"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.

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.

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.

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.

MODY 2 is a form of maturity onset diabetes of the young.

MODY 2 is due to any of several mutations in the "GCK" gene on chromosome 7 for glucokinase. Glucokinase serves as the glucose sensor for the pancreatic beta cell. Normal glucokinase triggers insulin secretion as the glucose exceeds about 90 mg/dl (5 mM). These loss-of-function mutations result in a glucokinase molecule that is less sensitive or less responsive to rising levels of glucose. The beta cells in MODY 2 have a normal ability to make and secrete insulin, but do so only above an abnormally high threshold (e.g., 126–144 mg/dl, or 7-8 mM). This produces a chronic, mild increase in blood sugar, which is usually asymptomatic. It is usually detected by accidental discovery of mildly elevated blood sugar (e.g., during pregnancy screening). An oral glucose tolerance test is much less abnormal than would be expected from the impaired (elevated) fasting blood sugar, since insulin secretion is usually normal once the glucose has exceeded the threshold for that specific variant of the glucokinase enzyme.

The degree of blood sugar elevation does not worsen rapidly with age, and long-term diabetic complications are rare. In healthy children and adults, a high blood sugar level can be avoided by a healthy diet and exercise, primarily avoiding large amounts of carbohydrates. However, as people who have MODY2 enter their 50's and 60's, even though they continue to eat a healthy diet and exercise, they sometimes are unable to control a high blood sugar level with these measures. In these cases, many medicines for type II diabetes mellitus are not effective, because MODY2 does not cause insulin resistance. Repaglinide (Prandin) can help the body regulate the amount of glucose in the blood by stimulating the pancreas to release insulin before meals. In some cases, the baseline glucose levels are too high as well and insulin is required.

MODY2 is an autosomal dominant condition. Autosomal dominance refers to a single, abnormal gene on one of the first 22 nonsex chromosomes from either parent which can cause an autosomal disorder. Dominant inheritance means an abnormal gene from one parent is capable of causing disease, even though the matching gene from the other parent is normal. The abnormal gene "dominates" the pair of genes. If just one parent has a dominant gene defect, each child has a 50% chance of inheriting the disorder.

This type of MODY demonstrates the common circulation but complex interplay between maternal and fetal metabolism and hormone signals in the determination of fetal size. A small number of infants will have a new mutation not present in their mothers. If the mother is affected and the fetus is not, the maternal glucose will be somewhat high and the normal pancreas of the fetus will generate more insulin to compensate, resulting in a large infant. If the fetus is affected but mother is not, glucoses will be normal and fetal insulin production will be low, resulting in intrauterine growth retardation. Finally, if both mother and fetus have the disease, the two defects will offset each other and fetal size will be unaffected.

When both "GCK" genes are affected the diabetes appears earlier and the hyperglycemia is more severe. A form of permanent neonatal diabetes has been caused by homozygous mutations in the GCK gene.

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.

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.

MODY 3 is a form of maturity onset diabetes of the young.

MODY 3 (also known as HNF1A-MODY) is caused by mutations of the HNF1-alpha; gene, a homeobox gene on chromosome 12. This is the most common type of MODY in populations with European ancestry, accounting for about 70% of all cases in Europe. HNF1α is a transcription factor (also known as transcription factor 1, TCF1) that is thought to control a regulatory network (including, among other genes, HNF1α) important for differentiation of beta cells. Mutations of this gene lead to reduced beta cell mass or impaired function. MODY 1 and MODY 3 diabetes are clinically similar. About 70% of people develop this type of diabetes by age 25 years, but it occurs at much later ages in a few. This type of diabetes can often be treated with sulfonylureas with excellent results for decades. However, the loss of insulin secretory capacity is slowly progressive and most eventually need insulin.

This is the form of MODY which can most resemble ordinary type 1 diabetes, and one of the incentives for diagnosing it is that insulin may be discontinued or deferred in favor of oral sulfonylureas. Some people treated with insulin for years due to a presumption of type 1 diabetes have been able to switch to pills and discontinue injections. Long-term diabetic complications can occur if the glucose is not adequately controlled.

High-sensitivity measurements of CRP may help to distinguish between HNF1A-MODY and other forms of diabetes

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).

MODY 1 is a form of maturity onset diabetes of the young.

MODY 1 is due to a loss-of-function mutation in the gene on chromosome 20. This gene codes for HNF4-α protein also known as transcription factor 14 (TCF14). HNF4α controls function of HNF1α (see MODY 3; ) and perhaps HNF1β (MODY 5) as well. This transcription network plays a role in the early development of the pancreas, liver, and intestines. In the pancreas these genes influence expression of, among others, the genes for insulin, the principal glucose transporter (GLUT2), and several proteins involved in glucose and mitochondrial metabolism.

Although pancreatic beta cells produce adequate insulin in infancy, the capacity for insulin production declines thereafter. Diabetes (persistent hyperglycemia) typically develops by early adult years, but may not appear until later decades. The degree of insulin deficiency is slowly progressive. Many patients with MODY 1 are treated with sulfonylureas for years before insulin is required.

Liver effects are subtle and not clinically significant. Many people with this condition have low levels of triglycerides, lipoprotein(a), apolipoproteins AII and CIII.

Mutations in the alternative promoter of HNF4A are linked to development of type 2 diabetes.

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.

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

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

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

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.

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.

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.

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.

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.

Possible causes include:

- Neoplasm

- Pancreatic cancer

- Polycystic ovary syndrome (PCOS)

- Trans fats

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.

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.

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.