The degree of hyperglycemia can change over time depending on the metabolic cause, for example, impaired glucose tolerance or fasting glucose, and it can depend on treatment. Temporary hyperglycemia is often benign and asymptomatic. Blood glucose levels can rise well above normal and cause pathological and functional changes for significant periods without producing any permanent effects or symptoms. During this asymptomatic period, an abnormality in carbohydrate metabolism can occur which can be tested by measuring plasma glucose. However, chronic hyperglycemia at above normal levels can produce a very wide variety of serious complications over a period of years, including kidney damage, neurological damage, cardiovascular damage, damage to the retina or damage to feet and legs. Diabetic neuropathy may be a result of long-term hyperglycemia. Impairment of growth and susceptibility to certain infection can occur as a result of chronic hyperglycemia.

Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). It is most often seen in persons who have uncontrolled insulin-dependent diabetes.

The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad:

- Polyphagia – frequent hunger, especially pronounced hunger

- Polydipsia – frequent thirst, especially excessive thirst

- Polyuria – increased volume of urination (not an increased frequency for urination)

- Blurred vision

- Fatigue

- Restlessness

- Weight loss

- Poor wound healing (cuts, scrapes, etc.)

- Dry mouth

- Dry or itchy skin

- Tingling in feet or heels

- Erectile dysfunction

- Recurrent infections, external ear infections (swimmer's ear)

- Cardiac arrhythmia

- Stupor

- Coma

- Seizures

Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response. This hunger is not usually as pronounced as in Type I diabetes, especially the juvenile onset form, but it makes the prescription of oral hypoglycemic medication difficult to manage.

Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys, which leads to the presence of glucose in the urine. This produces an osmotic diuresis.

Signs and symptoms of diabetic ketoacidosis may include:

- Ketoacidosis

- Kussmaul hyperventilation: deep, rapid breathing

- Confusion or a decreased level of consciousness

- Dehydration due to glycosuria and osmotic diuresis

- Acute hunger and/or thirst

- 'Fruity' smelling breath odor

- Impairment of cognitive function, along with increased sadness and anxiety

Hyperglycemia caused a decrease in cognitive performance, specifically in processing speed, and executive function and performance. Decreased cognitive performance may cause forgetfulness and concentration loss

Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.

- Shakiness, anxiety, nervousness

- Palpitations, tachycardia

- Sweating, feeling of warmth (sympathetic muscarinic rather than adrenergic)

- Pallor, coldness, clamminess

- Dilated pupils (mydriasis)

- Hunger, borborygmus

- Nausea, vomiting, abdominal discomfort

- Headache

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms, if symptoms even occur. Specific manifestations may also vary by age, by severity of the hypoglycemia and the speed of the decline. In young children, vomiting can sometimes accompany morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person may be similar from episode to episode, but are not necessarily so and may be influenced by the speed at which glucose levels are dropping, as well as previous incidents.

In newborns, hypoglycemia can produce irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating, hypothermia, somnolence, hypotonia, refusal to feed, and seizures or "spells." Hypoglycemia can resemble asphyxia, hypocalcemia, sepsis, or heart failure.

In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed "hypoglycemia unawareness" and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.

Hypoglycemic symptoms can also occur when one is sleeping. Examples of symptoms during sleep can include damp bed sheets or clothes from perspiration. Having nightmares or the act of crying out can be a sign of hypoglycemia. Once the individual is awake they may feel tired, irritable, or confused and these may be signs of hypoglycemia as well.

In nearly all cases, hypoglycemia that is severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.

Research in healthy adults shows that mental efficiency declines slightly but measurably as blood glucose falls below 3.6 mM (65 mg/dL). Hormonal defense mechanisms (adrenaline and glucagon) are normally activated as it drops below a threshold level (about 55 mg/dL (3.0 mM) for most people), producing the typical hypoglycemic symptoms of shakiness and dysphoria. Obvious impairment may not occur until the glucose falls below 40 mg/dL (2.2 mM), and many healthy people may occasionally have glucose levels below 65 in the morning without apparent effects. Since the brain effects of hypoglycemia, termed neuroglycopenia, determine whether a given low glucose is a "problem" for that person, most doctors use the term "hypoglycemia" only when a moderately low glucose level is accompanied by symptoms or brain effects.

Determining the presence of both parts of this definition is not always straightforward, as hypoglycemic symptoms and effects are vague and can be produced by other conditions; people with recurrently low glucose levels can lose their threshold symptoms so that severe neuroglycopenic impairment can occur without much warning, and many measurement methods (especially glucose meters) are imprecise at low levels.

It may take longer to recover from severe hypoglycemia with unconsciousness or seizure even after restoration of normal blood glucose. When a person has not been unconscious, failure of carbohydrate to reverse the symptoms in 10–15 minutes increases the likelihood that hypoglycemia was not the cause of the symptoms. When severe hypoglycemia has persisted in a hospitalized person, the amount of glucose required to maintain satisfactory blood glucose levels becomes an important clue to the underlying etiology. Glucose requirements above 10 mg/kg/minute in infants, or 6 mg/kg/minute in children and adults are strong evidence for hyperinsulinism. In this context this is referred to as the "glucose infusion rate" (GIR). Finally, the blood glucose response to glucagon given when the glucose is low can also help distinguish among various types of hypoglycemia. A rise of blood glucose by more than 30 mg/dl (1.70 mmol/l) suggests insulin excess as the probable cause of the hypoglycemia.

In untreated hyperglycemia, a condition called ketoacidosis may develop because decreased insulin levels increase the activity of hormone sensitive lipase. The degradation of triacylglycerides by hormone-sensitive lipase produces free fatty acids that are eventually converted to acetyl-coA by beta-oxidation.

Ketoacidosis is a life-threatening condition which requires immediate treatment. Symptoms include: shortness of breath, breath that smells fruity (such as pear drops), nausea and vomiting, and very dry mouth.

Chronic hyperglycemia (high blood sugar) injures the heart in patients without a history of heart disease or diabetes and is strongly associated with heart attacks and death in subjects with no coronary heart disease or history of heart failure.

Also, life-threatening consequences of hyperglycemia is nonketotic hyperosmolar syndrome.

Diabetic hypoglycemia can be mild, recognized easily by the patient, and reversed with a small amount of carbohydrates eaten or drunk, or it may be severe enough to cause unconsciousness requiring intravenous dextrose or an injection of glucagon. Severe hypoglycemic unconsciousness is one form of diabetic coma. A common medical definition of severe hypoglycemia is "hypoglycemia severe enough that the person needs assistance in dealing with it". A co-morbidity is the issue of hypoglycemia unawareness. Recent research using machine learning methods have proved to be successful in predicting such severe hypoglycemia episodes.

Symptoms of diabetic hypoglycemia, when they occur, are those of hypoglycemia: neuroglycopenic, adrenergic, and abdominal. Symptoms and effects can be mild, moderate or severe, depending on how low the glucose falls and a variety of other factors. It is rare but possible for diabetic hypoglycemia to result in brain damage or death. Indeed, an estimated 2-4% of deaths of people with type 1 diabetes mellitus have been attributed to hypoglycemia.

In North America a mild episode of diabetic hypoglycemia is sometimes termed a "low" or an "insulin reaction," and in Europe a "hypo", although all of these terms are occasionally used interchangeably in North America, Europe, Australia and New Zealand. A severe episode is sometimes also referred to as "insulin shock".

In a counter-intuitive manifestation, hypoglycemia can trigger a Somogyi effect, resulting in a rebounding high blood sugar or hyperglycemia.

Symptoms vary according to individuals' hydration level and sensitivity to the rate and/or magnitude of decline of their blood glucose concentration.

A crash is usually felt within four hours or less of heavy carbohydrate consumption. Symptoms of reactive hypoglycemia include:

- double vision or blurry vision

- unclear thinking

- insomnia

- heart palpitation or fibrillation

- fatigue

- dizziness

- light-headedness

- sweating

- headaches

- depression

- nervousness

- muscle twitches

- irritability

- tremors

- flushing

- craving sweets

- increased appetite

- rhinitis

- nausea, vomiting

- panic attack

- numbness/coldness in the extremities

- confusion

- irrationality

- bad temper

- paleness

- cold hands

- disorientation

- the need to sleep or 'crash'

- coma can be a result in severe untreated episodes

The majority of these symptoms, often correlated with feelings of hunger, mimic the effect of inadequate sugar intake as the biology of a crash is similar in itself to the body’s response to low blood sugar levels following periods of glucose deficiency.

A commonly used "number" to define the lower limit of normal glucose is 70 mg/dl (3.9 mmol/l), though in someone with diabetes, hypoglycemic symptoms can sometimes occur at higher glucose levels, or may fail to occur at lower. Some textbooks for nursing and pre-hospital care use the range 80 mg/dl to 120 mg/dl (4.4 mmol/l to 6.7 mmol/l). This variability is further compounded by the imprecision of glucose meter measurements at low levels, or the ability of glucose levels to change rapidly.

The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels). In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as "Kussmaul respiration"). The abdomen may be tender to the point that an acute abdomen may be suspected, such as acute pancreatitis, appendicitis or gastrointestinal perforation. Coffee ground vomiting (vomiting of altered blood) occurs in a minority of people; this tends to originate from erosion of the esophagus. In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness).

On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, tachycardia (a fast heart rate) and low blood pressure may be observed. Often, a "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. If Kussmaul respiration is present, this is reflected in an increased respiratory rate.

Small children with DKA are relatively prone to cerebral edema (swelling of the brain tissue), which may cause headache, coma, loss of the pupillary light reflex, and progress to death. It occurs in 0.3–1.0% of children with DKA, and has been described in young adults, but is overall very rare in adults. It carries a 20–50% mortality.

Oxyhyperglycemia is a special type of impaired glucose tolerance characterized by a rapid and transient hyperglycemia (i.e. rise in blood glucose) spike after an oral intake of glucose, the peak of this spike being high enough to cause transient, symptom free glycosuria (i.e. detectable glucose in urine), but this hyperglycemia reverses rapidly and may even go to hypoglycemia in the later phase. This sharp downstroke overshooting towards hypoglycemia distinguishes this pathologic phenomenon from the artificial hyperglycemia inducible by an intravenous bolus dose of a large amount of glucose solution. Early dumping syndrome patients usually have oxyhyperglycemia associated with any meal or OGTT.

The Greek root "oxy" means "sharp" or "pointy". The OGTT curve in this condition appears sharp and somewhat pointy (at least relative to the other forms of hyperglycemia)- hence this name.

Dorlands dictionary defines oxyhyperglycemia as:

A blood level of approximately 180 mg/dL is the renal glucose threshold below which all glucose is reabsorbed from glomerular filtrate. But at blood concentrations above the renal threshold sugar starts appearing in the urine.

Oxyhyperglycemia, like other forms of Impaired glucose tolerance has also been suggested to be a prediabetic condition

Manifestations of hyperinsulinemic hypoglycemia vary by age and severity of the hypoglycemia. In general, most signs and symptoms can be attributed to (1) the effects on the brain of insufficient glucose (neuroglycopenia) or (2) to the adrenergic response of the autonomic nervous system to hypoglycemia. A few miscellaneous symptoms are harder to attribute to either of these causes. In most cases, all effects are reversed when normal glucose levels are restored.

There are uncommon cases of more persistent harm, and rarely even death due to severe hypoglycemia of this type. One reason hypoglycemia due to excessive insulin can be more dangerous is that insulin lowers the available amounts of most alternate brain fuels, such as ketones. Brain damage of various types ranging from stroke-like focal effects to impaired memory and thinking can occur. Children who have prolonged or recurrent hyperinsulinemic hypoglycemia in infancy can suffer harm to their brains and may be developmentally delayed.

There are often no visible symptoms of hyperinsulinemia unless hypoglycaemia (low blood sugar) is present.

Some patients may experience a variety of symptoms when hypoglycaemia is present, including:

- Temporary muscle weakness

- Brain fog

- Fatigue

- Temporary thought disorder, or inability to concentrate

- Visual problems such as blurred vision or double vision

- Headaches

- Shaking/Trembling

- Thirst

If a person experiences any of these symptoms, a visit to a qualified medical practitioner is advised, and diagnostic blood testing may be required.

Ketotic hypoglycemia more commonly refers to a common but mysterious "disease" of recurrent hypoglycemic symptoms with ketosis in young children. The cause and the homogeneity of the condition remain uncertain, but a characteristic presentation, precipitating factors, diagnostic test results, treatment, and natural history can be described. It remains one of the more common causes of hypoglycemia in the age range.

There are several genetic forms of hyperinsulinemic hypoglycemia:

Cats will generally show a gradual onset of the disease over a few weeks or months, and it may escape notice for even longer.

The first outward symptoms are a sudden weight loss (or occasionally gain), accompanied by excessive drinking and urination; for example, cats can appear to develop an obsession with water and lurk around faucets or water bowls. Appetite is suddenly either ravenous (up to three-times normal) or absent. These symptoms arise from the body being unable to use glucose as an energy source.

A fasting glucose blood test will normally be suggestive of diabetes at this point. The same home blood test monitors used in humans are used on cats, usually by obtaining blood from the ear edges or paw pads. As the disease progresses, ketone bodies will be present in the urine, which can be detected with the same urine strips as in humans.

In the final stages, the cat starts wasting and the body will breaking down its own fat and muscle to survive. Lethargy or limpness, and acetone-smelling breath are acute symptoms of ketoacidosis and/or dehydration and is a medical emergency.

Untreated, diabetes leads to coma and then death.

The typical patient with ketotic hypoglycemia is a young child between the ages of 10 months and 4 years. Episodes nearly always occur in the morning after an overnight fast, often one that is longer than usual. Symptoms include those of neuroglycopenia, ketosis, or both. The neuroglycopenic symptoms usually include lethargy and malaise, but may include unresponsiveness or seizures. The principal symptoms of ketosis are anorexia, abdominal discomfort, and nausea, sometimes progressing to vomiting.

If severe, parents usually take the child to a local emergency department, where blood is drawn. The glucose is usually found to be between 35 and 60 mg/dl (1.8-3.1 mMol/L). The total CO is usually somewhat low as well, (14-19 mMol/L is typical), and if urine is obtained, high levels of ketones are discovered. Ketones can also be measured in the blood at the bedside (Medisense glucometer). Other routine tests are normal. If given intravenous fluids with saline and dextrose, the child improves dramatically and is usually restored to normal health within a few hours. These symptoms are normally seen because of the child being unadapted to using fat as energy, typically when the child's daily glucose intake might be too high (more than 50g/day for a child). This is also associated with fluctuant glycemia throughout the day.

A first episode is usually attributed to a viral infection or acute gastroenteritis. However, in most of these children one or more additional episodes recur over next few years and become immediately recognizable to the parents. In mild cases, carbohydrates and a few hours of sleep will be enough to end the symptoms. Thus said, the required amount of carbohydrate intake of a child, as well as for an adult is close to 0, because the liver can supply the required glucose quantity needed for the body through gluconeogenesis.

Precipitating factors, conditions that trigger an episode, may include extended fasting (e.g., missing supper the night before), a low carbohydrate intake the previous day (e.g., a hot dog without a bun), or stress such as a viral infection. Most children affected by ketotic hypoglycemia have a slender build, many with a weight percentile below height percentile, though without other evidence of malnutrition. Overweight children are rarely affected.

Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within 4 hours after a high carbohydrate meal in people who do not have diabetes.

The condition is related to homeostatic systems utilised by the body to control blood sugar levels. It is variously described as a sense of tiredness, lethargy, irritation, or hangover, although the effects can be less if one has undertaken a lot of physical activity within the next few hours after consumption.

The alleged mechanism for the feeling of a crash is correlated with an abnormally rapid rise in blood glucose after eating. This normally leads to insulin secretion (known as an "insulin spike"), which in turn initiates rapid glucose uptake by tissues either accumulating it as glycogen or utilizing it for energy production. The consequent fall in blood glucose is indicated as the reason for the "sugar crash".. A deeper cause might be hysteresis effect of insulin action, i.e., the effect of insulin is still prominent even if both plasma glucose and insulin levels were already low, causing a plasma glucose level eventually much lower than the baseline level.

Sugar crashes are not to be confused with the after-effects of consuming large amounts of "protein", which produces fatigue akin to a sugar crash, but are instead the result of the body prioritising the digestion of ingested food.

The prevalence of this condition is difficult to ascertain because a number of stricter or looser definitions have been used. It is recommended that the term reactive hypoglycemia be reserved for the pattern of postprandial hypoglycemia which meets the Whipple criteria (symptoms correspond to measurably low glucose and are relieved by raising the glucose), and that the term idiopathic postprandial syndrome be used for similar patterns of symptoms where abnormally low glucose levels at the time of symptoms cannot be documented.

To assist diagnosis, a doctor can order an HbA1c test, which measures the blood sugar average over the two or three months before the test. The more specific 6-hour glucose tolerance test can be used to chart changes in the patient's blood sugar levels before ingestion of a special glucose drink and at regular intervals during the six hours following to see if an unusual rise or drop in blood glucose levels occurs.

According to the U.S. National Institute of Health (NIH), a blood glucose level below 70 mg/dL (3.9 mmol/L) at the time of symptoms followed by relief after eating confirms a diagnosis for reactive hypoglycemia.

Oxyhyperglycemia is most commonly caused by early dumping syndrome, but it can rarely caused by other conditions like Graves' disease. It was first described by Lawrence et al. in 1936 as often happening after gastroenterostomy. It is seen in most forms of gastrectomy, gastric bypass and gastrostomy procedures, all of which are surgical causes of dumping syndrome.

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes.

DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.

The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.

Rates of DKA vary around the world. In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost universally fatal. The risk of death with adequate and timely treatment is currently around 1–4%. Up to 1% of children with DKA develop a complication known as cerebral edema.

Hyperinsulinism due to reduced insulin sensitivity is usually asymptomatic. In contrast, hyperinsulinemic hypoglycemia can produce any of the entire range of hypoglycemic symptoms, from shakiness and weakness, to seizures or coma.

Diabetic ketoacidosis (DKA), if it progresses and worsens without treatment, can eventually cause unconsciousness, from a combination of a very high blood sugar level, dehydration and shock, and exhaustion. Coma only occurs at an advanced stage, usually after 36 hours or more of worsening vomiting and hyperventilation.

In the early to middle stages of ketoacidosis, patients are typically flushed and breathing rapidly and deeply, but visible dehydration, pale appearance from diminished perfusion, shallower breathing, and a fast heart rate are often present when coma is reached. However these features are variable and not always as described.

If the patient is known to have diabetes, the diagnosis of DKA is usually suspected from the appearance and a history of 1–2 days of vomiting. The diagnosis is confirmed when the usual blood chemistries in the emergency department reveal a high blood sugar level and severe metabolic acidosis.

Treatment of DKA consists of isotonic fluids to rapidly stabilize the circulation, continued intravenous saline with potassium and other electrolytes to replace deficits, insulin to reverse the ketoacidosis, and careful monitoring for complications.

Chronic Somogyi rebound is a contested explanation of phenomena of elevated blood sugars in the morning. Also called the Somogyi effect and posthypoglycemic hyperglycemia, it is a rebounding high blood sugar that is a response to low blood sugar. When managing the blood glucose level with insulin injections, this effect is counter-intuitive to insulin users who experience high blood sugar in the morning as a result of an overabundance of insulin at night.

This theoretical phenomenon was named after Michael Somogyi, a Hungarian-born professor of biochemistry at the Washington University and Jewish Hospital of St. Louis, who prepared the first insulin treatment given to a child with diabetes in the USA in October 1922. Somogyi showed that excessive insulin makes diabetes unstable and first published his findings in 1938.

Compare with the dawn phenomenon, which is a morning rise in blood sugar in response to waning insulin and a growth hormone surge (that further antagonizes insulin).

People with type 1 diabetes mellitus who must take insulin in full replacement doses are most vulnerable to episodes of hypoglycemia. It is usually mild enough to reverse by eating or drinking carbohydrates, but blood glucose occasionally can fall fast enough and low enough to produce unconsciousness before hypoglycemia can be recognized and reversed. Hypoglycemia can be severe enough to cause unconsciousness during sleep. Predisposing factors can include eating less than usual or prolonged exercise earlier in the day. Some people with diabetes can lose their ability to recognize the symptoms of early hypoglycemia.

Unconsciousness due to hypoglycemia can occur within 20 minutes to an hour after early symptoms and is not usually preceded by other illness or symptoms. Twitching or convulsions may occur. A person unconscious from hypoglycemia is usually pale, has a rapid heart beat, and is soaked in sweat: all signs of the adrenaline response to hypoglycemia. The individual is not usually dehydrated and breathing is normal or shallow. Their blood sugar level, measured by a glucose meter or laboratory measurement at the time of discovery, is usually low but not always severely, and in some cases may have already risen from the nadir that triggered the unconsciousness.

Unconsciousness due to hypoglycemia is treated by raising the blood glucose with intravenous glucose or injected glucagon.

Too little insulin over time can cause tissue starvation (as glucose can't reach the brain or body). In combination with dehydration, fasting, infection, or other body stresses, this can turn over a few hours into diabetic ketoacidosis, a medical emergency with a high fatality rate, that cannot be treated at home. Many undiagnosed diabetic cats first come to the vet in this state, since they haven't been receiving insulin. Symptoms include lethargy, acetone or fruity smell on breath, shortness of breath, high blood sugar, huge thirst drive. Emergency care includes fluid therapy, insulin, management of presenting symptoms and 24-hour hospitalization.

Although many factors influence insulin secretion, the most important control is the amount of glucose moving from the blood into the beta cells of the pancreas. In healthy people, even small rises in blood glucose result in increased insulin secretion. As long as the pancreatic beta cells are able to sense the glucose level and produce insulin, the amount of insulin secreted is usually the amount required to maintain a fasting blood glucose between 70 and 100 mg/dL (3.9-5.6 mmol/L) and a non-fasting glucose level below 140 mg/dL (<7.8 mmol/L).

When liver cells and other cells that remove glucose from the blood become less sensitive (more resistant) to the insulin, the pancreas increases secretion and the level of insulin in the blood rises. This increased secretion can compensate for reduced sensitivity for many years, with maintenance of normal glucose levels. However, if insulin resistance worsens or insulin secretion ability declines, the glucose levels will begin to rise. Persistent elevation of glucose levels is termed diabetes mellitus.

Typical fasting insulin levels found in this type of hyperinsulinism are above 20 μU/mL. When resistance is severe, levels can exceed 100 μU/mL.

In addition to being a risk factor for type 2 diabetes, hyperinsulinism due to insulin resistance may increase blood pressure and contribute to hypertension by direct action on vascular endothelial cells (the cells lining blood vessels). Hyperinsulinism has also been implicated as a contributing factor in the excessive production of androgens in polycystic ovary syndrome.

The principal treatments of hyperinsulinism due to insulin resistance are measures that improve insulin sensitivity, such as weight loss, physical exercise, and drugs such as thiazolidinediones or metformin.

A person with type 1 diabetes should balance insulin delivery to manage their blood glucose level. Occasionally, insufficient insulin can result in hyperglycemia. The appropriate response is to take a correction dose of insulin to reduce the blood sugar level and to consider adjusting the insulin regimen to deliver additional insulin in the future to prevent hyperglycemia. Conversely, excessive insulin delivery may result in hypoglycemia. The appropriate response is to treat the hypoglycemia and to consider adjusting the regimen to reduce insulin in the future.

Somogyi and others have claimed that if prolonged hypoglycemia is untreated, then stress due to low blood sugar can result in a high blood glucose rebound. The physiological mechanisms driving the rebound are defensive. When the blood glucose level falls below normal, the body responds by releasing the endocrine hormone glucagon as well as the stress hormones epinephrine, cortisol and growth hormone. Glucagon facilitates release of glucose from the liver that raises the blood glucose immediately, and the stress hormones cause insulin resistance for several hours, sustaining the elevated blood sugar.