Insulin resistance glucocorticoids

Congestive heart failure Hypertension Deep vein thrombosis Coronary artery disease Stroke Diabetes Insulin resistance Glucocorticoid imbalance Gall bladder disease Hypercholesterolemia Hypertriglyceridemia Gout Pancreatitis Liver disease Osteoarthritis Rheumatoid arthritis Bone fractures Lower back pain Carpal tunnel syndrome Depression Pain... 

Insulin is a powerful anabolic hormone but it is unlikely that insulin deficiency causes skeletal muscle atrophy by direct action on muscle fibers (as opposed to neurogenic atrophy) except in chronic untreated cases. There is however a close parallel between the catabolic states induced by glucocorticoid excess and by insulin deficiency. Moreover, impaired insulin action is implicated in other endocrine myopathies as a contributory cause of muscle wasting. Both acromegaly and thyrotoxicosis are associated with insulin resistance due to a postreceptor defect, and secondary hyperparathyroidism due to hypophosphatemia also gives rise to insulin insensitivity. 

Various hormonal agents (eg, glucocorticoids) lower the affinity of insulin receptors for insulin growth hormone in excess increases this affinity slightly. Aberrant serine and threonine phosphorylation of the insulin receptor subunits or IRS molecules may result in insulin resistance and functional receptor down-regulation. 

Weinstein, S. P., Holand, A., O Boyle, E., and Haber, R. S. (1993). Effects of Thia-zolidinediones on Glucocorticoid-Induced Insulin Resistance and GLUT4 Glucose Transporter Expression in Rat Skeletal Muscle. Metabolism 42, 1365-1369. 

The effect of counter-regulatory hormones (adrenaline, noradrenaline and glucocorticoids) on insulin-induced glucose utilization in individual tissues of normal rats was investigated in vivo. The main effect of these hormones was to reduce the insulin-induced glucose utilization in skeletal muscles, particularly the oxidative one (Marfaing et al.. 1991). These results support the notion that the increase in plasma concentrations of these hormones could play a role in states of insulin resistance such as obesity and diabetes (Marfaing et al.. 1991). 

Insulin stimulates peripheral tissue protein synthesis by stimulating amino acid uptake and protein synthesis at the level of translation and by inhibiting protein degradation. At low insulin levels, muscle proteolysis occurs. As the levels increase, proteolysis decreases and protein synthesis is favored. Exercise decreases proteolysis and increases protein synthesis, whereas disuse results in muscle wasting and depressed protein synthesis. Exercise increases sensitivity to insulin, whereas disuse makes the tissue insulin-resistant. Obesity, pregnancy, and glucocorticoids also increase insulin resistance. 

Liu Y, Nakagawa Y, Wang Y, Liu L, Du H, Wang W, Ren X, Lutfy K, Friedman TC (2008) Reduction of hepatic glucocorticoid receptor and hexose-6-phosphate dehydrogenase expression ameliorates diet-induced obesity and insulin resistance in mice. J Mol Endocrinol 41(2) 53-64... 

Glucocorticoid treatment can cause insulin resistence of muscle fibers, and often aggravates diabetes-2 or makes manifest type-2 diabetes in genetically predisposed and/or obese patients. 

In a patient who does have a close family history of diabetes-2, a glucocorticoid should be avoided if possible, because it can increase insulin resistance and make manifest diabetes-2 glucose dysmetabo-lism. Accordingly, asking about a close family history of diabetes-2 is very important in managing a chronic immune dysschwannian polyneuropathy (CIDP) (sometimes less precisely called chronic inflammatory demyelinating polyneuropathy), or other dysimmune patient. 

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