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

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.

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

The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss. Other symptoms that are commonly present at diagnosis include a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, and fatigue. Many people, however, have no symptoms during the first few years and are diagnosed on routine testing. A small number of people with type 2 diabetes mellitus can develop a hyperosmolar hyperglycemic state (a condition of very high blood sugar associated with a decreased level of consciousness and low blood pressure).

Low blood sugar is common in persons with type 1 and type 2 DM. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious issues such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases. Moderate hypoglycemia may easily be mistaken for drunkenness; rapid breathing and sweating, cold, pale skin are characteristic of hypoglycemia but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.

People (usually with type 1 DM) may also experience episodes of diabetic ketoacidosis, a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness.

A rare but equally severe possibility is hyperosmolar hyperglycemic state, which is more common in type 2 DM and is mainly the result of dehydration.

The classic symptoms of untreated diabetes are weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 DM, while they usually develop much more slowly and may be subtle or absent in type 2 DM.

Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known ones above, they include blurry vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.

The classical symptoms of type 1 diabetes include: polyuria (excessive urination), polydipsia (increased thirst), dry mouth, polyphagia (increased hunger), fatigue, and weight loss.

Many type 1 diabetics are diagnosed when they present with diabetic ketoacidosis. The signs and symptoms of diabetic ketoacidosis include dry skin, rapid deep breathing, drowsiness, increased thirst, frequent urination, abdominal pain, and vomiting.

About 12 percent of people with type 1 diabetes have clinical depression.

About 6 percent of people with type 1 diabetes have celiac disease, but in most cases there are no digestive symptoms or are mistakenly attributed to poor control of diabetes, gastroparesis or diabetic neuropathy. In most cases, celiac disease is diagnosed after onset of type 1 diabetes. The association of celiac disease with type 1 diabetes increases the risk of complications, such as retinopathy and mortality. This association can be explained by shared genetic factors, and inflammation or nutritional deficiencies caused by untreated celiac disease, even if type 1 diabetes is diagnosed first.

Some people with type 1 diabetes experience dramatic and recurrent swings in glucose levels, often occurring for no apparent reason; this is called "unstable diabetes" or "labile diabetes", and sometimes "brittle diabetes", although this term is no longer used. The results of such swings can be irregular and unpredictable hyperglycemias, sometimes involving ketoacidosis, and sometimes serious hypoglycemias. Brittle diabetes occurs no more frequently than in 1% to 2% of diabetics.

Impaired fasting glucose, or Impaired Fasting "Glycemia" (IFG) is a type of prediabetes, in which a person's blood sugar levels during fasting are consistently above the normal range, but below the diagnostic cut-off for a formal diagnosis of diabetes mellitus. Together with impaired glucose tolerance, it is a sign of insulin resistance. In this manner, it is also one of the conditions associated with Metabolic Syndrome.

Those with impaired fasting glucose are at an increased risk of vascular complications of diabetes, though to a lesser extent. The risks are cumulative, with both higher blood glucose levels, and the total amount of time it spends elevated, increasing the overall complication rate.

IFG can eventually progress to type 2 diabetes mellitus without intervention, which typically involves lifestyle modification. Those with impaired fasting glucose have a 1.5 fold increased risk of developing clinical diabetes within 10 years, when compared to the general population. Some studies suggest that without lifestyle changes, IFG will progress to clinically diagnosable diabetes in just under 3 years, on average.

Impaired fasting glucose is often, though not always, associated with impaired glucose tolerance, though it may occur in isolation, with such persons having a normal response to a glucose tolerance test.

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.

Type 2 diabetes is typically a chronic disease associated with a ten-year-shorter life expectancy. This is partly due to a number of complications with which it is associated, including: two to four times the risk of cardiovascular disease, including ischemic heart disease and stroke; a 20-fold increase in lower limb amputations, and increased rates of hospitalizations. In the developed world, and increasingly elsewhere, type 2 diabetes is the largest cause of nontraumatic blindness and kidney failure. It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia. Other complications include acanthosis nigricans, sexual dysfunction, and frequent infections.

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.

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.

The following characteristics suggest the possibility of a diagnosis of MODY in hyperglycemic and diabetic patients:

- Mild to moderate hyperglycemia (typically 130–250 mg/dl, or 7–14 mmol/l) discovered before 30 years of age. However, anyone under 50 can develop MODY.

- A first-degree relative with a similar degree of diabetes.

- Absence of positive antibodies or other autoimmunity (e.g., thyroiditis) in patient and family. However, Urbanova et al. found that about one quarter of Central European MODY patients are positive for islet cell autoantibodies (GADA and IA2A). Their expression is transient but highly prevalent. The autoantibodies were found in patients with delayed diabetes onset, and in times of insufficient diabetes control. The islet cell autoantibodies are absent in MODY in at least some populations (Japanese, Britons).

- Persistence of a low insulin requirement (e.g., less than 0.5 u/kg/day) past the usual "honeymoon" period.

- Absence of obesity (although overweight or obese people can get MODY) or other problems associated with type 2 diabetes or metabolic syndrome (e.g., hypertension, hyperlipidemia, polycystic ovary syndrome).

- Insulin resistance very rarely happens.

- Cystic kidney disease in patient or close relatives.

- Non-transient neonatal diabetes, or apparent type 1 diabetes with onset before six months of age.

- Liver adenoma or hepatocellular carcinoma in MODY type 3

- Renal cysts, rudimentary or bicornuate uterus, vaginal aplasia, absence of the vas deferens, epidymal cysts in MODY type 5

The diagnosis of MODY is confirmed by specific gene testing available through commercial laboratories.

The symptoms of latent autoimmune diabetes of adults are similar to those of other forms of diabetes: polydipsia (excessive thirst and drinking), polyuria (excessive urination), and often blurred vision. Compared to juvenile type 1 diabetes, the symptoms develop comparatively slowly, over a period of at least six months.

Currently, MODY is the final diagnosis in 1%–2% of people initially diagnosed with diabetes. The prevalence is 70–110 per million population. 50% of first-degree relatives will inherit the same mutation, giving them a greater than 95% lifetime risk of developing MODY themselves. For this reason, correct diagnosis of this condition is important. Typically patients present with a strong family history of diabetes (any type) and the onset of symptoms is in the second to fifth decade.

There are two general types of clinical presentation.

- Some forms of MODY produce significant hyperglycemia and the typical signs and symptoms of diabetes: increased thirst and urination (polydipsia and polyuria).

- In contrast, many people with MODY have no signs or symptoms and are diagnosed either by accident, when a high glucose is discovered during testing for other reasons, or screening of relatives of a person discovered to have diabetes. Discovery of mild hyperglycemia during a routine glucose tolerance test for pregnancy is particularly characteristic.

MODY cases may make up as many as 5% of presumed type 1 and type 2 diabetes cases in a large clinic population. While the goals of diabetes management are the same no matter what type, there are two primary advantages of confirming a diagnosis of MODY.

- Insulin may not be necessary and it may be possible to switch a person from insulin injections to oral agents without loss of glycemic control.

- It may prompt screening of relatives and so help identify other cases in family members.

As it occurs infrequently, many cases of MODY are initially assumed to be more common forms of diabetes: type 1 if the patient is young and not overweight, type 2 if the patient is overweight, or gestational diabetes if the patient is pregnant. Standard diabetes treatments (insulin for type 1 and gestational diabetes, and oral hypoglycemic agents for type 2) are often initiated before the doctor suspects a more unusual form of diabetes.

"Common symptoms of NDM includes:"

- Thirst and Frequent Urination

An excessive thirst (also known as polydipsia) and increased urination (also known as polyuria) are common signs of diabetes. An individual with diabetes, have accumulated blood glucose. Their kidneys are working overtime to filter and uptake excess sugar. However, their kidneys cannot keep up, excess sugar is excreted into their urine, and this drag along fluids from the diabetic's tissues. This may lead to more frequent urination and lead to dehydration. As a diabetic individual drinks more fluids to satisfy their thirst, he or she urinates even more.

- Dehydration

Effected areas of the body are the eyes, mouth, kidneys, heart, and pancreas. Other symptoms of dehydration includes headache, thirst and dry mouth, dizziness, tiredness, and dark colored urine. In severe cases of dehydration in diabetics, low blood pressure, sunken eyes, a weak pulse or rapid heart beat, feeling confused or fatigue. Dehydration and high blood glucose for extended period of time, the diabetic's kidney would try to filter the blood of access glucose and excrete this as urine. As the kidneys are filtering the blood, water is being removed from the blood and would need to be replaced. This leads to an increased thirst when the blood glucose is elevated in a diabetic individual. Water is needed to re-hydrate the body. Therefore, the body would take available from other parts of the body, such as saliva, tears, and from cells of the body. If access water is not available, the body would not be able to pass excess glucose out of the blood by urine and can lead to further dehydration.

"Severe symptoms of NDM (Deficiency of insulin):"

- Ketoacidosis

Is a diabetic complication that occurs when the body produces high levels of acid in the blood (ketones). This effects the pancreas, fat cells, and kidneys. This condition occurs when the body cannot produce enough insulin. In the absence or lack of insulin, the body of an diabetic individual will break down fat as fuel. This process produces a buildup of acids in the bloodstream known as ketones, in which leads to ketoacidosis if left untreated. The symptoms of ketoacidosis develop rapidly or within 24 hours. Symptoms of ketoacidosis are excessive thirst, frequent urination, nausea or vomiting, stomach pain, tiredness, shortness or fruity smell on breath and confusion.

- Intrauterine Growth Restriction

A condition in which the unborn baby is smaller than he or she should be, due to the fact he or she not growing at a normal rate in the womb. Delayed growth puts the baby at risk of certain problems during pregnancy, delivery, and after birth. The problems are as follows: baby's birth weight is 90% less than normal weight, difficulty handling vaginal delivery, decreased oxygen levels, hypoglycemia (low blood glucose), low resistance to infection, low Apgar scores (a test given after birth to test the baby's physical condition and evaluate if special medical care is needed), Meconium aspiration (inhaling of stools passed while in the uterus) which causes breathing issues, irregular body temperature and high red blood cell count.

- Hyperglycemia

A condition characterized as high blood glucose, which occurs when the body has too little insulin or when the body cannot use insulin properly. Hyperglycemia affects the pancreas, kidneys, and body's tissues. Characterization of hyperglycemia is high blood glucose, high levels of sugar in the urine, frequent urination and increase thirst.

- Hypoglycemia

A condition characterized an extremely low blood glucose, usually less than 70 mg/dL. Areas of the body that are affected, pancreas, kidneys, and mental state.

Diabetes mellitus type 1 (also known as type 1 diabetes) is a form of diabetes mellitus in which not enough insulin is produced. This results in high blood sugar levels in the body. The classical symptoms are frequent urination, increased thirst, increased hunger, and weight loss. Additional symptoms may include blurry vision, feeling tired, and poor healing. Symptoms typically develop over a short period of time.

The cause of type 1 diabetes is unknown. However, it is believed to involve a combination of genetic and environmental factors. Risk factors include having a family member with the condition. The underlying mechanism involves an autoimmune destruction of the insulin-producing beta cells in the pancreas. Diabetes is diagnosed by testing the level of sugar or A1C in the blood. Type 1 diabetes can be distinguished from type 2 by testing for the presence of autoantibodies.

There is no known way to prevent type 1 diabetes. Treatment with insulin is required for survival. Insulin therapy is usually given by injection just under the skin but can also be delivered by an insulin pump. A diabetic diet and exercise are an important part of management. Untreated, diabetes can cause many complications. Complications of relatively rapid onset include diabetic ketoacidosis and nonketotic hyperosmolar coma. Long-term complications include heart disease, stroke, kidney failure, foot ulcers and damage to the eyes. Furthermore, complications may arise from low blood sugar caused by excessive dosing of insulin.

Type 1 diabetes makes up an estimated 5–10% of all diabetes cases. The number of people affected globally is unknown, although it is estimated that about 80,000 children develop the disease each year. Within the United States the number of people affected is estimated at one to three million. Rates of disease vary widely with approximately 1 new case per 100,000 per year in East Asia and Latin America and around 30 new cases per 100,000 per year in Scandinavia and Kuwait. It typically begins in children and young adults.

It is estimated that more than 50% of persons diagnosed as having non-obesity-related type 2 diabetes may actually have LADA. Glutamic acid decarboxylase autoantibody (GADA), islet cell autoantibody (ICA), insulinoma-associated (IA-2) autoantibody, and zinc transporter autoantibody (ZnT8) testing should be performed on all adults who are not obese who are diagnosed with diabetes. However, some overweight patients are misdiagnosed with type 2 due to their weight. Moreover, it is now becoming evident that autoimmune diabetes may be highly underdiagnosed in many individuals who have diabetes, and that the body mass index levels may have rather limited use in connections with latent autoimmune diabetes.

Persons with LADA typically have low, although sometimes moderate, levels of C-peptide as the disease progresses. Those with insulin resistance or type 2 diabetes are more likely to have high levels of C-peptide due to an over production of insulin.

Hypoglycemia, or abnormally low blood glucose, is an acute complication of several diabetes treatments. It is rare otherwise, either in diabetic or non-diabetic patients. The patient may become agitated, sweaty, weak, and have many symptoms of sympathetic activation of the autonomic nervous system resulting in feelings akin to dread and immobilized panic. Consciousness can be altered or even lost in extreme cases, leading to coma, seizures, or even brain damage and death. In patients with diabetes, this may be caused by several factors, such as too much or incorrectly timed insulin, too much or incorrectly timed exercise (exercise decreases insulin requirements) or not enough food (specifically glucose containing carbohydrates). The variety of interactions makes cause identification difficult in many instances.

It is more accurate to note that iatrogenic hypoglycemia is typically the result of the interplay of absolute (or relative) insulin excess and compromised glucose counterregulation in type 1 and advanced type 2 diabetes. Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine are the primary glucose counterregulatory factors that normally prevent or (more or less rapidly) correct hypoglycemia. In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephrine responses causes defective glucose counterregulation.

Furthermore, reduced sympathoadrenal responses can cause hypoglycemia unawareness. The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent incidents of hypoglycemia causes both defective glucose counterregulation and hypoglycemia unawareness. By shifting glycemic thresholds for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose concentrations, antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further impairment of glucose counterregulation. In many cases (but not all), short-term avoidance of hypoglycemia reverses hypoglycemia unawareness in affected patients, although this is easier in theory than in clinical experience.

In most cases, hypoglycemia is treated with sugary drinks or food. In severe cases, an injection of glucagon (a hormone with effects largely opposite to those of insulin) or an intravenous infusion of dextrose is used for treatment, but usually only if the person is unconscious. In any given incident, glucagon will only work once as it uses stored liver glycogen as a glucose source; in the absence of such stores, glucagon is largely ineffective. In hospitals, intravenous dextrose is often used.

Gestational diabetes is formally defined as "any degree of glucose intolerance with onset or first recognition during pregnancy". This definition acknowledges the possibility that a woman may have previously undiagnosed diabetes mellitus, or may have developed diabetes coincidentally with pregnancy. Whether symptoms subside after pregnancy is also irrelevant to the diagnosis.

A woman is diagnosed with gestational diabetes when glucose intolerance continues beyond 24–28 weeks of gestation.

The White classification, named after Priscilla White, who pioneered research on the effect of diabetes types on perinatal outcome, is widely used to assess maternal and fetal risk. It distinguishes between gestational diabetes (type A) and pregestational diabetes (diabetes that existed prior to pregnancy). These two groups are further subdivided according to their associated risks and management.

The two subtypes of gestational diabetes under this classification system are:

- Type A1: abnormal oral glucose tolerance test (OGTT), but normal blood glucose levels during fasting and two hours after meals; diet modification is sufficient to control glucose levels

- Type A2: abnormal OGTT compounded by abnormal glucose levels during fasting and/or after meals; additional therapy with insulin or other medications is required

Diabetes which existed prior to pregnancy is also split up into several subtypes under this system:

- Type B: onset at age 20 or older and duration of less than 10 years.

- Type C: onset at age 10–19 or duration of 10–19 years.

- Type D: onset before age 10 or duration greater than 20 years.

- Type E: overt diabetes mellitus with calcified pelvic vessels.

- Type F: diabetic nephropathy.

- Type R: proliferative retinopathy.

- Type RF: retinopathy and nephropathy.

- Type H: ischemic heart disease.

- Type T: prior kidney transplant.

An early age of onset or long-standing disease comes with greater risks, hence the first three subtypes.

Two other sets of criteria are available for diagnosis of gestational diabetes, both based on blood-sugar levels.

Criteria for diagnosis of gestational diabetes, using the 100 gram Glucose Tolerance Test, according to Carpenter and Coustan:

- Fasting 95 mg/dl

- 1 hour 180 mg/dl

- 2 hours 155 mg/dl

- 3 hours 140 mg/dl

Criteria for diagnosis of gestational diabetes according to National Diabetes Data Group:

- Fasting 105 mg/dl

- 1 hour 190 mg/dl

- 2 hours 165 mg/dl

- 3 hours 145 mg/dl

Diabetes mellitus is a disease in which the beta cells of the endocrine pancreas either stop producing insulin or can no longer produce it in enough quantity for the body's needs. The condition is commonly divided into two types, depending on the origin of the condition: Type 1 diabetes, sometimes called "juvenile diabetes", is caused by destruction of the beta cells of the pancreas. The condition is also referred to as insulin-dependent diabetes, meaning exogenous insulin injections must replace the insulin the pancreas is no longer capable of producing for the body's needs. Dogs can have insulin-dependent, or Type 1, diabetes; research finds no Type 2 diabetes in dogs. Because of this, there is no possibility the permanently damaged pancreatic beta cells could re-activate to engender a remission as may be possible with some feline diabetes cases, where the primary type of diabetes is Type 2. There is another less common form of diabetes, diabetes insipidus, which is a condition of insufficient antidiuretic hormone or resistance to it.

This most common form of diabetes affects approximately 0.34% of dogs. The condition is treatable and need not shorten the animal's life span or interfere with quality of life. If left untreated, the condition can lead to cataracts, increasing weakness in the legs (neuropathy), malnutrition, ketoacidosis, dehydration, and death. Diabetes mainly affects middle-age and older dogs, but there are juvenile cases. The typical canine diabetes patient is middle-age, female, and overweight at diagnosis.

The number of dogs diagnosed with diabetes mellitus has increased three-fold in thirty years. In survival rates from almost the same time, only 50% survived the first 60 days after diagnosis and went on to be successfully treated at home. Currently, diabetic dogs receiving treatment have the same expected lifespan as non-diabetic dogs of the same age and gender.

The main symptoms which occur in nearly all dogs with diabetes mellitus are:

- excessive water consumption, known as polydipsia,

- frequent and/or excessive urination, known as polyuria, often requiring the dog to be let outside to urinate during the night,

- greater than average appetite, known as polyphagia,

- weight loss.

Sometimes, the first sign of diabetes noticed by the owner may be that their dog either has become blind (due to the formation of cataracts in the eyes), or has vomiting, anorexia, lethargy and weakness (due to ketoacidosis).

The diagnostic criteria for steroid diabetes are those of diabetes (fasting glucoses persistently above 125 mg/dl (7 mM) or random levels above 200 mg/dl (11 mM)) occurring in the context of high-dose glucocorticoid therapy. Insulin levels are usually detectable, and sometimes elevated, but inadequate to control the glucose. In extreme cases the hyperglycemia may be severe enough to cause nonketotic hyperosmolar coma.

Steroid diabetes (also "steroid-induced diabetes") is a medical term referring to prolonged hyperglycemia due to glucocorticoid therapy for another medical condition. It is usually, but not always, a transient condition.

Neonatal diabetes mellitus (NDM) is defined as a disease that affects an infant and their body's ability to produce or use insulin. NDM is a monogenic (controlled by a single gene) form of diabetes that occurs in the first 6 months of life. Infants do not produce enough insulin, leading to an increase in . It is a rare disease, occurring in only one in 100,000 to 500,000 live births. NDM can be mistaken for the much more common type 1 diabetes, but type 1 diabetes usually occurs later than the first 6 months of life. There are two types of NDM: permanent neonatal diabetes mellitus (PNDM) is a lifelong condition. Transient neonatal diabetes mellitus (TNDM) is diabetes that disappears during the infant stage but may reappear later in life.

Specific genes that can cause NDM have been identified. The onset of NDM can be caused by abnormal pancreatic development, beta cell dysfunction or accelerated beta cell dysfunction. Individuals with monogenic diabetes can pass it on to their children or future generations. Each gene associated with NDM has a different inheritance pattern.