Impaired fasting glucose is often without any signs or symptoms, other than higher than normal glucose levels being detected in an individual's fasting blood sample. There may be signs and symptoms associated with elevated blood glucose, though these are likely to be minor, with significant symptoms suggestive of complete progression to type 2 diabetes. Such symptoms include:

- Increased thirst

- Increased urination, especially waking up in the night to urinate

- Tiredness and fatigue

- Blurred vision

- Slow healing of wounds

- Altered sensation, such as numbness or tingling, particularly of the hands and feet

- Recurrent, and difficult to clear infections, particularly of the urinary tract

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.

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

Prediabetes typically has no distinct signs or symptoms except the sole sign of high blood sugar. Patients should monitor for signs and symptoms of type 2 diabetes mellitus. These include the following:

- Constant hunger

- Unexplained weight loss

- Weight gain

- Flu-like symptoms, including weakness and fatigue

- Blurred vision

- Slow healing of cuts or bruises

- Tingling or loss of feeling in hands or feet

- Recurring gum or skin infections

- Recurring vaginal or bladder infections

- A high BMI (Body Mass Index) result

As impaired fasting glucose is considered a precursor condition for type 2 diabetes, it shares the same environmental and genetic risk factors.

Impaired glucose tolerance (IGT) is a pre-diabetic state of dysglycemia, that is associated with insulin resistance and increased risk of cardiovascular pathology. IGT may precede type 2 diabetes mellitus by many years. IGT is also a risk factor for mortality.

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.

Hyperinsulinemic hypoglycemia describes the condition and effects of low blood glucose caused by excessive insulin. Hypoglycemia due to excess insulin is the most common type of serious hypoglycemia. It can be due to endogenous or injected insulin.

These depend on poorly understood variations in individual biology and consequently may not be found with all people diagnosed with insulin resistance.

- Increased hunger

- Lethargy (tiredness)

- Brain fogginess and inability to focus

- High blood sugar

- Weight gain, fat storage, difficulty losing weight – for most people, excess weight is from high subcutaneous fat storage; the fat in IR is generally stored in and around abdominal organs in both males and females; it is currently suspected that hormones produced in that fat are a precipitating cause of insulin resistance

- Increased blood cholesterol levels

- Increased blood pressure; many people with hypertension are either diabetic or pre-diabetic and have elevated insulin levels due to insulin resistance; one of insulin's effects is to control arterial wall tension throughout the body

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.

According to the criteria of the World Health Organization and the American Diabetes Association, impaired glucose tolerance is defined as:

- two-hour glucose levels of 140 to 199 mg per dL (7.8 to 11.0 mmol/l) on the 75-g oral glucose tolerance test. A patient is said to be under the condition of IGT when he/she has an intermediately raised glucose level after 2 hours, but less than the level that would qualify for type 2 diabetes mellitus. The fasting glucose may be either normal or mildly elevated.

From 10 to 15 percent of adults in the United States have impaired glucose tolerance or impaired fasting glucose.

Possible causes include:

- Neoplasm

- Pancreatic cancer

- Polycystic ovary syndrome (PCOS)

- Trans fats

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.

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

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.

Impaired glucose tolerance (IGT) is a pre-diabetic state of hyperglycemia that is associated with insulin resistance and increased risk of cardiovascular pathology. IGT may precede type 2 diabetes mellitus by many years. IGT is also a risk factor for mortality.

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.

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

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.

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.

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.

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.

Insulin resistance (IR) is a pathological condition in which cells fail to respond normally to the hormone insulin. The body produces insulin when glucose starts to be released into the bloodstream from the digestion of carbohydrates in the diet. Normally this insulin response triggers glucose being taken into body cells, to be used for energy, and inhibits the body from using fat for energy. The concentration of glucose in the blood decreases as a result, staying within the normal range even when a large amount of carbohydrates is consumed. When the body produces insulin under conditions of insulin resistance, the cells are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level. This often remains undetected and can contribute to the development of type 2 diabetes or latent autoimmune diabetes of adults. Although this type of chronic insulin resistance is harmful, during acute illness it is actually a well-evolved protective mechanism. Recent investigations have revealed that insulin resistance helps to conserve the brain's glucose supply by preventing muscles from taking up excessive glucose. In theory, insulin resistance should even be strengthened under harsh metabolic conditions such as pregnancy, during which the expanding fetal brain demands more glucose.

People who develop type 2 diabetes usually pass through earlier stages of insulin resistance and prediabetes, although those often go undiagnosed. Insulin resistance is a syndrome (a set of signs and symptoms) resulting from reduced insulin activity; it is also part of a larger constellation of symptoms called the metabolic syndrome.

Insulin resistance may also develop in patients who have recently experienced abdominal or bariatric procedures. This acute form of insulin resistance that may result post-operatively tends to increase over the short term, with sensitivity to insulin typically returning to patients after about five days.

Some of the subtypes of Glycogen storage disease show ketotic hypoglycemia after fasting periods. Especially Glycogen storage disease type IX can be a common cause for ketotic hypoglycemia, with the most common sub-type IXa mainly affecting boys.

Diabetic coma is a medical emergency in which a person with diabetes mellitus is comatose (unconscious) because of one of the acute complications of diabetes:

1. Severe diabetic hypoglycemia

2. Diabetic ketoacidosis advanced enough to result in unconsciousness from a combination of severe hyperglycemia, dehydration and shock, and exhaustion

3. Hyperosmolar nonketotic coma in which extreme hyperglycemia and dehydration alone are sufficient to cause unconsciousness.