Effect of Dexamethasone on Oral Glucose Tolerance in Healthy Adults

Abdelmannan, Dima; Tahboub, Rundsara; Genuth, Saul; Ismail‐Beigi, Faramarz

doi:10.4158/ep09373.or

Cited by 42 publications

(20 citation statements)

References 13 publications

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“…These findings were supported by subsequent studies [56, 57]. Exogenous glucocorticoids could also interfere with the signalling pathways of various insulin secretagogues, but the exact mechanisms are still unknown.…”

Section: Hypercortisolism and Diabetessupporting

confidence: 60%

Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology

Dalmazi

Pagotto

Pasquali

et al. 2012

Journal of Nutrition and Metabolism

142

101

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Type 2 diabetes mellitus is the result of interaction between genetic and environmental factors, leading to heterogeneous and progressive pancreatic β-cell dysfunction. Overweight and obesity are major contributors to the development of insulin resistance and impaired glucose tolerance. The inability of β cells to secrete enough insulin produces type 2 diabetes. Abnormalities in other hormones such as reduced secretion of the incretin glucagon-like peptide 1 (GLP-1), hyperglucagonemia, and raised concentrations of other counterregulatory hormones also contribute to insulin resistance, reduced insulin secretion, and hyperglycaemia in type 2 diabetes. Clinical-overt and experimental cortisol excess is associated with profound metabolic disturbances of intermediate metabolism resulting in abdominal obesity, insulin resistance, and low HDL-cholesterol levels, which can lead to diabetes. It was therefore suggested that subtle abnormalities in cortisol secretion and action are one of the missing links between insulin resistance and other features of the metabolic syndrome. The aim of this paper is to address the role of glucocorticoids on glucose homeostasis and to explain the relationship between hypercortisolism and type 2 diabetes.

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Section: Hypercortisolism and Diabetessupporting

confidence: 60%

Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology

Dalmazi

Pagotto

Pasquali

et al. 2012

Journal of Nutrition and Metabolism

142

101

View full text Add to dashboard Cite

show abstract

“…Although there is some evidence that the underlying characteristics of the disease being treated with glucocorticoids may not influence the development of new-onset hyperglycemia [7,8,9], it is possible that the wide range of patient populations and disease states included in this meta-analysis may have influenced our findings. Also, none of the 13 included studies were prospective, randomized, controlled studies, and the analysis showed publication bias for glucocorticoid-induced diabetes.…”

Section: Discussionmentioning

confidence: 99%

“…Glucocorticoids also exacerbate hyperglycemia in patients with diabetes [1,6]. It is unlikely that the development of glucocorticoid-induced hyperglycemia is due to the underlying disease being treated since glucose metabolism abnormalities are observed in healthy subjects given these drugs [7,8,9]. Moreover, not all patients develop glucocorticoid-induced hyperglycemia, suggesting some populations of patients may be more susceptible than others [1].…”

Section: Introductionmentioning

confidence: 99%

Hyperglycemia Induced by Glucocorticoids in Nondiabetic Patients: A Meta-Analysis

et al. 2014

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Background/Aims: Glucocorticoids are associated with a number of side effects including the development of new-onset hyperglycemia or diabetes. The diagnosis and treatment of glucocorticoid-induced hyperglycemia are surprisingly undervalued by many health-care professionals, probably due to the lack of quality studies that assess specific reasons for and prevention of hyperglycemia. The aim of this meta-analysis was to evaluate the long-term incidence of glucocorticoid-induced hyperglycemia and diabetes in nondiabetic patients who received glucocorticoid treatment. Methods: We searched Medline, Embase, and the Cochrane Library (Central) until January 2014 for studies in which subjects received systematic glucocorticoid treatment and which evaluated whether subjects developed hyperglycemia or were diagnosed with diabetes following treatment. The primary outcome for this analysis was the incidence of hyperglycemia and the secondary outcome was the frequency of diabetes. Results: We identified 13 studies that met our inclusion criteria; 12 of the studies were retrospective or observational in design. We found that the rate at which patients developed glucocorticoid-induced hyperglycemia or diabetes was 32.3% (p = 0.003) and 18.6% (p = 0.002), respectively. Conclusions: Our meta-analysis indicated that glucocorticoid-induced hyperglycemia occurs fairly frequently and points to the need for the design of prospective, randomized, controlled studies to further investigate and better understand this medical problem.

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“…In matsuda index glucose and insulin values are in mg/dl and μu/mL, respectively. [9] This study was approved by the Isfahan Endocrine and Metabolism Research Center (IEMRC) Medical Ethics Committee and all patients signed a written consent form to enroll in this clinical trial.…”

Section: Methodsmentioning

confidence: 99%

Does the intramuscular injection of vitamin D increase insulin resistance?

Iraj¹,

Aminorroaya²,

Amini³

2012

J Res Pharm Pract

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Objective:Considering the physiologic roles of vitamin D on insulin regulation, the effects of vitamin D treatment on insulin sensitivity and resistance indexes and beta cell function in pre-diabetic vitamin D deficient patients were investigated.Methods:In a randomized open clinical trial, 61 pre-diabetic vitamin D deficient patients who were the first degree relatives of type 2 diabetic patients, were enrolled and randomized into three groups (A, B and C). Group A (n = 21) were treated with intramuscular injection of 300,000 units of vitamin D at the beginning of the study and one month later. In group B (n = 20), injection of vitamin D plus 500 mg/d calcium and in group C (n = 20), just calcium was administered for two months. At baseline and two months later, oral glucose tolerance test was done. Homeostasis Model of Assessment-Insulin Resistance (HOMA-IR), insulin resistance index, Homeostasis Model of Assessment-B (HOMA-B) which is a beta cell function index, and Matsuda index, an insulin sensitivity index, were calculated and compared before and after intervention and between three groups.Findings:In vitamin D treated groups (A + B), the mean (SD) of HOMA-IR increased from 2.46 (1.36) to 3.1 (2.3) (P = 0.02), and Matsuda index decreased from 11 (3) to 9.0 (2.3) (P = 0.001).Conclusion:Injection of vitamin D increased insulin resistance and decreased insulin sensitivity indexes.

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Effect of Dexamethasone on Oral Glucose Tolerance in Healthy Adults

Cited by 42 publications

References 13 publications

Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology

Glucocorticoids and Type 2 Diabetes: From Physiology to Pathology

Hyperglycemia Induced by Glucocorticoids in Nondiabetic Patients: A Meta-Analysis

Does the intramuscular injection of vitamin D increase insulin resistance?

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