Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance. Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue. In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood. The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion.
Family or personal history. Your risk increases if you have prediabetes — a precursor to type 2 diabetes — or if a close family member, such as a parent or sibling, has type 2 diabetes. You're also at greater risk if you had gestational diabetes during a previous pregnancy, if you delivered a very large baby or if you had an unexplained stillbirth.
Rosiglitazone, a thiazolidinedione, has not been found to improve long-term outcomes even though it improves blood sugar levels. Additionally it is associated with increased rates of heart disease and death. Angiotensin-converting enzyme inhibitors (ACEIs) prevent kidney disease and improve outcomes in those with diabetes. The similar medications angiotensin receptor blockers (ARBs) do not. A 2016 review recommended treating to a systolic blood pressure of 140 to 150 mmHg.
Injections of insulin may either be added to oral medication or used alone. Most people do not initially need insulin. When it is used, a long-acting formulation is typically added at night, with oral medications being continued. Doses are then increased to effect (blood sugar levels being well controlled). When nightly insulin is insufficient, twice daily insulin may achieve better control. The long acting insulins glargine and detemir are equally safe and effective, and do not appear much better than neutral protamine Hagedorn (NPH) insulin, but as they are significantly more expensive, they are not cost effective as of 2010. In those who are pregnant insulin is generally the treatment of choice.
Although urine can also be tested for the presence of glucose, checking urine is not a good way to monitor treatment or adjust therapy. Urine testing can be misleading because the amount of glucose in the urine may not reflect the current level of glucose in the blood. Blood glucose levels can get very low or reasonably high without any change in the glucose levels in the urine.
Monogenic diabetes is caused by mutations, or changes, in a single gene. These changes are usually passed through families, but sometimes the gene mutation happens on its own. Most of these gene mutations cause diabetes by making the pancreas less able to make insulin. The most common types of monogenic diabetes are neonatal diabetes and maturity-onset diabetes of the young (MODY). Neonatal diabetes occurs in the first 6 months of life. Doctors usually diagnose MODY during adolescence or early adulthood, but sometimes the disease is not diagnosed until later in life.
Diabetes mellitus is a chronic disease for which there is treatment but no known cure. Treatment is aimed at keeping blood glucose levels as close to normal as possible. This is achieved with a combination of diet, exercise and insulin or oral medication. People with type 1 diabetes need to be hospitalized right after they are diagnosed to get their glucose levels down to an acceptable level.
Whether you’re dealing with frequent UTIs or skin infections, undiagnosed diabetes may be to blame. The high blood sugar associated with diabetes can weaken a person’s immune system, making them more susceptible to infection. In more advanced cases of the disease, nerve damage and tissue death can open people up to further infections, often in the skin, and could be a precursor to amputation.
Excessive thirst typically goes hand-in-hand with increased urination. As your body pulls water out of the tissues to dilute your blood and to rid your body of sugar through the urine, the urge to drink increases. Many people describe this thirst as an unquenchable one. To stay hydrated, you drink excessive amounts of liquids. And if those liquids contain simple sugars (soda, sweet iced tea, lemonade, or juice, for example) your sugars will skyrocket even higher.
In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.
Type 1 diabetes mellitus is a chronic metabolic syndrome defined by an inability to produce insulin, a hormone which lowers blood sugar. This leads to inappropriate hyperglycaemia (increased blood sugar levels) and deranged metabolism of carbohydrates, fats and proteins. Insulin is normally produced in the pancreas, a glandular organ involved in the production of digestive enzymes and hormones such as insulin and glucagon. These functions are carried out in the exocrine and endocrine (Islets of Langerhans) pancreas respectively.
Several tests are helpful in identifying DM. These include tests of fasting plasma glucose levels, casual (randomly assessed) glucose levels, or glycosylated hemoglobin levels. Diabetes is currently established if patients have classic diabetic symptoms and if on two occasions fasting glucose levels exceed 126 mg/dL (> 7 mmol/L), random glucose levels exceed 200 mg/dL (11.1 mmol/L), or a 2-hr oral glucose tolerance test is 200 mg/dL or more. A hemoglobin A1c test that is more than two standard deviations above normal (6.5% or greater) is also diagnostic of the disease.
Jump up ^ Imperatore, Giuseppina; Boyle, James P.; Thompson, Theodore J.; Case, Doug; Dabelea, Dana; Hamman, Richard F.; Lawrence, Jean M.; Liese, Angela D.; Liu, Lenna L. (December 2012). "Projections of Type 1 and Type 2 Diabetes Burden in the U.S. Population Aged <20 Years Through 2050". Diabetes Care. 35 (12): 2515–20. doi:10.2337/dc12-0669. ISSN 0149-5992. PMC 3507562. PMID 23173134. Archived from the original on 2016-08-14.
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.
Gestational diabetes mellitus (GDM) resembles type 2 DM in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. However, after pregnancy approximately 5–10% of women with GDM are found to have DM, most commonly type 2. GDM is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.