Treatment of some forms of hypoglycemia, such as in diabetes, involves immediately raising the blood sugar to normal through the ingestion of carbohydrates, determining the cause, and taking measures to hopefully prevent future episodes. However, this treatment is not optimal in other forms such as reactive hypoglycemia, where rapid carbohydrate ingestion may lead to a further hypoglycemic episode.

Blood glucose can be raised to normal within minutes by taking (or receiving) 10–20 grams of carbohydrate. It can be taken as food or drink if the person is conscious and able to swallow. This amount of carbohydrate is contained in about 3–4 ounces (100–120 ml) of orange, apple, or grape juice although fruit juices contain a higher proportion of fructose which is more slowly metabolized than pure dextrose, alternatively, about 4–5 ounces (120–150 ml) of regular (non-diet) soda may also work, as will about one slice of bread, about 4 crackers, or about 1 serving of most starchy foods. Starch is quickly digested to glucose (unless the person is taking acarbose), but adding fat or protein retards digestion. Symptoms should begin to improve within 5 minutes, though full recovery may take 10–20 minutes. Overfeeding does not speed recovery and if the person has diabetes will simply produce hyperglycemia afterwards. A mnemonic used by the American Diabetes Association and others is the "rule of 15" – consuming 15 grams of carbohydrate followed by a 15-minute wait, repeated if glucose remains low (variable by individual, sometimes 70 mg/dl).

If a person is suffering such severe effects of hypoglycemia that they cannot (due to combativeness) or should not (due to seizures or unconsciousness) be given anything by mouth, medical personnel such as paramedics, or in-hospital personnel can establish IV access and give intravenous dextrose, concentrations varying depending on age (infants are given 2 ml/kg dextrose 10%, children are given dextrose 25%, and adults are given dextrose 50%). Care must be taken in giving these solutions because they can cause skin necrosis if the IV is infiltrated, sclerosis of veins, and many other fluid and electrolyte disturbances if administered incorrectly. If IV access cannot be established, the patient can be given 1 to 2 milligrams of glucagon in an intramuscular injection. More treatment information can be found in the article diabetic hypoglycemia. If a person is suffering less severe effects, and is conscious with the ability to swallow, medical personal such as EMT-B's may administer gelatinous oral glucose.

One situation where starch may be less effective than glucose or sucrose is when a person is taking acarbose. Since acarbose and other alpha-glucosidase inhibitors prevents starch and other sugars from being broken down into monosaccharides that can be absorbed by the body, patients taking these medications should consume monosaccharide-containing foods such as glucose tablets, honey, or juice to reverse hypoglycemia.

Treatment of hyperglycemia requires elimination of the underlying cause, such as diabetes. Acute hyperglycemia can be treated by direct administration of insulin in most cases. Severe hyperglycemia can be treated with oral hypoglycemic therapy and lifestyle modification.

In diabetes mellitus (by far the most common cause of chronic hyperglycemia), treatment aims at maintaining blood glucose at a level as close to normal as possible, in order to avoid these serious long-term complications. This is done by a combination of proper diet, regular exercise, and insulin or other medication such as metformin, etc.

Those with hyperglycaemia can be treated using sulphonylureas or metformin or both. These drugs help by improving glycaemic control

Dipeptidyl peptidase 4 inhibitor alone or in combination with basal insulin can be used as a treatment for hyperglycemia with patients still in the hospital.

The most effective means of preventing further episodes of hypoglycemia depends on the cause.

The risk of further episodes of diabetic hypoglycemia can often (but not always) be reduced by lowering the dose of insulin or other medications, or by more meticulous attention to blood sugar balance during unusual hours, higher levels of exercise, or decreasing alcohol intake.

Many of the inborn errors of metabolism require avoidance or shortening of fasting intervals, or extra carbohydrates. For the more severe disorders, such as type 1 glycogen storage disease, this may be supplied in the form of cornstarch every few hours or by continuous gastric infusion.

Several treatments are used for hyperinsulinemic hypoglycemia, depending on the exact form and severity. Some forms of congenital hyperinsulinism respond to diazoxide or octreotide. Surgical removal of the overactive part of the pancreas is curative with minimal risk when hyperinsulinism is focal or due to a benign insulin-producing tumor of the pancreas. When congenital hyperinsulinism is diffuse and refractory to medications, near-total pancreatectomy may be the treatment of last resort, but in this condition is less consistently effective and fraught with more complications.

Hypoglycemia due to hormone deficiencies such as hypopituitarism or adrenal insufficiency usually ceases when the appropriate hormone is replaced.

Hypoglycemia due to dumping syndrome and other post-surgical conditions is best dealt with by altering diet. Including fat and protein with carbohydrates may slow digestion and reduce early insulin secretion. Some forms of this respond to treatment with a glucosidase inhibitor, which slows starch digestion.

Reactive hypoglycemia with demonstrably low blood glucose levels is most often a predictable nuisance which can be avoided by consuming fat and protein with carbohydrates, by adding morning or afternoon snacks, and reducing alcohol intake.

Idiopathic postprandial syndrome without demonstrably low glucose levels at the time of symptoms can be more of a management challenge. Many people find improvement by changing eating patterns (smaller meals, avoiding excessive sugar, mixed meals rather than carbohydrates by themselves), reducing intake of stimulants such as caffeine, or by making lifestyle changes to reduce stress. See the following section of this article.

Potassium replacement is often required as the metabolic problems are corrected. It is generally replaced at a rate 10 mEq per hour as long as there is adequate urinary output.

To relieve reactive hypoglycemia, the NIH recommends taking the following steps:

- Avoiding or limiting sugar intake;

- Exercising regularly; exercise increases sugar uptake which decreases excessive insulin release

- Eating a variety of foods, including meat, poultry, fish, or nonmeat sources of protein, foods such as whole-grains, fruits, nuts, vegetables, and dairy products;

- Choosing high-fiber foods.

Other tips to prevent sugar crashes include:

- Avoiding eating meals or snacks composed entirely of carbohydrates; simultaneously ingest fats and proteins, which have slower rates of absorption.

- Consistently choosing longer lasting, complex carbohydrates to prevent rapid blood-sugar dips in the event that one does consume a disproportionately large amount of carbohydrates with a meal

- Monitoring any effects medication may have on symptoms.

Low-carbohydrate diet and/or frequent small split meals is the first treatment of this condition. The first important point is to add small meals at the middle of the morning and of the afternoon, when glycemia would start to decrease. If adequate composition of the meal is found, the fall in blood glucose is thus prevented. Patients should avoid rapidly absorbable sugars and thus avoid popular soft drinks rich in glucose or sucrose. They should also be cautious with drinks associating sugar and alcohol, mainly in the fasting state.

As it is a short-term ailment, a sugar crash does not usually require medical intervention in most people. The most important factors to consider when addressing this issue are the composition and timing of foods.

Acute low blood sugar symptoms are best treated by consuming small amounts of sweet foods, so as to regain balance in the body’s carbohydrate metabolism. Suggestions include sugary foods that are quickly digested, such as:

- Dried fruit

- Soft drinks

- Juice

- Sugar as sweets, tablets or cubes.

If a person cannot receive oral glucose gel or tablets, such as the case with unconsciousness, seizures, or altered mental status, then emergency personnel (EMTs/Paramedics and in-hospital personnel) can establish a peripheral or central IV line and administer a solution containing dextrose and saline. These are normally referred to as Dextrose (Concentration) Water, and come in 5%, 10%, 25% and 50%. Dextrose 5% and 10% come in IV bag and syringe form, and are mainly used in infants and to provide a fluid medium for medications. Dextrose 25% and 50% are heavily necrotic due to their hyperosmolarity, and should only be given through a patent IV line - Any infiltration can cause massive tissue necrosis. CAUTION: Dextrose 25% and 50% can easily cause necrosis in small veins. It is MUCH safer to use a Dextrose 10% solution when treating hypoglycemia via IV in children under the age of 14. When using Dextrose 25% in a child it is safer to administer it through a central line or an intra-oseous line.

Treatment of HHS begins with reestablishing tissue perfusion using intravenous fluids. People with HHS can be dehydrated by 8 to 12 liters. Attempts to correct this usually take place over 24 hours with initial rates of normal saline often in the range of 1 L/h for the first few hours or until the condition stabilizes.

The blood glucose can usually be raised to normal within minutes with 15-20 grams of carbohydrate, although overtreatment should be avoided if at all possible. It can be taken as food or drink if the person is conscious and able to swallow. This amount of carbohydrate is contained in about 3-4 ounces (100-120 mL) of orange, apple, or grape juice, about 4-5 ounces (120-150 mL) of regular (non-diet) soda, about one slice of bread, about 4 crackers, or about 1 serving of most starchy foods. Starch is quickly digested to glucose, but adding fat or protein retards digestion. Composition of the treatment should be considered, as fruit juice is typically higher in fructose which takes the body longer to metabolize than simple dextrose alone. Following treatment, symptoms should begin to improve within 5 to 10 minutes, although full recovery may take 10–20 minutes. It should be noted that over treatment does not speed recovery, and will simply produce hyperglycemia afterwards, which ultimately will need to be corrected. On the other hand, since the excess of insulin over the amount required to normalize blood sugar may continue to reduce blood sugar levels after treatment has produced an initial normalization, continued monitoring is required to determine if further treatment is necessary.

Treatment depends upon the underlying cause:

- Hypoglycaemic diabetic coma: administration of the hormone glucagon to reverse the effects of insulin, or glucose given intravenously.

- Ketoacidotic diabetic coma: intravenous fluids, insulin and administration of potassium and sodium.

- Hyperosmolar diabetic coma: plenty of intravenous fluids, insulin, potassium and sodium given as soon as possible.

The administration of sodium bicarbonate solution to rapidly improve the acid levels in the blood is controversial. There is little evidence that it improves outcomes beyond standard therapy, and indeed some evidence that while it may improve the acidity of the blood, it may actually worsen acidity inside the body's cells and increase the risk of certain complications. Its use is therefore discouraged, although some guidelines recommend it for extreme acidosis (pH<6.9), and smaller amounts for severe acidosis (pH 6.9–7.0).

Cerebral edema, if associated with coma, often necessitates admission to intensive care, artificial ventilation, and close observation. The administration of fluids is slowed. The ideal treatment of cerebral edema in DKA is not established, but intravenous mannitol and hypertonic saline (3%) are used—as in some other forms of cerebral edema—in an attempt to reduce the swelling.

Acute hypoglycemia is reversed by raising the blood glucose. Glucagon should be injected intramuscularly or intravenously, or dextrose can be infused intravenously to raise the blood glucose. Oral administration of glucose can worsen the outcome, as more insulin is eventually produced. Most people recover fully even from severe hypoglycemia after the blood glucose is restored to normal. Recovery time varies from minutes to hours depending on the severity and duration of the hypoglycemia. Death or permanent brain damage resembling stroke can occur rarely as a result of severe hypoglycemia. See hypoglycemia for more on effects, recovery, and risks.

Further therapy and prevention depends upon the specific cause.

Most hypoglycemia due to excessive insulin occurs in people who take insulin for type 1 diabetes. Management of this hypoglycemia is sugar or starch by mouth (or in severe cases, an injection of glucagon or intravenous dextrose). When the glucose has been restored, recovery is usually complete. Prevention of further episodes consists of maintaining balance between insulin, food, and exercise. Management of hypoglycemia due to treatment of type 2 diabetes is similar, and the dose of the oral hypoglycemic agent may need to be reduced. Reversal and prevention of hypoglycemia is a major aspect of the management of type 1 diabetes.

Hypoglycemia due to drug overdose or effect is supported with extra glucose until the drugs have been metabolized. The drug doses or combination often needs to be altered.

Hypoglycemia due to a tumor of the pancreas or elsewhere is usually curable by surgical removal. Most of these tumors are benign. Streptozotocin is a specific beta cell toxin and has been used to treat insulin-producing pancreatic carcinoma.

Hyperinsulinism due to diffuse overactivity of beta cells, such as in many of the forms of congenital hyperinsulinism, and more rarely in adults, can often be treated with diazoxide or a somatostatin analog called octreotide. Diazoxide is given by mouth, octreotide by injection or continuous subcutaneous pump infusion. When congenital hyperinsulinism is due to focal defects of the insulin-secretion mechanism, surgical removal of that part of the pancreas may cure the problem. In more severe cases of persistent congenital hyperinsulinism unresponsive to drugs, a near-total pancreatectomy may be needed to prevent continuing hypoglycemia. Even after pancreatectomy, continuous glucose may be needed in the form of gastric infusion of formula or dextrose.

High dose glucocorticoid is an older treatment used for presumptive transient hyperinsulinism but incurs side effects with prolonged use.

Treatment is typically achieved via diet and exercise, although metformin may be used to reduce insulin levels in some patients (typically where obesity is present). A referral to a dietician is beneficial. Another method used to lower excessively high insulin levels is cinnamon as was demonstrated when supplemented in clinical human trials.

A low carbohydrate diet is particularly effective in reducing hyperinsulinism.

A healthy diet that is low in simple sugars and processed carbohydrates, and high in fiber, and vegetable protein is often recommended. This includes replacing white bread with whole-grain bread, reducing intake of foods composed primarily of starch such as potatoes, and increasing intake of legumes and green vegetables, particularly soy.

Regular monitoring of weight, blood sugar, and insulin are advised, as hyperinsulinemia may develop into diabetes mellitus type 2.

It has been shown in many studies that physical exercise improves insulin sensitivity. The mechanism of exercise on improving insulin sensitivity is not well understood however it is thought that exercise causes the glucose receptor GLUT4 to translocate to the membrane. As more GLUT4 receptors are present on the membrane more glucose is taken up into cells decreasing blood glucose levels which then causes decreased insulin secretion and some alleviation of hyperinsulinemia. Another proposed mechanism of improved insulin sensitivity by exercise is through AMPK activity. The beneficial effect of exercise on hyperinsulinemia was shown in a study by Solomon et al. (2009), where they found that improving fitness through exercise significantly decreases blood insulin concentrations.

Diabetes can be treated but is life-threatening if left alone. Early diagnosis and treatment by a qualified veterinarian can help in preventing nerve damage, and, in rare cases, lead to remission. Cats do best with long-lasting insulin and low carbohydrate diets. Because diabetes is a disease of carbohydrate metabolism, a move to a primarily protein and fat diet reduces the occurrence of hyperglycemia.

Ketosis is deliberately induced by use of a ketogenic diet as a medical intervention in cases of intractable epilepsy. Other uses of low-carbohydrate diets remain controversial. Carbohydrate deprivation to the point of ketosis has been argued to have both negative and positive effects on health.

Oral medications like Glipizide that stimulate the pancreas, promoting insulin release (or in some cases, reduce glucose production), are less and less used in cats, and these drugs may be completely ineffective if the pancreas is not working. These drugs have also been shown in some studies to damage the pancreas further or to cause liver damage. Some owners are reluctant to switch from pills to insulin injections, but the fear is unjustified; the difference in cost and convenience is minor (most cats are easier to inject than to pill), and injections are more effective at treating the disease.

The primary treatment for insulin resistance is exercise and weight loss. Research shows that a low-carbohydrate diet may help. Both metformin and thiazolidinediones improve insulin resistance, but only are approved therapies for type 2 diabetes, not for insulin resistance. By contrast, growth hormone replacement therapy may be associated with increased insulin resistance.

Metformin has become one of the more commonly prescribed medications for insulin resistance. Unfortunately, Metformin also masks Vitamin B12 deficiency, so accompanying sub-lingual Vitamin B12 tablets are recommended.

Insulin resistance is often associated with abnormalities in lipids particularly high blood triglycerides and low high density lipoprotein.

The "Diabetes Prevention Program" (DPP) showed that exercise and diet were nearly twice as effective as metformin at reducing the risk of progressing to type 2 diabetes. However, the participants in the DPP trial regained about 40% of the weight that they had lost at the end of 2.8 years, resulting in a similar incidence of diabetes development in both the lifestyle intervention and the control arms of the trial. One 2009 study found that carbohydrate deficit after exercise, but not energy deficit, contributed to insulin sensitivity increase.

Resistant starch from high-amylose corn, amylomaize, has been shown to reduce insulin resistance in healthy individuals, in individuals with insulin resistance, and in individuals with type 2 diabetes. Animal studies demonstrate that it cannot reverse damage already done by high glucose levels, but that it reduces insulin resistance and reduces the development of further damage.

Some types of polyunsaturated fatty acids (omega-3) may moderate the progression of insulin resistance into type 2 diabetes, however, omega-3 fatty acids appear to have limited ability to reverse insulin resistance, and they cease to be efficacious once type 2 diabetes is established.

Caffeine intake limits insulin action, but not enough to increase blood-sugar levels in healthy persons. People who already have type 2 diabetes may see a small increase in levels if they take 2 or 2-1/2 cups of coffee per day.

The general form of this treatment is an intermediate-acting basal insulin with a regimen of food and insulin every 12 hours, with the insulin injection following the meal. The most commonly used intermediate-acting insulins are NPH, also referred to as isophane, or Caninsulin, also known as Vetsulin, a porcine Lente insulin. While the normal diabetes routine is timed feedings with insulin shots following the meals, dogs unwilling to adhere to this pattern can still attain satisfactory regulation. Most dogs do not require basal/bolus insulin injections; treatment protocol regarding consistency in the diet's calories and composition along with the established feeding and injection times is generally a suitable match for the chosen intermediate-acting insulin.

With Lantus and protamine zinc insulin (PZI) being unreliable in dogs, they are rarely used to treat canine diabetes. Bovine insulin has been used as treatment for some dogs, particularly in the UK. Pfizer Animal Health discontinued of all three types of its veterinary Insuvet bovine insulins in late 2010 and suggested patients be transitioned to Caninsulin. The original owner of the insulin brand, Schering-Plough Animal Health, contracted Wockhardt UK to produce them. Wockhardt UK has produced both bovine and porcine insulins for the human pharmaceutical market for some time.

In theory, avoidance is simply a matter of preventing hyperinsulinemia. In practice, the difficulty for a diabetic person to aggressively dose insulin to keep blood sugars levels close to normal and at the same time constantly adjust the insulin regimen to the dynamic demands of exercise, stress, and wellness can practically assure occasional hyperinsulinemia. The pharmacokinetic imperfections of all insulin replacement regimens is a severe limitation.

Some practical behaviors which are useful in avoiding chronic Somogyi rebound are:

- frequent blood glucose monitoring (8–10 times daily);

- continuous blood glucose monitoring;

- logging and review of blood glucose values, searching for patterns of low blood sugar values;

- conservative increases in insulin delivery;

- awareness to the signs of hypoglycemia;

- awareness to hyperglycemia in response to increased delivery of insulin;

- use of appropriate types of insulin (long-acting, short-acting, etc.) in appropriate amounts.

In terms of treatment, acute hypoglycemia is reversed by raising the blood glucose, but in most forms of congenital hyperinsulinism hypoglycemia recurs and the therapeutic effort is directed toward preventing falls and maintaining a certain glucose level. Some of the following measures are often tried:

Corn starch can be used in feeding; unexpected interruptions of continuous feeding regimens can result in sudden, hypoglycemia, gastrostomy tube insertion (requires a minor surgical procedure) is used for such feeding.Prolonged glucocorticoid use incurs the many unpleasant side effects of Cushing's syndrome, while diazoxide can cause fluid retention requiring concomitant use of a diuretic, and prolonged use causes hypertrichosis. Diazoxide works by opening the K channels of the beta cells. Octreotide must be given by injection several times a day or a subcutaneous pump must be inserted every few days, octreotide can cause abdominal discomfort and responsiveness to octreotide often wanes over time. Glucagon requires continuous intravenous infusion, and has a very short "half life".

Nifedipine is effective only in a minority, and dose is often limited by hypotension.

Pancreatectomy (removal of a portion or nearly all of the pancreas) is usually a treatment of last resort when the simpler medical measures fail to provide prolonged normal blood sugar levels. For some time, the most common surgical procedure was removal of almost all of the pancreas, this cured some infants but not all. Insulin-dependent diabetes mellitus commonly develops, though in many cases it occurs many years after the pancreatectomy.Later it was discovered that a sizeable minority of cases of mutations were focal, involving overproduction of insulin by only a portion of the pancreas. These cases can be cured by removing much less of the pancreas, resulting in excellent outcomes with no long-term problems.

Early diagnosis and interventive treatment can mean reduced incidence of complications such as cataracts and neuropathy. Since dogs are insulin dependent, oral drugs are not effective for them. They must be placed on insulin replacement therapy. Approved oral diabetes drugs can be helpful to sufferers of Type 2 diabetes because they work in one of three ways: by inducing the pancreas to produce more insulin, by allowing the body to more effectively use the insulin it produces, or by slowing the glucose absorption rate from the GI tract. Unapproved so-called "natural" remedies make similar claims for their products. All of this is based on the premise of having an endocrine pancreas with beta cells capable of producing insulin. Those with Type 1, or insulin-dependent diabetes, have beta cells which are permanently damaged, thus unable to produce insulin. This is the reason nothing other than insulin replacement therapy can be considered real and effective treatment. Canine diabetes means insulin dependency; insulin therapy must be continued for life.

The goal is to regulate the pet's blood glucose using insulin and some probable diet and daily routine changes. The process may take a few weeks or many months. It is basically the same as in Type 1 diabetic humans. The aim is to keep the blood glucose values in an acceptable range. The commonly recommended dosing method is by "starting low and going slow" as indicated for people with diabetes.

During the initial process of regulation and periodically thereafter, the effectiveness of the insulin dose at controlling blood glucose needs to be evaluated. This is done by a series of blood glucose tests called a curve. Blood samples are taken and tested at intervals of one to two hours over a 12- or 24-hour period. The results are generally transferred into graph form for easier interpretation. They are compared against the feeding and insulin injection times for judgment. The curve provides information regarding the action of the insulin in the animal. It is used to determine insulin dose adjustments, determine lowest and highest blood glucose levels, discover insulin duration and, in the case of continued hyperglycemia, whether the cause is insufficient insulin dose or Somogyi rebound, where blood glucose levels initially reach hypoglycemic levels and are brought to hyperglycemic ones by the body's counterregulatory hormones. Curves also provide evidence of insulin resistance which may be caused by medications other than insulin or by disorders other than diabetes which further testing can help identify.

Other diagnostic tests to determine the level of diabetic control are fructosamine and glycosylated hemoglobin (GHb) blood tests which can be useful especially if stress may be a factor. While anxiety or stress may influence the results of blood or urine glucose tests, both of these tests measure glycated proteins, which are not affected by them. Fructosamine testing provides information about blood glucose control for an approximate 2- to 4-week period, while GHb tests measure a 2- to 4-month period. Each of these tests has its own limitations and drawbacks and neither are intended to be replacements for blood glucose testing and curves, but are to be used to supplement the information gained from them. While HbA1c tests are a common diagnostic for diabetes in humans, there are no standards of measurement for use of the test in animals. This means the information from them may not be reliable.

The diabetic pet is considered regulated when its blood glucose levels remain within an acceptable range on a regular basis. Acceptable levels for dogs are between 5 and 10 mmol/L or 90 to 180 mg/dL. The range is wider for diabetic animals than non-diabetics, because insulin injections cannot replicate the accuracy of a working pancreas.

In many cases, neonatal diabetes may be treated with oral sulfonylureas such as glyburide. Physicians may order genetic tests to determine whether or not transitioning from insulin to sulfonylurea drugs is appropriate for a patient.

The transfer from insulin injections to oral glibenclamide therapy seems highly effective for most patients and safe. This illuminates how the molecular understanding of some monogenic form of diabetes may lead to an unexpected change of the treatment in children. This is a spectacular example of how the pharmacogenomic approach improves in a tremendous way the quality of life of the young diabetic patients.

Insulin Therapy

- Long Acting Insulin: (Insulin glargine)-is a hormone that works by lowering levels of blood glucose. It starts to work several hours after an injection and keeps working for 24 hours. It is used to manage blood glucose of diabetics. It is used to treat Type 1 and 2 diabetes in adults and Type 1 diabetes in kids as young as 6 years old.

- Short Acting Insulin (e.g. Novolin or Velosulin)-It works similarly to natural insulin and takes up to 30 minutes and lasts for about 8 hours depending on the dosage used.

- Intermediate Insulin: (e.g. NPH insulin)- Usually taken in combination with a short acting insulin. Intermediate acting insulin starts to activate within the first hour of injecting and enters a period of peak activity lasting for 7 hours.

Sulfonylureas

- Sulfonylureas: This medication signals the pancreas to release insulin and help the body's cells use insulin better. This medicaiton can lower A1C levels ( AIC is defined as a measurement of the blood glucose after previous 2–3 months) by 1-2%.

If there is no hypoglycemia at the time of the symptoms, this condition is called "postprandial syndrome." It might be an "adrenergic postprandial syndrome" — blood glucose levels are normal, but the symptoms are caused through autonomic adrenergic counterregulation. Often, this syndrome is associated with emotional distress and anxious behaviour of the patient. This is often seen in dysautonomic disorders as well. Dietary recommendations for reactive hypoglycemia can help to relieve symptoms of postprandial syndrome.

Certain medications increase the risk of hyperglycemia, including corticosteroids, octreotide, beta blockers, epinephrine, thiazide diuretics, niacin, pentamidine, protease inhibitors, L-asparaginase, and some antipsychotic agents. The acute administration of stimulants such as amphetamine typically produces hyperglycemia; chronic use, however, produces hypoglycemia. Some of the newer psychotropic medications, such as Zyprexa (Olanzapine) and Cymbalta (Duloxetine), can also cause significant hyperglycemia.

Thiazides are used to treat type 2 diabetes but it also causes severe hyperglycemia.

There is evidence that prediabetes is a curable disease state. Intensive weight loss and lifestyle intervention, if sustained, may improve glucose tolerance substantially and prevent progression from IGT to type 2 diabetes. The Diabetes Prevention Program (DPP) study found a 16% reduction in diabetes risk for every kilogram of weight loss. Reducing weight by 7% through a low-fat diet and performing 150 minutes of exercise a week is the goal. In observational studies, individuals following vegetarian diets are about half as likely to develop diabetes, compared with non-vegetarians. The ADA guidelines recommend modest weight loss (5–10% body weight), moderate-intensity exercise (30 minutes daily), and smoking cessation.

There are claims in the media that a high-fat, high-protein, low carbohydrates diet can reverse prediabetes, but scientific evidence is not conclusive as to whether this diet has any efficacy.

For patients with severe risk factors, prescription medication may be appropriate. This may be considered in patients for whom lifestyle therapy has failed, or is not sustainable, and who are at high-risk for developing type 2 diabetes. Metformin and acarbose help prevent the development of frank diabetes, and also have a good safety profile. Evidence also supports thiazolidinediones but there are safety concerns, and data on newer agents such as GLP-1 receptor agonists, DPP4 inhibitors or meglitinides are lacking.