I have been taking preds for a long time, now down from 40 mg per day to 15 mg neuro says no lower.
Was put on Azathioprine as a prednisolone sparing medication ended up taking both for about three years until it became obvious that Azathioprine was actually quite dangerous for me and it was stopped.
Preds make it very difficult to control blood sugars and insulin is normally the therapy of choice though I have never been offered it. I keep my blood sugars low by very strict control of carbs and calories it's a drag and makes me very low on energy a lot of the time.
This gives some insight into the effects of steroids
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Glucocorticoids
Glucocorticoids are widely used medications and clinical experience indicates that diabetes is a frequent side effect. Ingle first reported glucosuria in rats receiving glucocorticoid.1 A human retrospective epidemiological study of adult Medicaid patients carried out over 9 years identified almost 12 000 persons with new onset diabetes and closely matched controls which did not develop diabetes. Patients who were taking glucocorticoid were more likely to be in the diabetes group (relative risk 2.23) and the relative risk was dose dependent.2 One intuitive hypothesis for the mechanism by which glucocorticoids cause diabetes is development of insulin resistance. To test this hypothesis, hyperinsulinemic‐euglycemic clamps with tritiated glucose tracer were performed on 10 healthy subjects after 7 d of placebo and after 7 d of prednisolone.3 This study demonstrated that prednisolone induced insulin resistance in liver, muscle, and adipose tissue by decreasing the ability to suppress hepatic gluconeogenesis, as well as by decreasing peripheral glucose disposal in muscle and adipose tissue. There are multiple plausible biochemical mechanisms for development of insulin resistance in the postreceptor insulin‐signaling pathways in all tissues (reviewed by van Raalte4). In addition, there is evidence for decreased insulin‐induced vasodilation in muscle leading to reduced glucose delivery to muscle beds, reducing the opportunity for muscle to clear glucose from the blood.4
Glucocorticoids also have additional direct effects on release of insulin from beta cells.5 Six healthy subjects were given three mixed meal challenges at baseline on day 1, 2 h after 75 mg of prednisolone on day 2 and without any additional prednisolone on day 3. Plasma glucose was elevated during the day 2 challenge, but c‐peptide was unchanged from baseline suggesting that the beta cells were unable to release additional insulin to overcome the peripheral insulin resistance resulting from the acute exposure to glucocorticoid. There are also a number of plausible postreceptor biochemical targets in the beta cell for glucocorticoid suppression of insulin secretion.4
The initial common sense approach to glucocorticoid‐induced diabetes is to minimize the glucocorticoid dose as much as possible. There are few studies of optimal medical treatment for glucocorticoid‐induced diabetes.6, 7 Guidelines are largely based on expert opinion and therefore vary. The consensus is that postprandial excursions in blood glucose are more significant than fasting hyperglycemia in most instances, and therefore recommendations are made for use of glinides, thiazolidinediones (TZDs), glucagon‐like peptide 1 (GLP‐1) analogs, or dipeptidyl peptidase 4 (DPP‐4) inhibitors.6-10 The TZD, troglitazone, has been shown to improve postprandial glucose excursions (lower area under the glucose curve in an oral glucose tolerance test (OGTT)), decrease HbA1c, decrease low‐density lipoprotein, and increase insulin secretion in patients on chronic glucocorticoid,9 but is not widely recommended due to side effects of weight gain, heart failure, and bone fractures, all of which may be additive to similar side effects of glucocorticoids in the USA, the drug was removed from the market in 2000. There are few studies of metformin in glucocorticoid diabetes, and it has not generally been recommended as many patients taking glucocorticoid have renal failure or may be prone to lactic acidosis, which constitute contraindications to metformin.8, 10 Consensus is that blood glucose consistently over 200 mg/dL associated with glucocorticoid therapy should be treated with insulin."
I know the article is more aimed at pediatric diabetes but think it is still relevant
https://onlinelibrary.wiley.com/doi/full/10.1111/pedi.12406
