INS and Insulin resistance: This is due to their ability to impair the glucose uptake and metabolism in muscle through the inhibition of critical glycolytic enzymes [28,29]; i.e., to induce insulin resistance in the liver through modified intracellular signaling and altered gene expression (resulting in excessive hepatic glucose output) [30,31,32], as well as to decrease insulin secretion and stimulate apoptosis in β cells [33,34].