study demonstrates that nonobese normotensive men with hyperglycemia exhibit abnormalities in cortisol activity. The differences in cortisol metabolism and tissue sensitivity were more striking than any differences in HPA axis function. Specifically, these patients with DM or impaired glucose tolerance show: 1) normal cortisol secretion and circulating levels in the face of enhanced negative feedback sensitivity (as measured with dexamethasone); 2) enhanced in vivo peripheral tissue sensitivity to glucocorticoids (as measured by dermal blanching); 3) impaired hepatic 11β-HSD 1 activity but normal adipose 11β-HSD 1 activity, suggesting tissue-specific alterations in 11β-HSD 1 activity; and 4) increased relative excretion of A-ring reduced metabolites of cortisol. These findings suggest that isolated hyperglycemia is associated with some, but not all, of the changes in cortisol metabolism and action that have been observed in subjects with hypertension or obesity and the Metabolic Syndrome. This has implications for understanding underlying mechanisms predisposing to hyperglycemia, determinants of altered glucocorticoid signaling, and therapeutic opportunities to manipulate cortisol action to improve metabolic control in DM.

METS is a maturity onset disease and typically appears years after hormonal immune and metabolic aggression began.i believe you have described first signs of mets i.e hyperglycemia 11beta hsd1 activation and insulin resistance .to Dipti SARMA

A review about this subject.

http://onlinelibrary.wiley.com/doi/10.1111/j.1463-1326.2012.01582.x/abstract;jsessionid=36F2E8E2BC3F8BAEB9E39EFEEE369376.f03t03

There are so many research publications proven the role of cortisol and glucocorticoid receptor having an impact on glucose homeostasis.

http://www.ncbi.nlm.nih.gov/pubmed/18313837

http://www.ncbi.nlm.nih.gov/pubmed/17950991

Above pubmed link are some of my lab publication but they (my seniors) focused on Leydig cell glucose oxidation and insulin receptors. It may whole goods for insulin sensitive tissues also.

Not only cortisol even mineralocorticoid (Aldosterone), Sex Steroids (E2 and T) also have a role on glucose homeostasis in particular. In broad experimental setup excess glucocorticoid & mineralocorticoid favours glucose intolerance but inversely reduced testosterone and estradiol in general.

I agree with Rajesh Parsanathan, and Dipti Sarma. In METS we are faced with an extremely complex system resulting from interaction, at least, of cortisol, mineralcorticoids, sex steroids hormons and, of course, the immune system. In this integrated system the weak side is metabolism ( hyperglicemia,dyslipidemia, etc.), but when we recognize METS by its metabolic symptoms is late, then we have to find other markers of disease ( endocrine or immune) to allow prevention, but this is also difficult. In other words we can't cope METS without taking into consideration all systems involved. To continue discussIon , see my last paper full text .