In non-diabetic persons, ketonuria may occur during acute illness or severe stress. Approximately 15% of hospitalized patients may have ketonuria, even though they do not have diabetes. In a diabetic patient, ketone bodies in the urine suggest that the patient is not adequately controlled and that adjustments of medication, diet, or both should be made promptly. In the non diabetic patient, ketonuria reflects a reduced carbohydrate metabolism and an increased fat metabolism.

Screening for ketonuria is done frequently for acutely ill patients, presurgical patients, and pregnant women. Any diabetic patient who has elevated levels of blood and urine glucose should be tested for urinary ketones. In addition, when diabetic treatment is being switched from insulin to oral hypoglycemic agents, the patient's urine should be monitored for ketonuria. The development of ketonuria within 24 hours after insulin withdrawal usually indicates a poor response to the oral hypoglycemic agents. Diabetic patients should have their urine tested regularly for glucose and ketones, particularly when acute infection or other illness develops.

In conditions associated with acidosis, urinary ketones are tested to assess the severity of acidosis and to monitor treatment response. Urine ketones appear before there is any significant increase in blood ketones; therefore, urine ketone measurement is especially helpful in emergency situations.

In dairy cattle, ketosis is a common ailment that usually occurs during the first weeks after giving birth to a calf. Ketosis is in these cases sometimes referred to as "acetonemia". A study from 2011 revealed that whether ketosis is developed or not depends on the lipids a cow uses to create butterfat. Animals prone to ketosis mobilize fatty acids from adipose tissue, while robust animals create fatty acids from blood phosphatidylcholine (lecithin). Healthy animals can be recognized by high levels of milk glycerophosphocholine and low levels of milk phosphocholine. Point of care diagnostic tests are available and are reasonably useful.

In sheep, ketosis, evidenced by hyperketonemia with beta-hydroxybutyrate in blood over 0.7 mmol/L, occurs in pregnancy toxemia. This may develop in late pregnancy in ewes bearing multiple fetuses, and is associated with the considerable glucose demands of the conceptuses. In ruminants, because most glucose in the digestive tract is metabolized by rumen organisms, glucose must be supplied by gluconeogenesis, for which propionate (produced by rumen bacteria and absorbed across the rumen wall) is normally the principal substrate in sheep, with other gluconeogenic substrates increasing in importance when glucose demand is high or propionate is limited. Pregnancy toxemia is most likely to occur in late pregnancy because most fetal growth (and hence most glucose demand) occurs in the final weeks of gestation; it may be triggered by insufficient feed energy intake (anorexia due to weather conditions, stress or other causes), necessitating reliance on hydrolysis of stored triglyceride, with the glycerol moiety being used in gluconeogenesis and the fatty acid moieties being subject to oxidation, producing ketone bodies. Among ewes with pregnancy toxemia, beta-hydroxybutyrate in blood tends to be higher in those that die than in survivors. Prompt recovery may occur with natural parturition, Caesarean section or induced abortion. Prevention (through appropriate feeding and other management) is more effective than treatment of advanced stages of ovine ketosis.

Some clinicians regard eliminating carbohydrates as unhealthy and dangerous. However, it is not necessary to eliminate carbohydrates from the diet completely to achieve ketosis. Other clinicians regard ketosis as a safe biochemical process that occurs during the fat-burning state. Ketosis, which is accompanied by gluconeogenesis (the creation of glucose de novo from pyruvate), is the specific state that concerns some clinicians. However, it is unlikely for a normally functioning person to reach life-threatening levels of ketosis, defined as serum beta-hydroxybutyrate (B-OHB) levels above 15 millimolar (mM) compared to ketogenic diets among non diabetics, which "rarely run serum B-OHB levels above 3 mM." This is avoided with proper basal secretion of pancreatic insulin. People who are unable to secrete basal insulin, such as type 1 diabetics and long-term type II diabetics, are liable to enter an unsafe level of ketosis, eventually resulting in a coma that requires emergency medical treatment. The anti-ketosis conclusions have been challenged by a number of doctors and advocates of low-carbohydrate diets, who dispute assertions that the body has a preference for glucose and that there are dangers associated with ketosis.

The main risk factor is a history of diabetes mellitus type 2. Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1. Triggers include infections, stroke, trauma, certain medications, and heart attacks.

Other risk factors:

- Lack of sufficient insulin (but enough to prevent ketosis)

- Poor kidney function

- Poor fluid intake (dehydration)

- Older age (50–70 years)

- Certain medical conditions (cerebral vascular injury, myocardial infarction, sepsis)

- Some medications (glucocorticoids, beta-blockers, thiazide diuretics, calcium channel blockers, phenytoin)

HHS is usually precipitated by an infection, myocardial infarction, stroke or another acute illness. A relative insulin deficiency leads to a serum glucose that is usually higher than 33 mmol/L (600 mg/dL), and a resulting serum osmolarity that is greater than 320 mOsm. This leads to excessive urination (more specifically an osmotic diuresis), which, in turn, leads to volume depletion and hemoconcentration that causes a further increase in blood glucose level. Ketosis is absent because the presence of some insulin inhibits hormone-sensitive lipase mediated fat tissue breakdown.

Succinyl-CoA:3-oxoacid CoA transferase deficiency (SCOT deficiency) is an inborn error of ketone body utilization. Succinyl-CoA:3-oxoacid CoA transferase catalyzes the transfer of coenzyme A from succinyl-coenzyme A to acetoacetate. It can be caused by mutation in the "OXCT1" gene.

First described in 1972, more than 30 people have been reported in the medical literature with this inborn error of metabolism. They experience attacks of ketoacidosis during illness, and even when unwell may have elevated levels of ketone bodies in blood and urine (ketonemia and ketonuria, respectively). Not all people with SCOT deficiency have persistent ketonemia and ketonuria, particularly those with milder defects of enzyme activity.

If a person with Type 1 diabetes who has diabulimia suffers from the disease for more than a short time—usually due to alternating phases during which insulin is injected properly, and relapses, during which they have diabulimia—then the following longer-term symptoms can be expected:

- Severe kidney damage - high blood sugar can overwork the kidneys, eventually leading to kidney failure and the need for a kidney transplant

- Severe neuropathy (nerve damage to hands and feet)

- Extreme fatigue

- Edema (during blood sugars controlled phases)

- Heart problems

- High cholesterol

- Osteoporosis

- Death

Often, people with Type 1 diabetes who omit insulin injections will have already been diagnosed with an eating disorder such as anorexia nervosa, bulimia nervosa These individuals are often not aware that diabulimia is more common than they think and is also very difficult to overcome. Unlike anorexia and bulimia, diabulimia sometimes requires the afflicted individual to stop caring for a medical condition. Unlike vomiting or starving, there is sometimes no clear action or willpower involved. Diabulimia may be more appealing to individuals who want to lose weight.

Many articles and studies further conclude that diabetic females have, on average, higher body mass index (BMI) than do their nondiabetic counterparts. Girls and young adult woman with higher BMIs are also shown to be more likely to have disordered eating behavior (DEB). Many authoritative articles have been published which show that preteen and teenage girls with Type 1 diabetes have significantly higher rates of eating disorders of all types than do girls without diabetes. This condition can be triggered or exacerbated by the need for diabetics to exercise constant vigilance in regard to food, weight and glycemic control. In adolescent females, increased weight gain that insulin treatment can cause may play roles in the increased risk for onset of anorexia and/or bulimia.

There are no specific guidelines for the treatment of diabetes and disordered eating, but the standard approach for treatment of two complex conditions as multidisciplinary team of professionals which in this case could include an endocrinologist, psychiatrist, psychologist, dietician, etc.