The ADA recommends using patient age as one consideration in the establishment of glycemic goals, with different targets for preprandial, bedtime/overnight, and hemoglobin A1c (HbA1c) levels in patients aged 0-6, 6-12, and 13-19 years.  Benefits of tight glycemic control include not only continued reductions in the rates of microvascular complications but also significant differences in cardiovascular events and overall mortality.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose. people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).
Sugar doesn't cause diabetes. But there is one way that sugar can influence whether a person gets type 2 diabetes. Consuming too much sugar (or sugary foods and drinks) can make people put on weight. Gaining too much weight leads to type 2 diabetes in some people. Of course, eating too much sugar isn't the only cause of weight gain. Weight gain from eating too much of any food can make a person's chance of getting diabetes greater.
Patients need to ensure that their blood glucose levels are kept as normal as possible so that delicate tissues in the body (especially blood vessels in the eyes, kidneys and peripheral nerves) are not damaged by high glucose levels over a long period of time. To achieve this, patients need to measure their glucose regularly and learn how to adjust their insulin doses in order to optimise their glucose levels (diabetes control). Good diabetes control helps to minimise the risk of long-term diabetes complications, as well as short-term symptoms (such as thirst).
"Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used. Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, frequently with ketosis, and sometimes with serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.
According to the National Institutes of Health, the reported rate of gestational diabetes is between 2% to 10% of pregnancies. Gestational diabetes usually resolves itself after pregnancy. Having gestational diabetes does, however, put mothers at risk for developing type 2 diabetes later in life. Up to 10% of women with gestational diabetes develop type 2 diabetes. It can occur anywhere from a few weeks after delivery to months or years later.
Persons with diabetes who take insulin must be careful about indulging in unplanned exercise. Strenuous physical activity can rapidly lower their blood sugar and precipitate a hypoglycemic reaction. For a person whose blood glucose level is over 250 mg/dl, the advice would be not to exercise at all. At this range, the levels of insulin are too low and the body would have difficulty transporting glucose into exercising muscles. The result of exercise would be a rise in blood glucose levels.
Type I diabetes, sometimes called juvenile diabetes, begins most commonly in childhood or adolescence. In this form of diabetes, the body produces little or no insulin. It is characterized by a sudden onset and occurs more frequently in populations descended from Northern European countries (Finland, Scotland, Scandinavia) than in those from Southern European countries, the Middle East, or Asia. In the United States, approximately three people in 1,000 develop Type I diabetes. This form also is called insulin-dependent diabetes because people who develop this type need to have daily injections of insulin.
There is evidence that certain emotions can promote type 2 diabetes. A recent study found that depression seems to predispose people to diabetes. Other research has tied emotional stress to diabetes, though the link hasn't been proved. Researchers speculate that the emotional connection may have to do with the hormone cortisol, which floods the body during periods of stress. Cortisol sends glucose to the blood, where it can fuel a fight-or-flight response, but overuse of this system may lead to dysfunction.
If sugars in general are not associated with increased diabetes risk, but sodas are, it suggests the possibility that something other than sugar explains this relationship.16 Sodas are often accompanied by cheeseburgers, chicken nuggets, and other unhealthful foods. That is, soda consumption can be a sign of a diet focusing on fast foods or an overall unhealthful diet and lifestyle. And sugary snack foods (e.g., cookies and snack pastries) are often high in fat; the sugar lures us in to the fat calories hiding inside. Some, but not all, observational trials have sought to control for these confounding variables.
Insulin works like a key that opens the doors to cells and lets the glucose in. Without insulin, glucose can't get into the cells (the doors are "locked" and there is no key) and so it stays in the bloodstream. As a result, the level of sugar in the blood remains higher than normal. High blood sugar levels are a problem because they can cause a number of health problems.
A number of studies have looked for relationships between sugar and diabetes risk. A 2017 meta-analysis, based on nine reports of 15 cohort studies including 251,261 participants, found no significant effect of total sugars on the risk of developing type 2 diabetes.7 Those consuming the most sugar actually had a 9 percent lower risk of developing diabetes, compared with those consuming the least sugar, although the difference was not statistically significant (meaning that it could have been a chance result). Similarly, fructose was not significantly associated with diabetes risk. Sucrose appeared to have a significant protective association. Those consuming the most sucrose had 11 percent less risk of developing type 2 diabetes, compared with those consuming the least.
A second oral agent of another class or insulin may be added if metformin is not sufficient after three months. Other classes of medications include: sulfonylureas, thiazolidinediones, dipeptidyl peptidase-4 inhibitors, SGLT2 inhibitors, and glucagon-like peptide-1 analogs. As of 2015 there was no significant difference between these agents. A 2018 review found that SGLT2 inhibitors may be better than glucagon-like peptide-1 analogs or dipeptidyl peptidase-4 inhibitors.
Sequelae. The long-term consequences of diabetes mellitus can involve both large and small blood vessels throughout the body. That in large vessels is usually seen in the coronary arteries, cerebral arteries, and arteries of the lower extremities and can eventually lead to myocardial infarction, stroke, or gangrene of the feet and legs. atherosclerosis is far more likely to occur in persons of any age who have diabetes than it is in other people. This predisposition is not clearly understood. Some believe that diabetics inherit the tendency to develop severe atherosclerosis as well as an aberration in glucose metabolism, and that the two are not necessarily related. There is strong evidence to substantiate the claim that optimal control will mitigate the effects of diabetes on the microvasculature, particularly in the young and middle-aged who are at greatest risk for developing complications involving the arterioles. Pathologic changes in the small blood vessels serving the kidney lead to nephrosclerosis, pyelonephritis, and other disorders that eventually result in renal failure. Many of the deaths of persons with type 1 diabetes are caused by renal failure.
Type 1 DM is caused by autoimmune destruction of the insulin-secreting beta cells of the pancreas. The loss of these cells results in nearly complete insulin deficiency; without exogenous insulin, type 1 DM is rapidly fatal. Type 2 DM results partly from a decreased sensitivity of muscle cells to insulin-mediated glucose uptake and partly from a relative decrease in pancreatic insulin secretion.
People with type 2 diabetes have insulin resistance, which means the body cannot use insulin properly to help glucose get into the cells. In people with type 2 diabetes, insulin doesn’t work well in muscle, fat, and other tissues, so your pancreas (the organ that makes insulin) starts to put out a lot more of it to try and compensate. "This results in high insulin levels in the body,” says Fernando Ovalle, MD, director of the multidisciplinary diabetes clinic at the University of Alabama in Birmingham. This insulin level sends signals to the brain that your body is hungry.