While there are competing explanations of the link between obesity and type 2 diabetes, Gerald Shulman, MD, PhD, a professor of internal medicine and physiology at Yale University, believes the key is figuring out insulin resistance. He has studied the causes of insulin resistance for 25 years and thinks he may have the answer to the weight-diabetes link.
interventions The goal of treatment is to maintain insulin glucose homeostasis. Type 1 diabetes is controlled by insulin, meal planning, and exercise. The Diabetes Control and Complications Trial (DCCT), completed in mid-1993, demonstrated that tight control of blood glucose levels (i.e., frequent monitoring and maintenance at as close to normal as possible to the level of nondiabetics) significantly reduces complications such as eye disease, kidney disease, and nerve damage. Type 2 diabetes is controlled by meal planning; exercise; one or more oral agents, in combination with oral agents; and insulin. The results of the United Kingdom Prospective Diabetes Study, which involved more than 5000 people with newly diagnosed type 2 diabetes in the United Kingdom, were comparable to those of the DCCT where a relationship in microvascular complications. Stress of any kind may require medication adjustment in both type 1 and type 2 diabetes.
There is strong evidence that the long-term complications are related to the degree and duration of metabolic disturbances.2 These considerations form the basis of standard and innovative therapeutic approaches to this disease that include newer pharmacologic formulations of insulin, delivery by traditional and more physiologic means, and evolving methods to continuously monitor blood glucose to maintain it within desired limits by linking these features to algorithm-driven insulin delivery pumps for an “artificial pancreas.”
Insulin is needed to allow glucose to pass from the blood into most of the body cells. Only the cells of the brain and central nervous system can use glucose from the blood in the absence of insulin. Without insulin, most body cells metabolize substances other than glucose for energy. However, fat metabolism in the absence of glucose metabolism, creates ketone bodies which are poisonous and their build up is associated with hyperglycemic coma. In the absence of sufficient insulin, unmetabolized glucose builds up in the blood. Water is drawn from body cells by osmosis to dilute the highly concentrated blood, and is then excreted along with much of the glucose, once the renal threshold for glucose (usually 10 mmol/L) is exceeded. Dehydration follows.
Type 1 diabetes in pediatric patients has been linked to changes in cognition and brain structure, with a study by Siller et al finding lower volume in the left temporal-parietal-occipital cortex in young patients with type 1 diabetes than in controls. The study also indicated that in pediatric patients, higher severity of type 1 diabetes presentation correlates with greater structural differences in the brain at about 3 months following diagnosis. The investigators found that among study patients with type 1 diabetes, an association existed between the presence of diabetic ketoacidosis at presentation and reduced radial, axial, and mean diffusivity in the major white matter tracts on magnetic resonance imaging (MRI). In those with higher glycated hemoglobin (HbA1c) levels, hippocampal, thalamic, and cerebellar white matter volumes were lower, as was right posterior parietal cortical thickness, while right occipital cortical thickness was greater. Patients in the study were aged 7-17 years. 
Low blood sugar (hypoglycemia), is common in people with type 1 and type 2 DM. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases. Moderately low blood sugar may easily be mistaken for drunkenness; rapid breathing and sweating, cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Although age of onset and length of the disease process are related to the frequency with which vascular, renal, and neurologic complications develop, there are some patients who remain relatively free of sequelae even into the later years of their lives. Because diabetes mellitus is not a single disease but rather a complex constellation of syndromes, each patient has a unique response to the disease process.
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Fasting plasma glucose level: If your blood glucose level is 7.0 mmol/L or higher after having not eaten anything for at least 8 hours – called fasting – your doctor may diagnose diabetes. If your blood glucose level is between 6.1 to 6.9 mmol/L, your doctor may diagnose impaired fasting glucose or prediabetes (a condition that may later develop into diabetes).