Insulin is a hormone having multiple functions which include regulating sugar, protein, and fat metabolism. Insulin resistance is defined as a state of having a reduction in biological activity of insulin. Insulin resistance has multiple causes including obesity and excess caloric intake. The major health implications of insulin resistance include Type 2 diabetes mellitus (T2DM), hypertension, obesity, polycystic ovary syndrome, metabolic syndrome, and cardiac and vascular diseases. While exercise and diet managements improve insulin sensitivity, they are sometime not adequate in helping patients with T2DM controlling their blood sugar. Drugs are sometimes needed in combination with diet and exercise managements. Many drugs work to improve insulin sensitivity and help patients manage a normal blood sugar level. He biguanides and the thiazolidinediones are two classes of drugs that work to improve insulin sensitivity.

Insulin is synthesized by beta cells of the pancreas with its main function in regulating whole-body sugar (glucose) metabolism. Insulin is released into the bloodstream after every meal to lower the spiked blood sugar level that accompanies such meals. It accomplishes this task by stimulating proteins that transport glucose inside the cell where it can be used for energy or storage. Insulin's main targets include the liver, skeletal muscles, and fat tissues; however, there are insulin receptors on virtually all cells in the human body indicating that insulin exerts its effect basically on all cells.

Once inside the cell, sugars are destined for different metabolic fates. One of these fates for sugars is to be broken down via a series of reactions to harness energy (in the form of ATP) for cellular usage. Glucose within the cell could also be converted into glycogen (a storage form of sugar) or transformed into fat to be used in the future. In fat metabolism, insulin inhibits fat breakdown and stimulates fat synthesis. Insulin achieves these tasks by controlling the genes involved in fat synthesis and degradation. In protein metabolism, insulin helps maintain an equilibrium protein turnover rate--a balanced state of having the rate of proteins degradation equal to the rate of protein synthesis. It achieves this task by stabilizing various components in the protein synthetic machinery. Insulin also prevents protein breakdown. In insulin resistance, insulin essentially loses its biological effects, and cells and tissues no longer become sensitive to it. Insulin resistance has multiple causes including obesity and having too much caloric intake. Some of the consequences for insulin resistance include T2DM, hypertension, dyslipidemia, polycystic ovary syndrome, and cardiac and vascular diseases. On a cellular level, insulin resistance causes a decrease in glycogen synthesis as well as sugar transport.

Two families of drugs--targeting to improve insulin sensitivity and helping patients with T2DM managing a normal blood sugar level--include the biguanides and the thiazoglitazones. Many other drug families are available to treat T2DM including the alpha-glucosidase inhibitors, glucagon-like peptide 1s, sulfonylureas, and meglitinides. However, they do not work by directly increasing insulin sensitivity like the biguanides and the thiazoglitazones families mentioned. No matter which drugs are used, diet and exercise managements are recommended along with such drugs treatments for insulin resistance and T2DM.

The biguanides family includes metformin, phenformin, and buformin. Metformin can be utilized by itself along with diet and exercise to improve insulin sensitivity and to lower the high blood sugar associated with T2DM. It is the first line of defense for overweight patients with mild to moderate T2DM demonstrating insulin resistance. Metformin can also be used in combination with other antidiabetic drugs such as sulfonylureas or thiazolidinediones. Furthermore, metformin can be taken in combination with nateglinide (a meglitinides antidiabetic agent) when metformin in combination with exercise and diet management are no longer effective. Phenformin, another biguanides, was used briefly in the United States; however, it was taken of the market because it causes acid buildup in the blood. Buformin, the third biguanides introduced, had limited use.

The thiazolidinediones family, commonly referred to as the "glitazones," includes rosiglitazone, pioglitazone, and troglitazone. Patients with T2DM who benefit most from the glitazones are those with the most insulin resistance. Along with diet and exercise management, rosiglitazone can be taken alone as monotherapy or in combination with other antidiabetic drugs including sulfonylureas, metformin, or insulin. For patients who do not respond well to sulfonylureas or metformin separate monotherapies, rosiglitzone is used in combination with metformin and sulfonylureas. The combination therapy of rosiglitazone and metformin serves as a second line of defense for patients who cannot properly control their blood glucose with separate monotherapies. Along with diet and exercise, pioglitazone (a glitazone) can be taken as monotherapy or in combination with other antidiabetic agents including glimepiride (a sufonylureas), metformin, or insulin. Troglitazone, another member of the glitazone family, was taken of the market because it has toxic effects on the liver.

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