calcium signals." Journal of Endocrinology 133, no. 2 (May 1992): R13—R16. http://dx.doi.org/10.1677/joe.0.133r013.
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ABSTRACT Stress provokes a cohort of homeostatic reflexes by the central nervous, the immune as well as the metabolic control systems of the body. These powerful adaptive responses, which can cause a collapse of body homeostasis in the absence of feedback inhibition, are suppressed by adrenal glucocorticoid hormones. A prominent and physiologically significant early action of glucocorticoids that requires the induction of newly synthesized messenger RNA and protein is the suppression of ACTH release by anterior pituitary corticotroph cells. It is demonstrated here that glucocorticoids inhibit stimulated ACTH secretion in pituitary corticotroph tumour (AtT-20) cells by reducing stimulus-evoked intracellular free calcium transients. Thus, the data show for the first time that intracellular calcium signals may be modified by rapidly induced proteins. It is proposed that this is a general mechanism that underlies the early inhibitory effects of glucocorticoids during stress in various types of cell.
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Liu, J., R. M. Haigh, and C. T. Jones. "Enhancement of noradrenaline-induced inositol polyphosphate formation by glucocorticoids in rat vascular smooth muscle cells." Journal of Endocrinology 133, no. 3 (June 1992): 405—NP. http://dx.doi.org/10.1677/joe.0.1330405.
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ABSTRACT Glucocorticoids are known to regulate the contractility of vascular smooth muscle by increasing its response to noradrenaline. The molecular mechanisms for achieving this remain unclear. Recent results in our laboratory have demonstrated that glucocorticoids affect both α1-adrenoceptor number and coupling to G proteins. Whether this leads to an increase in second-messenger production has to be established. The present experiments, therefore, report the effects of dexamethasone on inositol polyphosphate production in vascular smooth muscle cells in culture. Noradrenaline induced the release of inositol polyphosphates from prelabelled [3H]inositol phosphoinositides in the membrane in a dose-dependent manner. The concentration of noradrenaline which caused half-maximal response was 1·26 μmol/l. Prazosin inhibited noradrenaline-induced inositol monophosphate formation to 10·26 ± 3·67% (mean ± s.e.m.; P < 0·01, n = 5) of control value whereas yohimbine reduced it to only 61·74 ± 11·82% (P < 0·05, n = 5), suggesting an action primarily through α1-adrenergic receptors. Dexamethasone (100 nmol/l, 48 h) enhanced noradrenaline-induced inositol monophosphate, bisphosphate and trisphosphate formation up to twofold (P < 0·001, n = 5). The enhancement of the response occurred despite the fact that dexamethasone reduced [3H]inositol prelabelling of membrane phosphoinositides by 49·5 ± 9·9% (P < 0·05, n = 3). The present results suggest that the potential action of glucocorticoids on vascular smooth muscle contractility is, at least in part, through controlling α1-adrenoceptor-mediated second-messenger production. Journal of Endocrinology (1992) 133, 405–411
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Solano, Joel M., and Lauren Jacobson. "Glucocorticoids reverse leptin effects on food intake and body fat in mice without increasing NPY mRNA." American Journal of Physiology-Endocrinology and Metabolism 277, no. 4 (October 1, 1999): E708—E716. http://dx.doi.org/10.1152/ajpendo.1999.277.4.e708.
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Glucocorticoid stimulation of appetite and leptin expression conflicts with leptin inhibition of food intake and suggests that glucocorticoids reduce sensitivity to leptin. To determine if glucocorticoids impair feeding and metabolic responses to leptin, we measured leptin-induced changes in food intake, body weight, hormones, carcass fat, and hypothalamic neuropeptide Y (NPY) mRNA in adrenalectomized mice with and without corticosterone replacement. Leptin infusion (0.5 μg/h) significantly decreased food intake and body weight in adrenalectomized mice. Corticosterone replacement approximating normal 24-h mean levels restored food intake but did not permit weight gain equivalent to PBS-infused controls. Corticosterone levels comparable to stress-induced production completely reversed leptin-induced reductions in weight gain and body fat, despite significant attenuation by leptin of corticosterone-induced increases in plasma insulin levels. Glucocorticoid replacement increased food intake without reversing leptin inhibition of hypothalamic NPY mRNA levels. We conclude that glucocorticoid levels within the physiological range can interfere with leptin action and that glucocorticoid effects are at least partly independent of NPY.
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Ratineau, C., C. Roche, F. Chuzel, M. Cordier-Bussat, M. Blanc, C. Bernard, J.-C. Cuber, and J.-A. Chayvialle. "Regulation of intestinal cholecystokinin gene expression by glucocorticoids." Journal of Endocrinology 151, no. 1 (October 1996): 137–45. http://dx.doi.org/10.1677/joe.0.1510137.
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Abstract The effect of glucocorticoids on the expression of intestinal cholecystokinin (CCK) was investigated both in vivo and in cell culture systems. In vivo, 2-day administration of methylprednisolone to adult male rats induced a decrease in CCK-like immunoreactivity (CCK-LI) and CCK mRNA levels in mucosal extracts. In two CCK-producing cell lines, RIN 1056E and STC-1 of pancreatic and intestinal origin respectively, dexamethasone induced dose-dependent decreases in both CCK-LI and steady-state CCK mRNA levels. The decrease in CCK mRNA was totally prevented by incubation of cells with an excess of RU 38486, a competitive inhibitor for the binding of glucocorticoids to their receptor. Actinomycin D, used to prevent RNA synthesis, did not modify CCK mRNA stability in dexamethasone-pretreated cells as compared with cells not exposed to dexamethasone. When cells were first incubated with actinomycin D, subsequent addition of dexamethasone left the steady-state CCK mRNA levels unaltered in both cell lines. Nuclear run-on assays performed in RIN 1056E cells showed that glucocorticoids decreased the rate of transcription of the CCK gene. In addition, cycloheximide, used to prevent protein synthesis, abolished the inhibitory effects of dexamethasone on steady-state CCK mRNA levels. These results demonstrate that glucocorticoids down-regulate CCK gene expression in the rat intestinal mucosa and in two CCK-producing cell lines. The effect is blocked by a glucocorticoid receptor antagonist. Inhibition of CCK gene expression may result from a decrease in the transcription rate, and probably involves one or several steps that depend on protein synthesis. Journal of Endocrinology (1996) 151, 137–145
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Dardevet, D., C. Sornet, I. Savary, E. Debras, P. Patureau-Mirand, and J. Grizard. "Glucocorticoid effects on insulin- and IGF-I-regulated muscle protein metabolism during aging." Journal of Endocrinology 156, no. 1 (January 1, 1998): 83–89. http://dx.doi.org/10.1677/joe.0.1560083.
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This study was performed to assess the effect of glucocorticoids (dexamethasone) on insulin- and IGF-I-regulated muscle protein metabolism in adult and old rats. Muscle atrophy occurred more rapidly in old rats, and recovery of muscle mass was impaired when compared with adults. Muscle wasting resulted mainly from increased protein breakdown in adult rat but from depressed protein synthesis in the aged animal. Glucocorticoid treatment significantly decreased the stimulatory effect of insulin and IGF-I on muscle protein synthesis in adult rats by 25.9 and 58.1% respectively. In old rats, this effect was even greater, being 49.3 and 100% respectively. With regard to muscle proteolysis, glucocorticoids blunted the anti-proteolytic action of insulin and IGF-I in both age groups. During the recovery period, adult rats reversed the glucocorticoid-induced resistance of muscle protein metabolism within 3 days, at which time old rats still exhibited the decrease in insulin-regulated proteolysis. In conclusion, the higher sensitivity of old rat muscle to glucocorticoids may in part result from the greater modification of the effects of insulin and IGF-I on muscle protein metabolism. These responses to glucocorticoids in old rats may be associated with the emergence of muscle atrophy with advancing age.
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Groves, TC, GF Wagner, and GE DiMattia. "cAMP signaling can antagonize potent glucocorticoid post-transcriptional inhibition of stanniocalcin gene expression." Journal of Endocrinology 171, no. 3 (December 1, 2001): 499–516. http://dx.doi.org/10.1677/joe.0.1710499.
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Stanniocalcin (STC) is a glycoprotein hormone first discovered in fish as a homeostatic regulator of calcium and phosphate transport; it has recently been discovered in mammals, in which it appears to have a similar role. It has also been implicated in a number of different physiological processes through correlative studies, but the factors regulating its production have not been elucidated. In this report, we show that steady-state STC mRNA levels in the mouse corticotrope tumor line, AtT-20, were exquisitely sensitive to glucocorticoids. Hydrocortisone and dexamethasone (Dex) induced a dramatic reduction in steady-state STC mRNA levels in AtT-20 cells through a post-transcriptional mechanism. Similarly, glucocorticoids down-regulated STC mRNA levels in the human fibrosarcoma cell line, HT1080. The specificity of the glucocorticoid-mediated decrease in STC mRNA abundance was shown using the glucocorticoid receptor antagonist, RU-486. Activation of the cAMP-signaling pathway in glucocorticoid-cultured AtT-20 cells transiently restored STC gene expression. Treatment of AtT-20 cells with the transcriptional inhibitor, actinomycin D, rescued steady-state STC mRNA levels from Dex-induced repression, indicating that the Dex-mediated decrease in STC gene expression requires current gene transcription. Taken together, these results describe a unique model system in which cAMP-stimulated events can reverse post-transcriptional repression of gene expression by glucocorticoids.
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Nadolnik, L. I., N. V. Emelyanov, I. P. Pasteur, and V. V. Vinogradov. "Corticosteroid-binding globulin in experimental hypothyroidism in male and female rats." Problems of Endocrinology 46, no. 5 (October 15, 2000): 35–39. http://dx.doi.org/10.14341/probl11875.
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Main parameters of complex formation of corticosteroid-binding globulin (CSG) were studied in young male and female rats with hypothyrosis induced by mercasolyl in a daily dose of 6 and 30 mg/kg. No pronounced differences in CSG, typical of adult animals, were observed in young rats under conditions of thyroid function inhibition. Steroidand androgen-inhibitory and estrogen-inducing effects of hormones towards CSG did not manifest in hypothyrosis. Decrease in the level of thyroid hormones is characterized by increased affinity of CSG for glucocorticoids and a decrease in the concentration of binding sites. These data indicate that thyroid hormones are the primary regulators of CSG activity. Possibility of modifying CSG affinity and role of this factor in regulation of biological activity of glucocorticoids are discussed.
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Van der Geyten, S., and V. M. Darras. "Developmentally defined regulation of thyroid hormone metabolism by glucocorticoids in the rat." Journal of Endocrinology 185, no. 2 (May 2005): 327–36. http://dx.doi.org/10.1677/joe.1.05974.
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Glucocorticoids are known regulators of thyroid function in vertebrates. In birds they have clear tissue-specific and age-dependent effects on thyroid hormone metabolism. In mammals, however, few studies exist addressing these aspects using an in vivo model system. We therefore set out to examine the acute effects of a single dose of dexamethasone (DEX) on plasma 3,5,3′-tri-iodothyronine (T3) and thyroxine (T4) levels, as well as on the activity of the different deiodinases in liver, kidney and brain in the developing rat. In 20-day-old fetuses (E20), glucocorticoids had no effects on circulating thyroid hormone levels despite their clear effects on hepatic and renal deiodinases, thereby indicating that under these conditions circulating thyroid hormone levels are more dependent on thyroidal secretion than on peripheral deiodination. In contrast, in 5-day-old rat pups, DEX did not seem to have any effects on hepatic and renal T3 production (via the type I deiodinase), whereas type III deiodinase (D3) activity in both these tissues increased significantly. These observations therefore suggested that the DEX-induced increase in circulating T3 levels is a direct consequence of the increase in plasma T4 levels. In 12-day-old pups (P12), however, the main effect of glucocorticoids on circulating levels was by increasing inner ring deiodination T3 through induction of D3 in both liver and kidney. Finally, in the brain, glucocorticoids stimulated thyroid hormone activity only during a short period of time (between E20 and P12) that largely overlaps with the transient window in time during which brain development is thyroid hormone sensitive. This was in contrast to the E20 and P12 brain, where the glucocorticoid-induced changes in type II deiodinase and D3 seemed to favor a status quo in local T3 availability.
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Dang, Thanh Q., Nanyoung Yoon, Helen Chasiotis, Emily C. Dunford, Qilong Feng, Pingnian He, Michael C. Riddell, Scott P. Kelly, and Gary Sweeney. "Transendothelial movement of adiponectin is restricted by glucocorticoids." Journal of Endocrinology 234, no. 2 (August 2017): 101–14. http://dx.doi.org/10.1530/joe-16-0363.
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Altered permeability of the endothelial barrier in a variety of tissues has implications both in disease pathogenesis and treatment. Glucocorticoids are potent mediators of endothelial permeability, and this forms the basis for their heavily prescribed use as medications to treat ocular disease. However, the effect of glucocorticoids on endothelial barriers elsewhere in the body is less well studied. Here, we investigated glucocorticoid-mediated changes in endothelial flux of Adiponectin (Ad), a hormone with a critical role in diabetes. First, we used monolayers of endothelial cells in vitro and found that the glucocorticoid dexamethasone increased transendothelial electrical resistance and reduced permeability of polyethylene glycol (PEG, molecular weight 4000 Da). Dexamethasone reduced flux of Ad from the apical to basolateral side, measured both by ELISA and Western blotting. We then examined a diabetic rat model induced by treatment with exogenous corticosterone, which was characterized by glucose intolerance and hyperinsulinemia. There was no change in circulating Ad but less Ad protein in skeletal muscle homogenates, despite slightly higher mRNA levels, in diabetic vs control muscles. Dexamethasone-induced changes in Ad flux across endothelial monolayers were associated with alterations in the abundance of select claudin tight junction (TJ) proteins. shRNA-mediated knockdown of one such gene, claudin-7, in HUVEC resulted in decreased TEER and increased adiponectin flux, confirming the functional significance of Dex-induced changes in its expression. In conclusion, our study identifies glucocorticoid-mediated reductions in flux of Ad across endothelial monolayers in vivo and in vitro. This suggests that impaired Ad action in target tissues, as a consequence of reduced transendothelial flux, may contribute to the glucocorticoid-induced diabetic phenotype.
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Shpilberg, Y., J. L. Beaudry, A. D'Souza, J. E. Campbell, A. Peckett, and M. C. Riddell. "A rodent model of rapid-onset diabetes induced by glucocorticoids and high-fat feeding." Disease Models & Mechanisms 5, no. 5 (December 19, 2011): 671–80. http://dx.doi.org/10.1242/dmm.008912.
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Chan, Junny, Elizabeth H. Rabbitt, Barbara A. Innes, Judith N. Bulmer, Paul M. Stewart, Mark D. Kilby, and Martin Hewison. "Glucocorticoid-induced apoptosis in human decidua: a novel role for 11β-hydroxysteroid dehydrogenase in late gestation." Journal of Endocrinology 195, no. 1 (October 2007): 7–15. http://dx.doi.org/10.1677/joe-07-0289.
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Glucocorticoids play a fundamental role in the endocrinology of pregnancy but excess glucocorticoids in utero may lead to abnormalities of fetal growth. Protection against fetal exposure to cortisol is provided by the enzyme 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) located in the human placental trophoblast. By contrast, relatively little is known concerning the function of glucocorticoid-activating 11β-HSD1, which is strongly expressed within human maternal decidua. To address this we have assessed: i) changes in decidual 11β-HSD1 expression across gestation and ii) the functional role of glucocorticoids in decidua. Human decidua was collected from women undergoing surgical termination of pregnancy in first (n = 32) and second (n = 10) trimesters, and elective caesarean sections in the third trimester (n = 9). Analysis of mRNA for 11β-HSD1 by real-time RT-PCR showed increased expression in second (9.3-fold, P < 0.01) and third (210-fold, P < 0.001) trimesters. Studies using primary cultures of decidual cells also revealed higher levels of cortisol generation in the third trimester. Changes in decidual 11β-HSD1 with gestation were paralleled by increased expression of the apoptosis markers caspase-3 and annexin-V, particularly in cluster designation (CD)10−VE non-stromal cells (20-fold in third trimester relative to first trimester). Apoptosis was also readily induced in primary cultures of third trimester decidual cells when treated with cortisol, cortisone, or dexamethasone (all 100 nM for 24 h). The effect of cortisone but not cortisol or dexamethasone was blocked by an 11β-HSD inhibitor confirming the functional significance of endogenous cortisol generation. These data show that autocrine metabolism of glucocorticoids is an important facet of the feto-placental unit in late gestation and we propose that a possible effect of this is to stimulate programmed cell death in human decidua.
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Rossiyah, Nella. "THE SAFETY OF GLUCOCORTICOIDS IN THE TREATMENT OF INFAMMATORY RHEUMATIC DISEASE : A SYSTEMATIC REVIEW." Journal of Advance Research in Medical & Health Science (ISSN: 2208-2425) 9, no. 3 (March 25, 2023): 110–15. http://dx.doi.org/10.53555/nnmhs.v9i3.1623.
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Glucocorticoids have been utilized as a component of the treatment for rheumatoid arthritis ever since their introduction some decades ago. It has been established that glucocorticoids are effective in lowering the inflammatory activity induced by this condition and in slowing the course of erosive joint degradation. Both of these benefits can be attained by taking the medication. Unfortunately, they also have a wide variety of potentially adverse consequences, the severity of which may vary depending on the dosage and the length of the therapy. Nevertheless, the benefits of these medications far outweigh the risks associated with them. As a result of the rise in popularity of many alternative therapy alternatives, the use of glucocorticoids as a treatment method is currently being debated (such as biologic and targeted synthetic disease-modifying antirheumatic medicines). It is possible to provide corticosteroids by injecting them directly into the joint. Many people are opposed to the use of glucocorticoids because of the dose-dependent adverse effects that they can have, despite the fact that they continue to be an essential component in the treatment of a wide variety of inflammatory rheumatic diseases. The usage of glucocorticoids for an extended period of time is connected with a greater risk of experiencing adverse consequences. These problems are associated with an increased chance of developing cardiovascular disease, diabetes, and possibly mortality.
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Shelat, SG, LM Flanagan-Cato, and SJ Fluharty. "Glucocorticoid and mineralocorticoid regulation of angiotensin II type 1 receptor binding and inositol triphosphate formation in WB cells." Journal of Endocrinology 162, no. 3 (September 1, 1999): 381–91. http://dx.doi.org/10.1677/joe.0.1620381.
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Mineralocorticoids, glucocorticoids, and angiotensin II (AngII) act cooperatively to maintain body fluid homeostasis. Mineralocorticoids, such as aldosterone and deoxycorticosterone-acetate (DOCA), function synergistically with AngII in the brain to increase salt appetite and blood pressure. In addition, glucocorticoids increase AngII-induced drinking and pressor responses and may also facilitate the actions of aldosterone on salt appetite. The AngII Type 1 (AT1) receptor mediates many of the physiological and behavioral actions of AngII. This receptor is coupled to the G-protein Gq, which mediates AngII-induced inositol triphosphate (IP3) formation. The WB cell line, a liver epithelial cell line that expresses the AT1 receptor, was used to examine the cellular basis of glucocorticoid and mineralocorticoid regulation of AT1 function. In this study corticosterone and dexamethasone treatments increased the number of AT1 receptors by activating the glucocorticoid receptor (GR). This increase in AT1 binding resulted in enhanced AngII-stimulated IP3 formation. However, only supraphysiological doses of aldosterone or DOCA increased AT1 binding, and this effect also was mediated by GR activation. Furthermore, despite evidence that mineralocorticoids and glucocorticoids function together to increase AngII-stimulated actions in vivo, aldosterone and dexamethasone did not act synergistically to affect AT1 binding, Gq expression, or IP3 formation. These results indicate that GR activation, and the subsequent increases in AT1 binding and in AngII-stimulated IP3 formation, may represent a cellular mechanism underlying the synergy between adrenal steroids and AngII.
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Manahan, Rachel, Jake Macey, Mallory Farrar, Conor O’Donoghue, Sarah Knight, Chloe Carmichael, Chris Marshall, et al. "PSAT097 Patient Preference Research: Preferred Adjunctive Medication Attributes of Adult Patients with Classic Congenital Adrenal Hyperplasia." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A118. http://dx.doi.org/10.1210/jendso/bvac150.240.
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Abstract Background People with classic congenital adrenal hyperplasia (CAH) often require supraphysiologic doses of glucocorticoids (e.g., hydrocortisone, dexamethasone) to treat cortisol deficiency and excess androgen production. Healthcare providers and patients continually try to balance androgen control with side effects from supraphysiologic glucocorticoids. This study aimed to understand the preferences of adults with classic CAH regarding benefits of a potential new adjunctive medication that may provide better androgen control and allow for lower glucocorticoid doses. Methods Discrete choice experiment (DCE) methodology was used to calculate the relative stated preferences for the additional therapy's hypothetical benefits (attributes). Seven attributes were developed for the DCE after review of relevant data and qualitative literature, interviews with eight adults with classic CAH and input from two endocrinologists. The online DCE survey was piloted via interviews with three adults with classic CAH and a soft launch, which confirmed survey content and functioning. Preference data and subgroup differences were analyzed using conditional logit and scale assessment modelling, respectively. Results US adults with classic CAH (N=118, 75% female, age 19–69) valued avoidance of glucocorticoid-induced weight gain by twice the magnitude of other treatment attributes (all coefficients p<0.001 compared to baseline levels of no avoidance/decrease/improvement): complete avoidance of weight gain from glucocorticoids (1.109); moderate decrease in risk of developing health conditions from long-term glucocorticoids: type 2 diabetes (0.540), osteopenia, osteoporosis, fractures (0.521) and cardiovascular disease (0.502); moderate improvement in: fatigue (0.439), fertility (0.437) and excessive body hair (females only) and acne (0.410). Avoidance of glucocorticoid-induced weight gain remained the most preferred attribute across all subgroup analyses. Avoidance of glucocorticoid-induced weight gain was relatively much more important to females (n=89) than males (n=28) and participants with a body mass index ≥30 (n=70) than <30 (n=48). Improvement in fertility was more important to males than females, was valued by participants aged 18–45 (n=82) but was not a significant preference in participants >45 (n=36) and was relatively more important to participants with fertility problems (n=31) than without (n=87). Improvement in hirsutism and acne was highly valued by participants with excessive hair growth (n=38) but had the lowest preference among those without (n=80). Improvement in fatigue was a significant preference for participants with energy problems (n=73) but was not significant for those without (n=45). Conclusions The strong and consistent preference for avoiding glucocorticoid-induced weight gain suggests that patients with classic CAH would most value a novel adjunctive therapy that helps mitigate glucocorticoid-induced weight gain. In relation to other potential adjunctive therapy benefits, reduced risk of glucocorticoid-driven side effects may be valued more than improvement in fatigue or androgen-driven adverse events (fertility and hirsutism/acne). However, subgroup analyses indicated that individuals’ characteristics impact their treatment preferences and priorities, after avoidance of glucocorticoid-induced weight gain. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
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Kaouass, M., J. Sulon, P. Deloyer, and G. Dandrifosse. "Spermine-induced precocious intestinal maturation in suckling rats: possible involvement of glucocorticoids." Journal of Endocrinology 141, no. 2 (May 1994): 279–83. http://dx.doi.org/10.1677/joe.0.1410279.
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Abstract The mechanism(s) involved in the spermine-induced precocious postnatal maturation of the intestine in the unweaned rat was examined. Spermine given orally to 11-day-old rats stimulated ACTH and corticosterone secretion. Maximum serum levels of ACTH and corticosterone were observed between 4 and 6 h after spermine ingestion and were five- and sevenfold greater respectively than those of control rats receiving saline alone. Intraperitoneal injection of the polyamine had no effect on corticosterone production. Repeated intraperitoneal administration of gastrin, cholecystokinin, glucagon(1–37) and secretin to 11-day-old rats had no effect on the specific activity of intestinal disaccharidases. These data indicate that (1) the hypophysial-adrenal axis is implicated in the postnatal development of the gastro-intestinal tract induced by spermine and (2) spermine affects ACTH and corticosterone secretion indirectly, probably by stimulating the release of gastrointestinal hormone(s). Journal of Endocrinology (1994) 141, 279–283
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Liu, Zhenqi, Guolian Li, Scot R. Kimball, Linda A. Jahn, and Eugene J. Barrett. "Glucocorticoids modulate amino acid-induced translation initiation in human skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 287, no. 2 (August 2004): E275—E281. http://dx.doi.org/10.1152/ajpendo.00457.2003.
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Amino acids are unique anabolic agents in that they nutritively signal to mRNA translation initiation and serve as substrates for protein synthesis in skeletal muscle. Glucocorticoid excess antagonizes the anabolic action of amino acids on protein synthesis in laboratory animals. To examine whether excessive glucocorticoids modulate mixed amino acid-signaled translation initiation in human skeletal muscle, we infused an amino acid mixture (10% Travasol) systemically to 16 young healthy male volunteers for 6 h in the absence ( n = 8) or presence ( n = 8) of glucocorticoid excess (dexamethasone 2 mg orally every 6 h for 3 days). Vastus lateralis muscles were biopsied before and after amino acid infusion, and the phosphorylation of eukaryotic initiation factor (eIF) 4E-binding protein 1 (4E-BP1), ribosomal protein S6 kinase (p70S6K), and eIF2α and the guanine nucleotide exchange activity of eIF2B were measured. Systemic infusion of mixed amino acids significantly stimulated the phosphorylation of 4E-BP1 ( P < 0.04) and p70S6K ( P < 0.001) and the dephosphorylation of eIF2α ( P < 0.003) in the control group. Dexamethasone treatment did not alter the basal phosphorylation state of 4E-BP1, p70S6K, or eIF2α; however, it abrogated the stimulatory effect of amino acid infusion on the phosphorylation of 4E-BP1 ( P = 0.31) without affecting amino acid-induced phosphorylation of p70S6K ( P = 0.002) or dephosphorylation of eIF2α ( P = 0.003). Neither amino acid nor dexamethasone treatment altered the guanine nucleotide exchange activity of eIF2B. We conclude that changes of amino acid concentrations within the physiological range stimulate mRNA translation by enhancing the binding of mRNA to the 43S preinitiation complex, and the activity of p70S6K and glucocorticoid excess blocks the former action in vivo in human skeletal muscle.
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Heuck, C., and OD Wolthers. "A placebo-controlled study of three osteocalcin assays for assessment of prednisolone-induced suppression of bone turnover." Journal of Endocrinology 159, no. 1 (October 1, 1998): 127–31. http://dx.doi.org/10.1677/joe.0.1590127.
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Serum osteocalcin is a sensitive marker of suppressive effects of exogenous glucocorticoids on bone turnover. It has been suggested, however, that the degree of suppression detected by different assays may vary. Whether discrepancies between various assays influence conclusions from group studies of exogenous glucocorticoids has not been evaluated. The aim of the present study was to compare the CAP fluoroimmunoassay (FEIA), OSTK-PR and ELSA-OSTEO assays for assessment of prednisolone-induced effects on serum osteocalcin. Twelve men and eight premenopausal women aged 19-45 (mean 31) years were studied. All subjects were healthy. The design was a randomised double-blind, placebo-controlled parallel- group study with 2 days run-in, 3 days treatment and 4 days run-out. During run-in and run-out no medication was given. During the treatment period the subjects took either 20 mg prednisolone twice daily or placebo. Blood was collected on the last day of each period. Intra- and intergroup comparisons showed prednisolone treatment to be associated with a statistically significant suppression of osteocalcin which was detected by all assays (ANOVA;P<0.0001). In the individual subjects the response to prednisolone was the same for each assay. The CAP FEIA, OSTK-PR and ELSA-OSTEO assays seem equally sensitive for evaluation of osteocalcin in group studies of oral glucocorticoids.
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Araujo-Castro, Marta, Martin Reincke, and Cristina Lamas. "Epidemiology and Management of Hypertension and Diabetes Mellitus in Patients with Mild Autonomous Cortisol Secretion: A Review." Biomedicines 11, no. 12 (November 22, 2023): 3115. http://dx.doi.org/10.3390/biomedicines11123115.
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Mild autonomous cortisol secretion (MACS) is associated with a higher cardiometabolic risk than that observed in patients with nonfunctioning adrenal adenomas and in the general population. In patients with MACS, the excess of glucocorticoids affects various metabolic pathways, leading to different manifestations of metabolic syndrome and other comorbidities. Hypertension and diabetes mellitus are two of the most common cardiometabolic comorbidities associated with MACS, reaching a prevalence of up to 80% and up to 40%, respectively. In addition, they are the comorbidities that experienced a greater improvement after adrenalectomy in patients with MACS. Hypertension pathogenesis is multifactorial, including the coexistence of comorbidities such as obesity or diabetes and the role of the different polymorphisms of the glucocorticoid receptor gene, among others. Glucocorticoid-induced diabetes mellitus is mainly related to the detrimental effects of glucocorticoids on insulin-dependent glucose uptake in peripheral tissues, gluconeogenesis and insulin secretion. There are no specific recommendations for hypertension and diabetes treatment in patients with MACS. Thus, considering the similar underlying pathogenesis of hypertension and diabetes mellitus in overt and mild hypercortisolism, our recommendation is to follow this general stepwise approach: surgically remove the adrenal culprit lesion to induce remission from hypercortisolism; control hypercortisolism with steroidogenesis inhibitors; and treat elevated blood pressure or high glucose levels using carefully selected anti-hypertensives and glucose-lowering medications if blood pressure and glucose levels remain uncontrolled, respectively. In this review, we summarize the epidemiology, physiopathology and management of diabetes mellitus and hypertension in patients with MACS.
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Greer, Christopher L., and Joshua J. Neumiller. "Multidisciplinary Diabetes Management and Education Strategies in the Inpatient Rehabilitation Setting." Diabetes Spectrum 37, no. 3 (August 1, 2024): 227–33. http://dx.doi.org/10.2337/dsi24-0012.
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People with diabetes receiving inpatient rehabilitation have multiple unique care needs. Although the condition, event, or disability resulting in admission to an inpatient rehabilitation facility (IRF) may not have a causal relationship with chronic conditions such as diabetes, the condition precipitating referral to IRF care may increase a person’s risk for worsening cardiometabolic disease. Furthermore, diabetes management in the IRF setting may be complicated by stress hyperglycemia from illness and/or drug-induced hyperglycemia from the use of glucocorticoids or other offending medications. The availability of a multidisciplinary team of clinicians and therapists in the IRF setting holds great opportunity for development of robust diabetes care and education programs to optimize therapy, teach or reinforce diabetes self-management survival skills, and facilitate safe transitions of care to individuals’ next setting of care.
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Chrysis, D., EM Ritzen, and L. Savendahl. "Growth retardation induced by dexamethasone is associated with increased apoptosis of the growth plate chondrocytes." Journal of Endocrinology 176, no. 3 (March 1, 2003): 331–37. http://dx.doi.org/10.1677/joe.0.1760331.
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Glucocorticoids cause significant growth retardation in mammals and humans and decreased proliferation of chondrocytes has been considered as the main local mechanism. Death by apoptosis is an important regulator of homeostasis in multicellular organisms. Here we chose to study the role of apoptosis in growth retardation caused by glucocorticoid treatment. We treated 7-week-old male rats with dexamethasone (5 mg/kg/day) for 7 days. Apoptosis was studied in tibiae growth plates by the TUNEL method. Immunoreactivity for parathyroid hormone-related peptide (PTHrP), caspase-3, and the anti-apoptotic proteins Bcl-2 and Bcl-x was also studied. Apoptosis was mainly localized in terminal hypertropic chondrocytes (THCs) in both control and dexamethasone-treated animals. Dexamethasone caused an increase in apoptosis which was fourfold in THCs (2.45+/-0.12 vs 0.62+/-0.09 apoptotic cells/mm growth plate, P<0.001), and 18-fold in proliferative chondrocytes (0.18+/-0.04 vs 0.01+/-0.007 apoptotic cells/mm growth plate, P<0.001). Increased apoptosis after dexamethasone treatment was accompanied by increased immunoreactivity for caspase-3 and decreased immunoreactivity for the anti-apoptotic proteins Bcl-2 and Bcl-x, which further supports our apoptosis results. Dexamethasone also decreased the immunoreactivity for PTHrP, suggesting a role in the mechanism by which glucocorticoids induce apoptosis in the growth plate. We conclude that apoptosis is one mechanism involved in growth retardation induced by glucocorticoids. Premature loss of resting/proliferative chondrocytes by apoptosis could contribute to incomplete catch-up seen after prolonged glucocorticoid treatment.
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Shapiro, Lawrence E., Claire P. Katz, Susan H. S. Wasserman, Charles R. DeFesi, and Martin I. Surks. "Heat stress and hydrocortisone are independent stimulators of triiodothyronine-induced growth hormone production in cultured rat somatotrophic tumour cells." Acta Endocrinologica 124, no. 4 (April 1991): 417–24. http://dx.doi.org/10.1530/acta.0.1240417.
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Abstract. We have reported that, in cultured GC cells, the stress of incubation at 41°C enhances thyroid hormone stimulation of growth hormone (GH) in a manner similar to the effects observed in a model of nonthyroidal disease in rats. Since glucocorticoids are potentially involved in stress responses both in vivo and in cell culture, we studied the role of glucocorticoid in the enhancement of (which are rat somatotrophic tumor cells) triiodothyronine (T3)-induced GH synthesis due to heat stress. Hydrocortisone addition increased T3-induced GH synthesis and GH mRNA content in cultured GC cells at both 37°C and 41°C. Depletion of glucocorticoid endogenous to serum supplement of the tissue culture medium did not prevent the enhancement of T3-induced GH synthesis that occurred during incubation at 41°C. The levels and affinity of glucocorticoid cytosolic receptors were not enhanced during incubation at 41°C. Lastly, no change in the sedimentation coefficient of the cytosolic glucocorticoid receptor or in its translocation into the nucleus occurred during incubation at 41°C. Thus, the enhancement of T3-induced GH production in GC cells by heat stress appeared independent of the effect of glucocorticoids and not mediated through glucocorticoid receptors.
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Valentini, S. R., and M. C. S. Armelin. "Cloning of glucocorticoid-regulated genes in C6/ST1 rat glioma phenotypic reversion." Journal of Endocrinology 148, no. 1 (January 1996): 11–17. http://dx.doi.org/10.1677/joe.0.1480011.
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Abstract The C6 rat glioma cell line is responsive to glucocorticoid hormones. C6 variants that are hyper-responsive (ST1) and resistant (P7) to hormone treatment have been derived previously. Glucocorticoid treatment of ST1 cells leads to complete reversion of the transformed phenotype and loss of tumorigenic potential. Production of C type retrovirus particles is also induced by glucocorticoids in ST1 cells. Cloning of the genes regulated by glucocorticoids in this cell system was used here as a strategy to uncover the gene products involved in the transformed-to-normal phenotypic change. Construction of a cDNA library from glucocorticoid-treated ST1 cells and screening by differential hybridization resulted in the isolation of three cellular sequences that code for rat metallothioneins (C27 and C41) and α1-acid glycoprotein (C36). Northern blot analysis revealed that expression of these genes was dramatically induced by hydrocortisone in ST1 but not in P7 cells. Viral genomic RNA was used to isolate and characterize retrovirus-related sequences that could also be responsible for the phenotypic reversion phenomenon. Journal of Endocrinology (1996) 148, 11–17
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Dąbrowski, Piotr, and Maria Majdan. "Glucose tolerance disorders during treatment with glucocorticoids in patients with inflammatory diseases of the musculoskeletal system – based on the analysis of data from the literature and own research results." Postępy Higieny i Medycyny Doświadczalnej 71, no. 1 (May 4, 2017): 0. http://dx.doi.org/10.5604/01.3001.0010.3815.
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Glucocorticoids are among the most frequently used anti-inflammatory and immunosuppressive drugs. They are widely used in the treatment of numerous autoimmune disorders. However, the treatment with glucocorticoids is connected with the risk of a number of side effects. Among them, glucose tolerance disorders play an important role. The results of meta-analyses show that the risk of diabetes is from 1.4 to 2.5 times higher in the case of treated patients in comparison to the general population. Glucocorticoids can directly impair pancreatic β-cell secretion. Nevertheless, a crucial role in the hyperglycemic activity seems to be played by a peripheral glucose uptake reduction, principally in the skeletal muscle, which is responsible for the decrease of insulin sensitivity, and can manifest itself in the increase of postprandial blood glucose levels. If they are used in higher doses and for a prolonged period, they can also reduce the inhibitory effect of insulin on hepatic glucose production, which can lead to an increase of fasting plasma glucose. Numerous literature data indicate that in the case of patients who suffer from inflammatory diseases of the musculoskeletal system, the treatment with low to moderate doses of glucocorticoids, for a short period, does not significantly increase the metabolic risk. The beneficial role in this area may be connected with an anti-inflammatory and immunosuppressive effect. The regular assessment of the postprandial glucose, especially in the afternoon and evening, has the highest diagnostic sensitivity of glucocorticoid-induced glucose tolerance disorders. In the case of patients without a prior diagnosis of diabetes, after discontinuation of treatment, the oral glucose tolerance test should be considered in order to identify the presence of persistent disorders.
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Vidal, NO, H. Brandstrom, KB Jonsson, and C. Ohlsson. "Osteoprotegerin mRNA is expressed in primary human osteoblast-like cells: down-regulation by glucocorticoids." Journal of Endocrinology 159, no. 1 (October 1, 1998): 191–95. http://dx.doi.org/10.1677/joe.0.1590191.
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Osteoprotegerin (OPG) is a recently cloned member of the tumour necrosis factor receptor family. It has been suggested that this secreted glycoprotein acts as an inhibitor of osteoclastic differentiation. Expression of OPG has previously been demonstrated in a number of tissues. However, it is still unclear whether or not OPG is expressed by human osteoblasts. We have used the RNase protection assay to demonstrate the OPG transcript in primary cultured human osteoblast-like cells, human marrow stroma cells and osteosarcoma cell lines. Furthermore, we have studied the effect of glucocorticoids on OPG mRNA levels in these cells. We demonstrate that glucocorticoids decrease the OPG transcript in a dose- and time-dependent manner. The time-course study reveals that hydrocortisone (10(-6) M) decreases OPG mRNA levels within 2 h. This decrease is transient, reaching control levels again after 24 h. Our findings demonstrate that human osteoblasts express the mRNA corresponding to OPG, an inhibitor of osteoclast differentiation. The finding that OPG mRNA levels are decreased by glucocorticoids indicates that a reduced production of OPG from osteoblasts and/or marrow stroma cells could, in part, explain glucocorticoid-induced bone resorption.