A patient diagnosed with type 2 diabetes (HbA1c of 6.5% or above) will always have type 2 diabetes. Interventions such as medication (including insulin), staying active and making good diet choices must be maintained to prevent the disease from progressing further. However, even if the patient undergoes strict medication, diet and exercise adherence and manages to lower the HbA1c they will still have type 2 diabetes.
Although a defect in mitochondrial function is associated with extremes of insulin resistance in skeletal muscle (30), this does not appear to be relevant to the etiology of type 2 diabetes. No defect is present in early type 2 diabetes but rather is directly related to ambient plasma glucose concentration (31). Observed rates of mitochondrial ATP production can be modified by increasing or decreasing plasma fatty acid concentration (32,33). Additionally, the onset of insulin stimulation of mitochondrial ATP synthesis is slow, gradually increasing over 2 h, and quite distinct from the acute onset of insulin’s metabolic effects (34). Although it remains possible that secondary mitochondrial effects of hyperglycemia and excess fatty acids exist, there is no evidence for a primary mitochondrial defect underlying type 2 diabetes.
They would often say to me, “Doctor. You’ve always said that weight loss is the key to reversing diabetes. Yet you prescribed me a drug that made me gain 25 pounds. How is that good?” I never had a good answer, because none existed. The truth was that insulin was not good for type 2 diabetes — it was only good for reducing blood glucose. The key was weight loss, whereupon the diabetes often goes away or at least gets significantly better. So, logically, insulin does not help reverse the disease, but actually worsens it.
The primary issue requiring management is that of the glucose cycle. In this, glucose in the bloodstream is made available to cells in the body; a process dependent upon the twin cycles of glucose entering the bloodstream, and insulin allowing appropriate uptake into the body cells. Both aspects can require management. Another issue that ties along with the glucose cycle is getting a balanced amount of the glucose to the major organs so they are not affected negatively.
The term diabetes includes several different metabolic disorders that all, if left untreated, result in abnormally high concentration of a sugar called glucose in the blood. Diabetes mellitus type 1 results when the pancreas no longer produces significant amounts of the hormone insulin, usually owing to the autoimmune destruction of the insulin-producing beta cells of the pancreas. Diabetes mellitus type 2, in contrast, is now thought to result from autoimmune attacks on the pancreas and/or insulin resistance. The pancreas of a person with type 2 diabetes may be producing normal or even abnormally large amounts of insulin. Other forms of diabetes mellitus, such as the various forms of maturity onset diabetes of the young, may represent some combination of insufficient insulin production and insulin resistance. Some degree of insulin resistance may also be present in a person with type 1 diabetes.
Metformin is a biguanide drug that increases the sensitivity of the body’s cells to insulin. It also decreases the amount of glucose produced by the liver.. In 1994, the FDA approved the use of the biguanide called metformin (Glucophage) for the treatment of type 2 diabetes. Today, this is still typically the first drug prescribed for type 2 diabetes.