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iStock-629430458.jpgFolate deficiency has been associated with the onset of varied metabolic abnormalities, “including insulin resistance, by altering epigenetic processes on key regulatory genes,” such as the calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2). CAMKK2 is part of the calcium-triggered signaling cascade, and influences obesity and glucose metabolism.

This study looked at subjects with a total folate intake lower than 300 μg/d, more “fat mass (especially trunk fat), as well as statistically higher levels of glucose, insulin, homeostatic model assessment–insulin resistance (HOMA-IR) index, cortisol, and plasminogen activator inhibitor-1, and compared [these levels] to those consuming ≥ 300 μg/d [of folate].”  They determined that “folate deficiency was related to lower CAMKK2 methylation.

In this study, the methylation of CAMKK2 was “negatively correlated with the Homeostatic model assessment (HOMA-IR),” a method used to assess β-cell function and insulin resistance (IR) from basal (fasting) glucose and insulin or C-peptide concentrations.[1]  Furthermore, they observed that CAMKK2 expression directly correlated with HOMA-IR values, and that folate deficiency was related to lower CAMKK2 methylation.

In conclusion, this summary proposed “associations between low folate intakes, lower CAMKK2 gene methylation, and insulin resistance in obese individuals.”


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