The genes identified so far in people with type 2 include many that affect the insulin-producing beta cells of the pancreas, says Craig Hanis, PhD, a professor at the Human Genetics Center at the University of Texas Health Science Center in Houston. And yet he emphasizes that why people get type 2 isn't at all clear yet: "What it tells us is that diabetes is a complicated disease."
In an otherwise healthy individual, blood glucose levels usually do not rise above 180 mg/dL (9 mmol/L). In a child with diabetes, blood sugar levels rise if insulin is insufficient for a given glucose load. The renal threshold for glucose reabsorption is exceeded when blood glucose levels exceed 180 mg/dL (10 mmol/L), causing glycosuria with the typical symptoms of polyuria and polydipsia. (See Pathophysiology, Clinical, and Treatment.)
Can diabetes be prevented? Why are so many people suffering from it now over decades past? While there will never be anyway to possibly avoid genetic diabetes, there have been cases where dietary changes could perhaps have been made to delay or prevent the ailment from further developing. Doctors report that obesity plays a role, as well as activity levels, and even overall mental health often can be common threads of pre-diabetic patients.
Diabetes that's triggered by pregnancy is called gestational diabetes (pregnancy, to some degree, leads to insulin resistance). It is often diagnosed in middle or late pregnancy. Because high blood sugar levels in a mother are circulated through the placenta to the baby, gestational diabetes must be controlled to protect the baby's growth and development.
Autonomic changes involving cardiovascular control (eg, heart rate, postural responses) have been described in as many as 40% of children with diabetes. Cardiovascular control changes become more likely with increasing duration and worsening control.  In a study by 253 patients with type 1 diabetes (mean age at baseline 14.4 y), Cho et al reported that the prevalence of cardiac autonomic dysfunction increases in association with higher body mass index and central adiposity. 
Type 2 diabetes, the most common type of diabetes, is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes mainly from the food you eat. Insulin, a hormone made by the pancreas, helps glucose get into your cells to be used for energy. In type 2 diabetes, your body doesn’t make enough insulin or doesn’t use insulin well. Too much glucose then stays in your blood, and not enough reaches your cells.
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).
Diabetes mellitus, or as it's more commonly known diabetes, is a disease characterized by an excess of blood glucose, or blood sugar, which builds up in the bloodstream when your body isn't able to adequately process the sugar in food. High blood sugar is an abnormal state for the body and creates specific symptoms and possible long-term health problems if blood sugar is not managed well.
FIGURE 19-1 ■. This figure shows the hyperbolic relationship of insulin resistance and beta cell function. On the y-axis is beta cell function as reflected in the first-phase insulin response during intravenous (IV) glucose infusion; on the x-axis is insulin sensitivity and its mirror image resistance. In a subject with normal glucose tolerance (NGT) and beta-cell reserve, an increase in insulin resistance results in increased insulin release and normal glucose tolerance. In an individual for whom the capacity to increase insulin release is compromised, increasing insulin resistance with partial or no beta-cell compensation results in progression from normal glucose tolerance, to impaired glucose tolerance (IGT), and finally to diabetes (T2D). Differences between these categories are small at high insulin sensitivity, which may be maintained by weight reduction, exercise, and certain drugs. At a critical degree of insulin resistance, due to obesity or other listed factors, only a further small increment in resistance requires a large increase in insulin output. Those that can increase insulin secretion to this extent retain normal glucose tolerance; those who cannot achieve this degree of insulin secretion (e.g., due to a mild defect in genes regulating insulin synthesis, insulin secretion, insulin action, or an ongoing immune destruction of beta cells) now unmask varying degrees of carbohydrate intolerance. The product of insulin sensitivity (the reciprocal of insulin resistance) and acute insulin response (a measurement beta-cell function) has been called the “disposition index.” This index remains constant in an individual with normal beta cell compensation in response to changes in insulin resistance. IGT, impaired glucose tolerance; NGT, normal glucose tolerance; T2D, type 2 diabetes.
The woman’s weight may also play a role. Changing hormone levels and weight gain are part of a healthy pregnancy, but both changes make it more difficult for the body to keep up with its need for insulin. This may lead to gestational diabetes. As pregnancy progresses, the placenta also produces insulin-blocking hormones, which might result in a woman’s blood-glucose levels becoming elevated if there isn’t enough insulin to counter this effect.
Type 2 DM is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 DM is the most common type of diabetes mellitus.
The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.
Infections. Poorly controlled diabetes can lead to a variety of tissue infections. The most commonly encountered is a yeast infection (Candida) and the presence of dry mouth further increases one’s risk (see PATIENT INFORMATION SHEET – Oral Yeast Infections). Typically, affected areas appear redder than the surrounding tissue and commonly affected sites include the tongue, palate, cheeks, gums, or corners of the mouth (see Right). There is conflicting data regarding cavity risk in the diabetic patient, but those who have dry mouth are clearly at increased risk for developing cavities.
It is clearly established that diabetes mellitus is not a single disease but a genetically heterogeneous group of disorders that share glucose intolerance in common (4–7). The concept of genetic heterogeneity (i.e. that different genetic and/or environmental etiologic factors can result in similar phenotypes) has significantly altered the genetic analysis of this common disorder. Diabetes and glucose intolerance are not diagnostic terms, but, like anemia, simply describe symptoms and/or laboratory abnormalities that can have a number of distinct etiologies.
All types of diabetes mellitus have something in common. Normally, your body breaks down the sugars and carbohydrates you eat into a special sugar called glucose. Glucose fuels the cells in your body. But the cells need insulin, a hormone, in your bloodstream in order to take in the glucose and use it for energy. With diabetes mellitus, either your body doesn't make enough insulin, it can't use the insulin it does produce, or a combination of both.