Diabetes is a costly disease, placing a high financial burden on the patient and the healthcare system. If poorly managed or left untreated, it can cause blindness, loss of kidney function, and conditions that require the amputation of digits or limbs. The CDC reports that it’s also a major cause of heart disease and stroke and the seventh leading cause of death in the United States.
A OGTT glucose of less than 140 ml/dl is considered normal, with 141-199 being pre-diabetic and levels above 200 mg/dL considered full-blown diabetes. From my research, I believe that  OGTT blood sugar levels above 140 mg/dL , especially regularly, can increase risk of vision problems, cancer, stroke and cardiovascular disease, even without an official diabetes diagnosis.
Pancreatic islet transplantation is an experimental treatment for poorly controlled type 1 diabetes. Pancreatic islets are clusters of cells in the pancreas that make the hormone insulin. In type 1 diabetes, the body’s immune system attacks these cells. A pancreatic islet transplant replaces destroyed islets with new ones that make and release insulin. This procedure takes islets from the pancreas of an organ donor and transfers them to a person with type 1 diabetes. Because researchers are still studying pancreatic islet transplantation, the procedure is only available to people enrolled in research studies. Learn more about islet transplantation studies.
Type 2 diabetes is on the rise and is associated with insulin resistance. There are many factors which contribute to developing this disease some of which are modifiable and some of which are nonmodifiable. Modifiable risks which individuals can impact include weight, diet and exercise. It has been reported that gastric bypass patients who have T2DM are “cured” of the disease after surgery. That is a more drastic measure which many people are not ready or willing to consider.
Type 2 diabetes develops when the body cannot use insulin properly or make enough insulin, so the body cannot properly use or store glucose (a form of sugar) and sugar backs up into the bloodstream, raising blood sugar levels. In the United States, some 8.9 percent of adults 20 and older have been found to have diabetes, and health officials estimate that another 3.5 percent have undiagnosed diabetes.

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.
Called ALA for short, this vitamin-like substance neutralizes many types of free radicals. A build-up of free radicals, caused in part by high blood sugar, can lead to nerve damage and other problems. ALA may also help muscle cells take up blood sugar. In a German study, a team of scientists had 40 adults take either an ALA supplement or a placebo. At the end of the four-week study, the ALA group had improved their insulin sensitivity 27 percent. The placebo group showed no improvement. Other studies have shown a decrease in nerve pain, numbness, and burning.

Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.
The problem is, glucose is actually toxic if it is just floating around in your bloodstream, so that body has a defense mechanism. Any glucose that is not immediately used is stored as glycogen in the liver and the muscles. This would be all well and good except that your body has a limited number of glycogen receptors. When these are full, as they almost always are in inactive people, the body only has one option left: to store all the excess glucose as saturated fat within the body.
Each day in the United States, some 18 million people with diabetes walk a tightrope between too little sugar in the bloodstream and too much. Too little, which may come from a complication of medication, and they may quickly be overcome by dizziness, fatigue, headache, sweating, trembling, and, in severe cases, loss of consciousness and coma. Too much, which can happen after eating too much, especially if the person is older and overweight, and the person may experience weakness, fatigue, excessive thirst, labored breathing, and loss of consciousness.
Whole-body insulin resistance is the earliest predictor of type 2 diabetes onset, and this mainly reflects muscle insulin resistance (26). However, careful separation of the contributions of muscle and liver have shown that early improvement in control of fasting plasma glucose level is associated only with improvement in liver insulin sensitivity (20,21). It is clear that the resumption of normal or near-normal diurnal blood glucose control does not require improvement in muscle insulin sensitivity. Although this finding may at first appear surprising, it is supported by a wide range of earlier observations. Mice totally lacking in skeletal muscle insulin receptors do not develop diabetes (27). Humans who have the PPP1R3A genetic variant of muscle glycogen synthase cannot store glycogen in muscle after meals but are not necessarily hyperglycemic (28). Many normoglycemic individuals maintain normal blood glucose levels with a degree of muscle insulin resistance identical to those with type 2 diabetes (29).
All of the above contributing factors don’t usually happen by themselves. Since the body functions as a whole, a problem in one area will usually correlate to problems in others. A combination of the factors above can be the catalyst for a full blown case of diabetes (or a lot of other diseases). While researchers often look at a single variable when trying to discover a cure for a disease, often the best approach is one that addresses the body as a whole. As with all diseases, the best cure is good prevention, but certain measures can help reverse disease once it has occurred.

These are a relatively new class of drugs used to treat type 2 diabetes. They are oral medications that work by blocking the kidneys' reabsorption of glucose, leading to increased glucose excretion and reduction of blood sugar levels. The US FDA approved the SGLT2 inhibitors canagliflozin (Invokana) in March 2013 and dapagliflozin (Farxiga) in January 2014.

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