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Antidiabetic Herbal Formulations
Published in Parimelazhagan Thangaraj, Medicinal Plants, 2018
Binu Thomas, Krishna M. Chinchu
Diabetes is a chronic disorder of carbohydrate, fat and protein metabolism characterized by increased fasting and postprandial blood sugar levels. It is a complex metabolic disorder resulting from either insulin insufficiency or insulin dysfunction (Ramachandran et al. 2002). The different types of diabetes have been identified and categorized as type I, II and gestational diabetes. Type I is also referred as insulin-dependent diabetes mellitus or juvenile diabetes (IDDM), which results from the body’s failure to produce insulin and presently requires the person to inject insulin. Type II diabetes also referred as non-insulin-dependent diabetes mellitus or adult-onset diabetes (NIDDM). This result from insulin resistance, a condition in which cells fail to use insulin properly (Binu Thomas et al. 2012). The other type is gestational diabetes, which is observed in pregnant women who have never had diabetes before and who have a high blood glucose level during pregnancy. It may precede development of type II. The other forms of diabetes mellitus include congenital diabetes, which is due to the genetic defect of insulin secretion; cystic fibrosis–related diabetes; steroid diabetes, induced by high dose of glucocorticoids; and several forms of monogenic diabetes (Manisha et al. 2012).
Epidemiology, Risks, and Health-Care Expenditures for Diabetes and Its Complications
Published in Emmanuel Opara, NUTRITION and DIABETES, 2005
Posttransplantation diabetes (PTDM) is, as the name implies, the development of diabetes after transplantation. Steroid diabetes was first reported in renal-transplant recipients (38). Its early frequency was 40 percent to 60 percent (38). The incidence ranges from 2 percent to 50 percent, with most cases being diagnosed within three months of transplantation (39, 40). Risk factors for posttransplant diabetes include age, non-Caucasian ethnicity (risk of posttransplantation diabetes is higher in African American recipients than Caucasian recipients), and immunosuppression (39). Transplant recipients with posttransplant diabetes tend to be 0 to 12 years older than those without (39). Non-Caucasian patients had a twofold increased risk of posttransplant diabetes (RR 3.3, 95 percent CI 1.7–7.0) (39). There is an increased incidence of posttransplant diabetes in patients treated with glucocorticoid therapy, cyclosporine, and those treated with high doses of tacrolimus (39, 41). The mean time from transplantation to development of PTDM is 1.2 years (range from one day to 6.2 years), with most cases occurring during the first three months after transplant or after treatment for rejection (41, 42). Significant risk-factor development of PTDM included: first-degree family history of type 2 diabetes mellitus, tacrolimus use, and hyperglycemia in the two weeks immediately after transplantation (42). Patients that developed persistent PTDM had later onset disease (mean 1.9 years) compared to those with transient PTDM (0.3 years) (42).
Research Models of Diabetes Mellitus
Published in Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla, Heart Dysfunction in Diabetes, 2019
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla
Another way in which diabetes mellitus can be induced in animals is via the injection of large quantities of naturally occurring hormones. D. J. Ingle177 was first to document that the administration of a large dose of 17-hydroxy-11-dihydrocorticosterone to a normal rat could induce diabetes. Since then, epinephrine, glucagon, growth hormone, progestogens, and various glucocorticoids have been shown to produce diabetes in animals.1,178,179 Steroid diabetes is not restricted to animals. Over 30 years ago, it had been observed that patients treated with cortisone or corticotropin over an extended period of time developed diabetes. If the drug was discontinued the diabetic symptoms disappeared.180 This remains a serious medical problem for the endocrinologists today. Glucocorticoids are frequently administered to patients after certain types of traumatic surgery in order to suppress immune system reactions. A recent study181 of 145 renal transplant patients who were placed on a high-dose glucocortico-steroid regimen for up to 2 years found persistent diabetes had developed in 25% of the patients and transient diabetes had developed in another 22%. The incidence of diabetes in the patients correlated with the steroid dose, age, weight, and diabetic heredity of the patient. Of those patients who required some type of treatment to control their diabetes, half of the patients needed insulin. It is evident, therefore, that steroid diabetes is an important clinical problem. However, because of the numerous side effects which are associated with massive doses of steroids over an extended period of time, steroids have been discontinued as diabetogenic agents in studies which are principally interested in diabetes per se.
Etiology of posterior subcapsular cataracts based on a review of risk factors including aging, diabetes, and ionizing radiation
Published in International Journal of Radiation Biology, 2020
Richard B. Richardson, Elizabeth A. Ainsbury, Christina R. Prescott, Frank J. Lovicu
High or prolonged doses of steroids — specifically glucocorticoids, which repress NF-ĸB pro-inflammatory genes — cause vacuolated PSCs; the biological mechanisms however are not fully understood (Jobling and Augusteyn 2002; James 2007). These PSCs are characterized by superficial cortical vacuolation of fiber cells in the posterior region and by some LEC-like nucleated cells and Wedl cells with degenerating nuclei at the PSC margin. Cortical vacuoles are linked to elevated free water content in the lens. Prolonged glucocorticoid treatments cause hyperglycemia (steroid diabetes). Steroid-induced PSC exhibit increased ocular glucose levels and oxidative stress, as well as decreased lenticular GSH (Figure 4, Path. 9 onwards). Steroids have a major effect on the metabolism of calcium, vitamin D and growth factors, and long-term use can lead to steroid-induced osteoporosis, a disease associated with cataractogenesis (Nemet et al. 2013). Steroids lessen the viscosity of hyaluronic acid (Conrozier et al. 2016), although their effects on the calcium homeostasis of the vitreous hydrogel are unknown. Glucocorticoids disrupt normal LEC proliferation and differentiation by binding to LEC glucocorticoid receptors. Occupied receptors can reduce cell adhesion molecules such as E-cadherin and activate growth factors such as FGF (Figure 4, Paths. 3, 14) (Lovicu et al. 2004; Celojevic et al. 2012).
How should rheumatologists manage glucocorticoid-induced hyperglycemia?
Published in Modern Rheumatology, 2021
Hiroyuki Nakamura, Yuichiro Fujieda, Akinobu Nakamura, Tatsuya Atsumi
However, management of GIH is challenging to rheumatologists due to lack of detailed guidelines with clear evidence. The review aimed to help rheumatologists to manage GIH in their daily clinical practice through a systematic literature search and meta-analysis. We first describe about risk factors for the development of GIH, and then about therapeutic strategy for GIH including oral hypoglycemic agents as well as insulin. References were systematically searched through MEDLINE, the Cochrane Library and Japan Medical Abstracts Society in April 2020 using the following search terms: ‘steroid diabetes’, ‘steroid induced diabetes’, ‘steroid induced hyperglycemia’, ‘glucocorticoid induced diabetes’ or ‘glucocorticoid induced hyperglycemia’. Randomized or non-randomized controlled trials, retrospective studies and case series to evaluate risk factors and/or treatment for GIH were included. Studies enrolling children (<18 years old), subjects with type 1 diabetes or those with gestational diabetes were excluded. References were restricted to English or Japanese articles. A meta-analysis was performed to combine the results of studies when there were multiple studies addressing the same question. Flow diagram of literature search, screening and selection was shown as Supplemental Figure. The meta-analysis was based on the inverse variance statistical method and the random-effects model to calculate mean difference for continuous valuables or odds ratio (OR) for categorical valuables with their 95% confidence intervals (CI). Statistical significance was inferred when 95% CI of the pooled results did not cross the null point. Review Manager Version 5.3 (The Cochrane Collaboration, London, UK) was used for the analysis.