When we use the term diabetes mellitus, we’re referring to a disease of the pancreas. Over 80 percent of the time, diabetes refers to type 2 diabetes. Type 1 diabetes accounts for another 5 to 10 percent, with the remainder of cases due to other causes (see below).
Type 1 diabetes is characterized by destruction of the pancreatic beta cells, the cells responsible for making insulin. This is usually caused by the body attacking itself, which is why this is considered an autoimmune disease. Testing for islet-cell antibodies (ICA) or other autoantibodies (such as antibodies to glutamic acid decarboxylase (anti-GAD), insulin, and to the tyrosine phosphatase IA-2) is helpful in the diagnosis, though some patients may not have antibodies at all.
Patients with type 1 diabetes have an absolute requirement for insulin therapy and will develop diabetic ketoacidosis (DKA) if not given insulin. Type 1 is also referred to as juvenile diabetes, or insulin dependent diabetes. READ MORE ABOUT TYPE 1 DIABETES
Adult-onset type 1 diabetes (LADA)
Since the discovery of autoantibodies directed against pancreatic beta-cell antigens, it has been recognized that some adults considered to have type 2 diabetes probably have type 1 diabetes. Among adults with apparent type 2 diabetes, approximately 7.5 to 10 percent have type 1 diabetes as defined by the presence of circulating islet-cell antibodies (ICA) or antibodies to glutamic acid decarboxylase (GAD). This is also called “latent autoimmune diabetes in adults” or LADA.
These patients tend to be older than the average Type 1 patient, but the age of onset is usually less than 50 years. LADA patients are often thin, tend to have acute symptoms, and have a personal or family history of autoimmune disease.
The presence of either anti-ICA or anti-GAD antibodies identify patients thought to have type 2 diabetes who are likely to respond poorly to oral hypoglycemic drug therapy. These patients require insulin, and are at increased risk for developing ketoacidosis.
Type 2 diabetes is by far the most common type of diabetes, and is characterized by variable degrees of insulin deficiency and resistance. Many patients with type 2 diabetes lose beta cell function over time and require insulin for glucose control. Thus, the need for insulin does not distinguish between type 1 and type 2 diabetes. While ketoacidosis (DKA) is more commonly seen in type 1 diabetes, it can also happen in type 2 diabetes. READ MORE ABOUT TYPE 2 DIABETES
Type 1 and Type 2 can occur in the same persons — In the past, poor control of sugars in type 1 diabetes patients prevented most patients from gaining weight. Now, with the intense therapy commonly used to manage type 1 diabetes, and given all the societal changes that lead to obesity, 20 to 30 percent of type 1 diabetic patients become overweight or obese. When type 1 patients gain weight they may be at risk for type 2 diabetes, just like anyone else, especially those who also have a family history of type 2 diabetes.
This form of diabetes occurs in pregnant women, usually during the 2nd or 3rd trimester of pregnancy. Gestational diabetes occurs because the placenta starts to produce hormones which make it more difficult for insulin to work (increased insulin resistance) and if the woman cannot compensate for the increased insulin demand, then blood sugar levels start to rise. It is estimated to occur in approximately 2.1 percent of pregnant women in the United States. MORE ON GESTATIONAL DIABETES
SPECIFIC GENETIC DEFECTS — New information has led to increased understanding of genetic defects related to diabetes, and the formerly termed MODY syndromes (maturity onset diabetes of the young) have now been linked to specific genetic defects. These account for approximately two to five percent of patients with type 2 diabetes. These patients present at a young age, and have a mild form of the disease, which is genetic (autosomal dominant). As we learn more about the human genome we will start to understand that perhaps diabetes is a big umbrella of many, many different subtypes of genetic defects. Here are the genes that so far have been identified for the type of diabetes formally known as MODY: Hepatocyte nuclear factor-4-alpha (formerly MODY 1), Glucokinase gene (formerly MODY 2), Hepatocyte nuclear factor-1-alpha (formerly MODY3), Insulin promoter factor 1 (formerly MODY 4), Hepatocyte nuclear factor-1-beta (formerly MODY 5) and Neurogenic differentiation factor-1 (formerly MODY 6).
DISEASES OF THE PANCREAS — Any disease that damages the pancreas can lead to diabetes. It is more likely to occur if there is a history of type 1 or type 2 diabetes in the family. Some of the diseases that can damage the pancreas are cystic fibrosis, hereditary hemochromatosis, chronic pancreatitis (usually appears late in life). Hepatitis C is also associated with an increased risk of diabetes.
OTHER ENDOCRINE DISEASES– other endocrine diseases such as acromegaly (too much growth hormone), Cushing’s syndrome (too much cortisol), pheochromocytoma (too much epinephrine), and rare tumors such as glucagonomas and somatostatinomas can lead to hyperglycemia and diabetes.
DRUG-INDUCED DIABETES — A large number of drugs can lead to a lower production of insulin, or an increase in insulin resistance. Some the drugs are steroids, oral contraceptives, tacrolimus and cyclosporine, niacin, HIV medications –Protease inhibitors, thiazide diuretics (at the higher doses), atypical antipsychotics, pentamidine, and others.