Although the pathophysiologic basis of hyperglycemia/DM in TB has not been fully elucidated, a role has been postulated for adipokine-mediated alterations in the microenvironment, resulting in increased susceptibility to hyperglycemia through the release of counterregulatory stress hormones (e.g., glucagon, cortisol and growth hormone) [66,67]. Here, GH1 is linked to tuberculosis.