"Secondary" diabetes refers to elevated blood sugar levels from another medical condition. Secondary diabetes may develop when the pancreatic tissue responsible for the production of insulin is destroyed by disease, such as chronic pancreatitis (inflammation of the pancreas by toxins like excessive alcohol), trauma, or surgical removal of the pancreas.
Although there are dozens of known type 1 genes, about half of the risk attributable to heredity comes from a handful that coordinate a part of the immune system called HLA, which helps the body recognize nefarious foreign invaders, such as viruses, bacteria, and parasites. Type 1 diabetes is an autoimmune disease, in which the body's own immune system destroys the cells in the pancreas that produce insulin, so perhaps it is no surprise that immunity genes are involved. Other autoimmune diseases share the HLA gene link, which may be why people with type 1 are more likely to develop additional auto­immune disorders.
nephrogenic diabetes insipidus a rare form caused by failure of the renal tubules to reabsorb water; there is excessive production of antidiuretic hormone but the tubules fail to respond to it. Characteristics include polyuria, extreme thirst, growth retardation, and developmental delay. The condition does not respond to exogenous vasopressin. It may be inherited as an X-linked trait or be acquired as a result of drug therapy or systemic disease.
Type 2 diabetes (formerly named non-insulin-dependent) which results from the body's inability to respond properly to the action of insulin produced by the pancreas. Type 2 diabetes is much more common and accounts for around 90% of all diabetes cases worldwide. It occurs most frequently in adults, but is being noted increasingly in adolescents as well.
All children with type 1 diabetes mellitus require insulin therapy. Most require 2 or more injections of insulin daily, with doses adjusted on the basis of self-monitoring of blood glucose levels. Insulin replacement is accomplished by giving a basal insulin and a preprandial (premeal) insulin. The basal insulin is either long-acting (glargine or detemir) or intermediate-acting (NPH). The preprandial insulin is either rapid-acting (lispro, aspart, or glulisine) or short-acting (regular).
If sugars in general are not associated with increased diabetes risk, but sodas are, it suggests the possibility that something other than sugar explains this relationship.16 Sodas are often accompanied by cheeseburgers, chicken nuggets, and other unhealthful foods. That is, soda consumption can be a sign of a diet focusing on fast foods or an overall unhealthful diet and lifestyle. And sugary snack foods (e.g., cookies and snack pastries) are often high in fat; the sugar lures us in to the fat calories hiding inside. Some, but not all, observational trials have sought to control for these confounding variables. 
Reduce Your Carbohydrate Intake: One of the most important components involved in a diabetes diet is knowing how to eat a modified carbohydrate diet. Carbohydrates are the nutrient that impacts blood sugars the most. Carbohydrates are found in starches, fruit, some vegetables like potatoes, sweets, and grains. Eating the right kinds of carbohydrate in the right quantities can help you manage your weight and your blood sugars. Knowing how to identify and count carbohydrates is very important in managing diabetes. Eating a consistent carbohydrate diet is ideal because it can help you body regulate blood sugars.
Insulin — the hormone that allows your body to regulate sugar in the blood — is made in your pancreas. Essentially, insulin resistance is a state in which the body’s cells do not use insulin efficiently. As a result, it takes more insulin than normal to transport blood sugar (glucose) into cells, to be used immediately for fuel or stored for later use. A drop in efficiency in getting glucose to cells creates a problem for cell function; glucose is normally the body’s quickest and most readily available source of energy.
Insulin-dependent diabetes mellitus is believed to result from autoimmune, environmental, and/or genetic factors. Whatever the cause, the end result is destruction of insulin-producing pancreatic beta cells, a dramatic decrease in the secretion of insulin, and hyperglycemia. Non-insulin-dependent diabetes mellitus is presumably heterogeneous in origin. It is associated with older age, obesity, a family history of diabetes, and ethnicity (genetic components). The vast majority of those with non-insulin-dependent diabetes are overweight Kahn (2003). This form of the disorder has a much slower rate of progression than insulin-dependent diabetes. Over time the ability to respond to insulin decreases, resulting in increased levels of blood glucose. The pancreatic secretion of insulin increases in an attempt to compensate for the elevated levels of glucose. If the condition is untreated, the pancreatic production of insulin decreases and may even cease.
People with type 2 diabetes have insulin resistance, which means the body cannot use insulin properly to help glucose get into the cells. In people with type 2 diabetes, insulin doesn’t work well in muscle, fat, and other tissues, so your pancreas (the organ that makes insulin) starts to put out a lot more of it to try and compensate. "This results in high insulin levels in the body,” says Fernando Ovalle, MD, director of the multidisciplinary diabetes clinic at the University of Alabama in Birmingham. This insulin level sends signals to the brain that your body is hungry.
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