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Objective: To determine serum CPK variation based on TSH e free T4 (FT4), and to assess serum CPK in pathological states of the thyroid (hyperthyroidism and hypothyroidism), in relation to the euthyroidism., Material and Methods: We evaluated retrospectively 6,230 laboratory results of TSH and CPK from 2007 to 2011. From these, 3,369 had free T4 results. We evaluated the correlation between CPK and TSH and the pathological states of the thyroid., Results: The correlation between TSH and CPK was positive (r = 0.065), while that between CPK and FT4 was negative (r = -0.091, p < 0.05). From the total of results analyzed, 586 (9.4%) were measures of hyperthyroidism, with a median (range) of CPK of 98 U/L (27 to 1,113), and 556 (8.9%) were of hypothyroidism, with CPK of 114 U/L (25-4,182)., Conclusion: A positive correlation was found between serum CPK and TSH, and a negative correlation between CPK and FT4. CPK was lower in the group with hyperthyroidism, and greater in that with hypothyroidism.

Metformin is one of the most commonly prescribed oral antidiabetic agents worldwide. However, its mechanism of action remains unknown. The Diabetes Prevention Program Research Group studies have shown that metformin administration and lifestyle-intervention (diet and exercise) reduce the incidence of Diabetes Mellitus type 2 (DM2). A possible biochemical connection between both therapies may be the AMP-activated protein kinase (AMPK). This enzyme was originally described as a sensor of cellular energy status, being activated in exercise. On the other hand, several experimental evidences indicate that AMPK may be an important target of metformin action. This paper discusses various ways for AMPK regulation, suggesting a possible mechanism for its activation by metformin that involves the production of reactive nitrogen species. AMPK activation determines a wide variety of physiological effects, including enhanced glucose uptake by skeletal muscle and enhanced lipid catabolism. Thus, it may be a key player not only in the prevention and treatment of DM2, but also in the development of new treatments for obesity and the metabolic syndrome. The finding of AMPK activation by metformin draws attention to this enzyme as an important pharmacological target.