Insulin is essential to process carbohydrates, fat, and protein. Insulin reduces blood glucose levels by allowing glucose to enter muscle cells and by stimulating the conversion of glucose to glycogen (glycogenesis) as a carbohydrate store. Insulin also inhibits the release of stored glucose from liver glycogen (glycogenolysis) and slows the breakdown of fat to triglycerides, free fatty acids, and ketones. It also stimulates fat storage. Additionally, insulin inhibits the breakdown of protein and fat for glucose production (gluconeogenesis) in the liver and kidneys.
Environmental factors are important, because even identical twins have only a 30-60% concordance for type 1 diabetes mellitus and because incidence rates vary in genetically similar populations under different living conditions.  No single factor has been identified, but infections and diet are considered the 2 most likely environmental candidates.
Diabetes mellitus, or simply diabetes, is a group of diseases in which a person does not produce enough insulin, or because it does not respond to the insulin that is produced. Insulin is a hormone that controls the amount of glucose (sugar) in the blood. Diabetes leads to high blood sugar levels, which can lead to damage of blood vessels, organs, and nerves.
In patients with type 2 diabetes, stress, infection, and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Accompanied by dehydration, severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). This condition can worsen and lead to coma (hyperosmolar coma). A hyperosmolar coma usually occurs in elderly patients with type 2 diabetes. Like diabetic ketoacidosis, a hyperosmolar coma is a medical emergency. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. Unlike patients with type 1 diabetes, patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. Since in general, type 2 diabetes occurs in an older population, concomitant medical conditions are more likely to be present, and these patients may actually be sicker overall. The complication and death rates from hyperosmolar coma is thus higher than in diabetic ketoacidosis.
Higher levels of sugar in the urine and the vagina can become a breeding ground for the bacteria and yeast that cause these infections. Recurrent infections are particularly worrisome. “Usually when you keep getting infections, doctors will check for diabetes if you don’t already have it,” says Cypress. “Even women who go to the emergency room for urinary tract infections are often checked.” Don’t miss these other silent diabetes complications you need to know about.
So what determines where fat is stored, and thus a person's propensity for insulin resistance and type 2 diabetes? Well, just having more fat in the body increases the risk that some of it will get misplaced. But exercise may also have a role in fat placement. Exercise is known to reduce insulin resistance; one way it may do this is by burning fat out of the muscle. Because of this, getting enough exercise may stave off type 2 in some cases. Genes may also help orchestrate the distribution of fat in the body, which illustrates how lifestyle and genetics interact.
The above tips are important for you. But it's also crucial to allow yourself time to cope with the diagnosis and commit to making lifestyle changes that will benefit you forever. The good news is the diabetes is a manageable disease; the tough part is that you must think about it daily. Consider finding support—someone that you can talk to about your struggles—be that a friend, another person with diabetes, or a loved one. This may seem trivial, but it truly can help you take control of diabetes so that it doesn't control you. Some next steps that may help you to get on the right track at this early stage in your journey:
Diabetes mellitus (DM) is best defined as a syndrome characterized by inappropriate fasting or postprandial hyperglycemia, caused by absolute or relative insulin deficiency and its metabolic consequences, which include disturbed metabolism of protein and fat. This syndrome results from a combination of deficiency of insulin secretion and its action. Diabetes mellitus occurs when the normal constant of the product of insulin secretion times insulin sensitivity, a parabolic function termed the “disposition index” (Figure 19-1), is inadequate to prevent hyperglycemia and its clinical consequences of polyuria, polydipsia, and weight loss. At high degrees of insulin sensitivity, small declines in the ability to secrete insulin cause only mild, clinically imperceptible defects in glucose metabolism. However, irrespective of insulin sensitivity, a minimum amount of insulin is necessary for normal metabolism. Thus, near absolute deficiency of insulin must result in severe metabolic disturbance as occurs in type 1 diabetes mellitus (T1DM). By contrast, with decreasing sensitivity to its action, higher amounts of insulin secretion are required for a normal disposition index. At a critical point in the disposition index curve (see Figure 19-1), a further small decrement in insulin sensitivity requires a large increase in insulin secretion; those who can mount these higher rates of insulin secretion retain normal glucose metabolism, whereas those who cannot increase their insulin secretion because of genetic or acquired defects now manifest clinical diabetes as occurs in type 2 diabetes (T2DM).
Before blood glucose levels rise, the body of a person destined for type 2 becomes resistant to insulin, much as bacteria can become resistant to antibiotics. Insulin is the signal for the muscles, fat, and liver to absorb glucose from the blood. As the body becomes resistant to insulin, the beta cells in the pancreas must pump out more of the hormone to compensate. People with beta cells that can't keep up with insulin resistance develop the high blood glucose of type 2 diabetes.
Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk. The type of fats in the diet are important, with saturated fats and trans fatty acids increasing the risk, and polyunsaturated and monounsaturated fat decreasing the risk. Eating a lot of white rice appears to play a role in increasing risk. A lack of exercise is believed to cause 7% of cases. Persistent organic pollutants may play a role.
Another area of pathologic changes associated with diabetes mellitus is the nervous system (diabetic neuropathy), particularly in the peripheral nerves of the lower extremities. The patient typically experiences a “stocking-type” anesthesia beginning about 10 years after the onset of the disease. There may eventually be almost total anesthesia of the affected part with the potential for serious injury to the part without the patient being aware of it. In contrast, some patients experience debilitating pain and hyperesthesia, with loss of deep tendon reflexes.
The prognosis for a person with this health condition is estimated to be a life expectancy of 10 years less than a person without diabetes. However, good blood sugar control and taking steps to prevent complications is shortening this gap and people with the condition are living longer than ever before. It can be reversed with diligent attention to changing lifestyle behaviors.
In this health topic, we discuss hyperglycemic hyperosmolar nonketotic syndrome (HHNS), an extremely serious complication that can lead to diabetic coma and even death in type 2 diabetes. This serious condition occurs when the blood sugar gets too high and the body becomes severely dehydrated. To prevent HHNS and diabetic coma in type 2 diabetes, check your blood sugar regularly as recommended by your health care provider; check your blood sugar more frequently when you are sick, drink plenty of fluids, and watch for signs of dehydration.