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).
Yet carbs are processed differently in the body based on their type: While simple carbs are digested and metabolized quickly, complex carbs take longer to go through this system, resulting in more stable blood sugar. “It comes down to their chemical forms: A simple carbohydrate has a simpler chemical makeup, so it doesn’t take as much for it to be digested, whereas the complex ones take a little longer,” Grieger explains.
Nerve damage from diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. In essence, the blood flow to the nerves is limited, leaving the nerves without blood flow, and they get damaged or die as a result (a term known as ischemia). Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. When the nerve disease causes a complete loss of sensation in the feet, patients may not be aware of injuries to the feet, and fail to properly protect them. Shoes or other protection should be worn as much as possible. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Because of poor blood circulation, diabetic foot injuries may not heal. Sometimes, minor foot injuries can lead to serious infection, ulcers, and even gangrene, necessitating surgical amputation of toes, feet, and other infected parts.
Metformin is generally recommended as a first line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose. Several other groups of drugs, mostly given by mouth, may also decrease blood sugar in type II DM. These include agents that increase insulin release, agents that decrease absorption of sugar from the intestines, and agents that make the body more sensitive to insulin. When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications. Doses of insulin are then increased to effect.
If, on the other hand, you are already starting to develop complications or your medication regimen has changed because your blood sugars are getting higher, remember that diabetes is a progressive disease—and sometimes these things just happen without any influence from your own actions. As you age, beta cells in the pancreas get tired and stop working. If you've had diabetes for 20 years and now need to start insulin, for example, it doesn't mean you've failed. It just means that your body needs some help. Make sure you continue to receive education and that you continue to have someone to lean on when you need it, and keep the lines of communication open with your doctor. It truly can make a difference.
A population-based, nationwide cohort study in Finland examined the short -and long-term time trends in mortality among patients with early-onset and late-onset type 1 diabetes. The results suggest that in those with early-onset type 1 diabetes (age 0-14 y), survival has improved over time. Survival of those with late-onset type 1 diabetes (15-29 y) has deteriorated since the 1980s, and the ratio of deaths caused by acute complications has increased in this group. Overall, alcohol was noted as an important cause of death in patients with type 1 diabetes; women had higher standardized mortality ratios than did men in both groups. 
Type 1 diabetes occurs because the insulin-producing cells of the pancreas (beta cells) are damaged. In type 1 diabetes, the pancreas makes little or no insulin, so sugar cannot get into the body's cells for use as energy. People with type 1 diabetes must use insulin injections to control their blood glucose. Type 1 is the most common form of diabetes in people who are under age 30, but it can occur at any age. Ten percent of people with diabetes are diagnosed with type 1.
At present, the American Diabetes Association does not recommend general screening of the population for type 1 diabetes, though screening of high risk individuals, such as those with a first degree relative (sibling or parent) with type 1 diabetes should be encouraged. Type 1 diabetes tends to occur in young, lean individuals, usually before 30 years of age; however, older patients do present with this form of diabetes on occasion. This subgroup is referred to as latent autoimmune diabetes in adults (LADA). LADA is a slow, progressive form of type 1 diabetes. Of all the people with diabetes, only approximately 10% have type 1 diabetes and the remaining 90% have type 2 diabetes.
Diabetes is a condition in which the body cannot properly store and use fuel for energy. The body's main fuel is a form of sugar called glucose, which comes from food (after it has been broken down). Glucose enters the blood and is used by cells for energy. To use glucose, the body needs a hormone called insulin that's made by the pancreas. Insulin is important because it allows glucose to leave the blood and enter the body's cells.
Blurred vision can result from elevated blood sugar. Similarly, fluid that is pulled from the cells into the bloodstream to dilute the sugar can also be pulled from the lenses of your eyes. When the lens of the eye becomes dry, the eye is unable to focus, resulting in blurry vision. It's important that all people diagnosed with type 2 diabetes have a dilated eye exam shortly after diagnosis. Damage to the eye can even occur before a diagnosis of diabetes exists.
The most common complication of treating high blood glucose levels is low blood glucose levels (hypoglycemia). The risk is greatest for older people who are frail, who are sick enough to require frequent hospital admissions, or who are taking several drugs. Of all available drugs to treat diabetes, long-acting sulfonylurea drugs are most likely to cause low blood glucose levels in older people. When they take these drugs, they are also more likely to have serious symptoms, such as fainting and falling, and to have difficulty thinking or using parts of the body due to low blood glucose levels.
To treat diabetic retinopathy, a laser is used to destroy and prevent the recurrence of the development of these small aneurysms and brittle blood vessels. Approximately 50% of patients with diabetes will develop some degree of diabetic retinopathy after 10 years of diabetes, and 80% retinopathy after 15 years of the disease. Poor control of blood sugar and blood pressure further aggravates eye disease in diabetes.
“I don’t think that anybody has put their finger on what the true cause of diabetes is, or that we’re going to find a single cause,” Grieger says. So if you’ve been diagnosed with prediabetes or have other risk factors for the disease, avoiding any one food group entirely — even sugar — won’t completely offset your risk. Rather, it’s important to prioritize proper nutrition, exercise regularly, and maintain a healthy weight — all steps the American Diabetes Association recommends for preventing type 2 diabetes.
It will surely be tough eating salads and vegetables when everyone else at your dinner table is eating pizza. Decide that this diagnosis can benefit the health of the entire family. Educate your family about the benefits of eating a healthy diet. Take your children grocery shopping with you. Practice the plate method: Aim to make half your plate non-starchy vegetables; a quarter lean protein; and a quarter whole grains or starchy vegetables, like sweet potatoes. Make exercise part of your daily routine and include your family. Go for walks after dinner. Head to the pool on the weekends, or enroll in an exercise class. If you don't have children, aim to find others with diabetes or friends that can act as your workout partners.
Blood sugar should be regularly monitored so that any problems can be detected and treated early. Treatment involves lifestyle changes such as eating a healthy and balanced diet and regular physical exercise. If lifestyle changes alone are not enough to regulate the blood glucose level, anti-diabetic medication in the form of tablets or injections may be prescribed. In some cases, people who have had type 2 diabetes for many years are eventually prescribed insulin injections.
Some people with type 2 diabetes are treated with insulin. Insulin is either injected with a syringe several times per day, or delivered via an insulin pump. The goal of insulin therapy is to mimic the way the pancreas would produce and distribute its own insulin, if it were able to manufacture it. Taking insulin does not mean you have done a bad job of trying to control your blood glucose—instead it simply means that your body doesn’t produce or use enough of it on its own to cover the foods you eat.
^ Jump up to: a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.