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Artículos de revistas sobre el tema "Glucocorticoids-Induced diabetes"

Autor: Grafiati
Publicado: 15 de febrero de 2025
Última modificación: 31 de julio de 2025

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1

Nurullina, G. I. "Glucocorticoid pulse therapy аnd carbohydrate metabolism in rheumatic diseases". Kazan medical journal 94, № 6 (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 assoc
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2

Wardani, Indah Sapta. "Steroid Induced Diabetes Mellitus: An Overview." JURNAL SAINS TEKNOLOGI & LINGKUNGAN 9, no. 1 (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 ch
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3

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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4

Rana, M. Asim, Mujtaba H. Siddiqui, Sitara Raza, et al. "Incidence of Steroid-induced Diabetes in COVID-19 patients." Pakistan Journal of Medical and Health Sciences 15, no. 10 (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 kn
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5

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 facto
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6

Schakman, O., H. Gilson, and J. P. Thissen. "Mechanisms of glucocorticoid-induced myopathy." Journal of Endocrinology 197, no. 1 (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 degra
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7

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 (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 informa
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8

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 (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 im
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9

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 (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 perifu
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10

Thompson, E. Brad. "Mechanisms of T-cell Apoptosis Induced by Glucocorticoids." Trends in Endocrinology & Metabolism 10, no. 9 (1999): 353–58. http://dx.doi.org/10.1016/s1043-2760(99)00187-3.

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11

Fruchter, Oren, Tomoshige Kino, Emmanouil Zoumakis та ін. "The Human Glucocorticoid Receptor (GR) Isoform β Differentially Suppresses GRα-Induced Transactivation Stimulated by Synthetic Glucocorticoids". Journal of Clinical Endocrinology & Metabolism 90, № 6 (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 ma
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12

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 (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 deve
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13

Kashino, Chiaki, Toru Hasegawa, Yasuhiro Nakano, et al. "Involvement of BMP-15 in Glucocorticoid Actions on Ovarian Steroidogenesis by Rat Granulosa Cells." Journal of the Endocrine Society 5, Supplement_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 pr
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14

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, M
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15

Akshaya, N., Ravi Krishna, and N. Venkateswaramurthy. "Steroids Induced Hyperglycemia: Its Effects and Management." Journal of Drug Delivery and Therapeutics 13, no. 6 (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
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16

Vagnerová, K., M. Kverka, P. Klusoňová та ін. "Intestinal inflammation modulates expression of 11β-hydroxysteroid dehydrogenase in murine gut". Journal of Endocrinology 191, № 2 (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-inf
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17

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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18

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 (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 apopto
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19

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 (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 activat
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20

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 (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)
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21

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 patient
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22

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 (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 antiarrh
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23

Feilleux-Duche, S., M. Garlatti, R. Burcelin, et al. "Acinar zonation of the hormonal regulation of cytosolic aspartate aminotransferase in the liver." American Journal of Physiology-Cell Physiology 266, no. 4 (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.
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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 (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 clampe
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25

Paredes, Sílvia, and Marta Alves. "Abordagem e Tratamento da Hiperglicemia Induzida por Glicocorticóides." Acta Médica Portuguesa 29, no. 9 (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-induc
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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 (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 dexamethaso
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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 (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
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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 (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
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29

Burke, Susan J., Heidi M. Batdorf, Maggie P. Ducote, et al. "High-Protein Diet Prevents Glucocorticoid-Induced Fat Mass Accumulation and Hyperglycemia." International Journal of Molecular Sciences 26, no. 9 (2025): 4212. https://doi.org/10.3390/ijms26094212.

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Glucocorticoid-induced diabetes is the most common form of drug-induced hyperglycemia. In addition, chronic exposure to glucocorticoids promotes lean mass loss and fat mass accumulation. In this study, we hypothesized that a high-protein diet (60% kcal; HPD) would help to offset sarcopenia during oral administration of corticosterone to C57BL/6J mice. Carbohydrates were reduced in the HPD to ensure it was isocaloric with the normal-protein diet (20% kcal; NPD). We found that the HPD prevented fat mass accumulation but did not protect against reductions in lean mass in both male and female mice
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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 (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 re
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Ratineau, C., C. Roche, F. Chuzel, et al. "Regulation of intestinal cholecystokinin gene expression by glucocorticoids." Journal of Endocrinology 151, no. 1 (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 ex
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32

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 (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 e
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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 (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 dram
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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 (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 b
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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 (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 circulat
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36

Dang, Thanh Q., Nanyoung Yoon, Helen Chasiotis, et al. "Transendothelial movement of adiponectin is restricted by glucocorticoids." Journal of Endocrinology 234, no. 2 (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 a
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37

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 (2011): 671–80. http://dx.doi.org/10.1242/dmm.008912.

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38

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 (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
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39

Chan, Junny, Elizabeth H. Rabbitt, Barbara A. Innes та ін. "Glucocorticoid-induced apoptosis in human decidua: a novel role for 11β-hydroxysteroid dehydrogenase in late gestation". Journal of Endocrinology 195, № 1 (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 o
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40

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 (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 med
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41

Manahan, Rachel, Jake Macey, Mallory Farrar, 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 (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
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42

Greer, Christopher L., and Joshua J. Neumiller. "Multidisciplinary Diabetes Management and Education Strategies in the Inpatient Rehabilitation Setting." Diabetes Spectrum 37, no. 3 (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 medication
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43

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 (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 g
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44

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 (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(
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45

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 (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
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46

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 (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
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47

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 (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
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48

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 (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. Co
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49

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 (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
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50

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 (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-apoptot
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