The most common cause of hypoglycemia is medications used to treat diabetes mellitus such as insulin, sulfonylureas, and biguanides. Risk is greater in diabetics who have eaten less than usual, exercised more than usual, or drunk alcohol. Other causes of hypoglycemia include kidney failure, certain tumors, liver disease, hypothyroidism, starvation, inborn errors of metabolism, severe infections, reactive hypoglycemia, and a number of drugs including alcohol. Low blood sugar may occur in babies who are otherwise healthy who have not eaten for a few hours. Inborn errors of metabolism may include the lack of an enzyme to make glycogen (glycogen storage type 0).

Significant hypoglycemia appears to increase the risk of cardiovascular disease.

Since hyperinsulinemia and obesity are so closely linked it is hard to determine whether hyperinsulinemia causes obesity or obesity causes hyperinsulinemia, or both.

Obesity is characterized by an excess of adipose tissue – insulin increases the synthesis of fatty acids from glucose, facilitates the entry of glucose into adipocytes and inhibits breakdown of fat in adipocytes.

On the other hand, adipose tissue is known to secrete various metabolites, hormones and cytokines that may play a role in causing hyperinsulinemia. Specifically cytokines secreted by adipose tissue directly affect the insulin signalling cascade, and thus insulin secretion. Adiponectins are cytokines that are inversely related to percent body fat; that is people with a low body fat will have higher concentrations of adiponectins where as people with high body fat will have lower concentrations of adiponectins. Weyer "et al." (2011) reported that hyperinsulinemia is strongly associated with low adiponectin concentrations in obese people, though whether low adiponectin has a causal role in hyperinsulinemia remains to be established.

- May lead to hypoglycemia or diabetes

- Increased risk of PCOS

- Increased synthesis of VLDL (hypertriglyceridemia)

- Hypertension (insulin increases sodium retention by the renal tubules)

- Coronary Artery Disease (increased insulin damages endothelial cells)

- Increased risk of cardiovascular disease

- Weight gain and lethargy (possibly connected to an underactive thyroid)

Possible causes include:

- Neoplasm

- Pancreatic cancer

- Polycystic ovary syndrome (PCOS)

- Trans fats

In fructose bisphosphatase deficiency, there is not enough fructose bisphosphatase for gluconeogenesis to occur correctly. Glycolysis (the breakdown of glucose) will still work, as it does not use this enzyme.

Without effective gluconeogenesis (GNG), hypoglycaemia will set in after about 12 hours of fasting. This is the time when liver glycogen stores have been exhausted, and the body has to rely on GNG. When given a dose of glucagon (which would normally increase blood glucose) nothing will happen, as stores are depleted and GNG doesn't work. (In fact, the patient would already have high glucagon levels.)

There is no problem with the metabolism of glucose or galactose, but fructose and glycerol cannot be used by the liver to maintain blood glucose levels. If fructose or glycerol are given, there will be a buildup of phosphorylated three-carbon sugars. This leads to phosphate depletion within the cells, and also in the blood. Without phosphate, ATP cannot be made, and many cell processes cannot occur.

High levels of glucagon will tend to release fatty acids from adipose tissue, and this will combine with glycerol that cannot be used in the liver, to make triacylglycerides causing a fatty liver.

As three carbon molecules cannot be used to make glucose, they will instead be made into pyruvate and lactate. These acids cause a drop in the pH of the blood (a metabolic acidosis). Acetyl CoA (acetyl co-enzyme A) will also build up, leading to the creation of ketone bodies.

In some forms of MODY, standard treatment is appropriate, though exceptions occur:

- In MODY2, oral agents are relatively ineffective and insulin is unnecessary.

- In MODY1 and MODY3, insulin may be more effective than drugs to increase insulin sensitivity.

- Sulfonylureas are effective in the K channel forms of neonatal-onset diabetes. The mouse model of MODY diabetes suggested that the reduced clearance of sulfonylureas stands behind their therapeutic success in human MODY patients, but Urbanova et al. found that human MODY patients respond differently to the mouse model and that there was no consistent decrease in the clearance of sulfonylureas in randomly selected HNF1A-MODY and HNF4A-MODY patients.

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.

A broad classification for genetic disorders that result from an inability of the body to produce or utilize one enzyme that is required to oxidize fatty acids. The enzyme can be missing or improperly constructed, resulting in it not working. This leaves the body unable to produce energy within the liver and muscles from fatty acid sources.

The body's primary source of energy is glucose; however, when all the glucose in the body has been expended, a normal body digests fats. Individuals with a fatty-acid metabolism disorder are unable to metabolize this fat source for energy, halting bodily processes. Most individuals with a fatty-acid metabolism disorder are able to live a normal active life with simple adjustments to diet and medications.

If left undiagnosed many complications can arise. When in need of glucose the body of a person with a fatty-acid metabolism disorder will still send fats to the liver. The fats are broken down to fatty acids. The fatty acids are then transported to the target cells but are unable to be broken down, resulting in a build-up of fatty acids in the liver and other internal organs.

Fatty-acid metabolism disorders are sometimes classified with the lipid metabolism disorders, but in other contexts they are considered a distinct category.

The term fatty acid oxidation disorder (FAOD) is sometimes used, especially when there is an emphasis on the oxidation of the fatty acid.

In addition to the fetal complications, they can also cause complications for the mother during pregnancy.

Examples include:

- trifunctional protein deficiency

- MCADD, LCHADD, and VLCADD

In sheep, intrauterine growth restriction can be caused by heat stress in early to mid pregnancy. The effect is attributed to reduced placental development causing reduced fetal growth. Hormonal effects appear implicated in the reduced placental development. Although early reduction of placental development is not accompanied by concurrent reduction of fetal growth; it tends to limit fetal growth later in gestation. Normally, ovine placental mass increases until about day 70 of gestation, but high demand on the placenta for fetal growth occurs later. (For example, research results suggest that a normal average singleton Suffolk x Targhee sheep fetus has a mass of about 0.15 kg at day 70, and growth rates of about 31 g/day at day 80, 129 g/day at day 120 and 199 g/day at day 140 of gestation, reaching a mass of about 6.21 kg at day 140, a few days before parturition.)

In adolescent ewes (i.e. ewe hoggets), overfeeding during pregnancy can also cause intrauterine growth restriction, by altering nutrient partitioning between dam and conceptus. Fetal growth restriction in adolescent ewes overnourished during early to mid pregnancy is not avoided by switching to lower nutrient intake after day 90 of gestation; whereas such switching at day 50 does result in greater placental growth and enhanced pregnancy outcome. Practical implications include the importance of estimating a threshold for "overnutrition" in management of pregnant ewe hoggets. In a study of Romney and Coopworth ewe hoggets bred to Perendale rams, feeding to approximate a conceptus-free live mass gain of 0.15 kg/day (i.e. in addition to conceptus mass), commencing 13 days after the midpoint of a synchronized breeding period, yielded no reduction in lamb birth mass, where compared with feeding treatments yielding conceptus-free live mass gains of about 0 and 0.075 kg/day.

In both of the above models of IUGR in sheep, the absolute magnitude of uterine blood flow is reduced. Evidence of substantial reduction of placental glucose transport capacity has been observed in pregnant ewes that had been heat-stressed during placental development.

Maple syrup urine disease (MSUD) is a rare, inherited metabolic disorder. Its prevalence in the United States population is approximately 1 newborn out of 180,000 live births. However, in populations where there is a higher frequency of consanguinity, such as the Mennonites in Pennsylvania or the Amish, the frequency of MSUD is significantly higher at 1 newborn out of 176 live births. In Austria, 1 newborn out of 250,000 live births inherits MSUD. It also is believed to have a higher prevalence in certain populations due in part to the founder effect since MSUD has a much higher prevalence in children of Amish, Mennonite, and Jewish descent.

Control of metabolism is vital during pregnancy of women with MSUD. To prevent detrimental abnormalities in development of the embryo or fetus, dietary adjustments should be made and plasma amino acid concentrations of the mother should be observed carefully and frequently. Amino acid deficiency can be detected through fetal growth, making it essential to monitor development closely.

The prognosis is very poor. Two studies reported typical age of deaths in infancy or early childhood, with the first reporting a median age of death of 2.6 for boys and less than 1 month for girls.

Seizures in cats are caused by various onsets. Cats can have reactive, primary (idiopathic) or secondary seizures. Idiopathic seizures are not as common in cats as in dogs however a recent study conducted showed that of 91 feline seizures, 25% were suspected to have idiopathic epilepsy. In the same group of 91 cats, 50% were secondary seizures and 20% reactive.

Idiopathic epilepsy does not have a classification due to the fact there are no known causes of these seizures, however both reactive and symptomatic secondary epilepsy can be placed into classifications.

IUGR affects 3-10% of pregnancies. 20% of stillborn infants have IUGR. Perinatal mortality rates are 4-8 times higher for infants with IUGR, and morbidity is present in 50% of surviving infants.

According to the theory of thrifty phenotype, intrauterine growth restriction triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment rich in food it may be more prone to metabolic disorders, such as obesity and type II diabetes.

Historically mortality has been high, being in excess of 80%. In recent years the advent of liver transplantation and multidisciplinary intensive care support have improved survival significantly. At present overall short-term survival with transplant is more than 65%.

Several prognostic scoring systems have been devised to predict mortality and to identify who will require an early liver transplant. These include King's College Hospital criteria, MELD score, APACHE II, and Clichy criteria.

Response to treatment is variable and the long-term and functional outcome is unknown. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation and outcome of these diseases their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies a patient registry was established by the noncommercial International Working Group on Neurotransmitter Related Disorders (iNTD).

Glycogen storage disease type XI is a form of glycogen storage disease. It is also known as "Fanconi–Bickel syndrome", for Guido Fanconi and Horst Bickel, who first described it in 1949.

It is associated with GLUT2, a glucose transport protein which, when functioning normally, allows glucose to exit several tissues, including the liver, nephrons, and enterocytes of the intestines, and enter the blood. The syndrome results in hepatomegaly secondary to glycogen accumulation, glucose and galactose intolerance, fasting hypoglycaemia, a characteristic proximal tubular nephropathy and severe short stature.

Panayiotopoulos syndrome is probably genetically determined, though conventional genetic influences may be less important than other mechanisms. Usually, there is no family history of similar seizures, although siblings with Panayiotopoulos syndrome or Panayiotopoulos syndrome and rolandic epilepsy or, less common, Panayiotopoulos syndrome and idiopathic childhood occipital epilepsy of Gastaut have been reported. There is a high prevalence of febrile seizures (about 17%).

SCN1A mutations have been reported in a child and in 2 siblings with relatively early onset of seizures, prolonged time over which many seizures have occurred, and strong association of seizures with febrile precipitants even after the age of 5 years. However, no such mutations were found in another couple of siblings and many other cases with typical Panayiotopoulos syndrome. These data indicate that SCN1A mutations when found contribute to a more severe clinical phenotype of Panayiotopoulos syndrome.

Hyponatraemia is an almost universal finding due to water retention and a shift in intracellular sodium transport from inhibition of Na/K ATPase. Hypoglycaemia (due to depleted hepatic glycogen store and hyperinsulinaemia), hypokalaemia, hypophosphataemia and Metabolic alkalosis are often present, independent of renal function. Lactic acidosis occurs predominantly in paracetomol (also known as acetaminophen) overdose.

Lightheadedness can be simply (and most commonly) an indication of a temporary shortage of blood or oxygen to the brain due to a drop in blood pressure, rapid dehydration from vomiting, diarrhea, or fever. Other causes are: low blood sugar, hyperventilation, Postural Orthostatic Tachycardia Syndrome, panic attacks, and anemia. It can also be a symptom of many other conditions, some of them serious, such as heart problems (including abnormal heart rhythm or heart attack), respiratory problems such as pulmonary embolism, and also stroke, bleeding, and shock. If any of these serious disorders is present, the individual will usually have additional symptoms such as chest pain, a feeling of a racing heart, loss of speech or change in vision.

Many people, especially as they age, experience lightheadedness if they arise too quickly from a lying or seated position. Lightheadedness often accompanies the flu, hypoglycaemia, common cold, or allergies.

Dizziness could be provoked by the use of antihistamine drugs, like levocetirizine or by some antibiotics or SSRIs. Nicotine or tobacco products can cause lightheadedness for inexperienced users. Narcotic drugs, such as codeine can also cause lightheadedness.

In a study comparing the central nervous depression due to supra-therapeutic doses of Triazolam (Benzodiazepine), Pentobarbital (Barbiturate) and GHB it appeared as if GHB had the strongest dose-effect function. Since, GHB had a high correlation between its dose and its central nervous system depression it has a high risk of accidental overdose. In the case of accidental overdose of GHB, patients could become drowsy, fall asleep and may enter a coma. Although GHB had higher sedative effects at high doses as compared to Triazolam and Pentobarbital, it had less amnestic effects as compared to Triazolam and Pentobarbital. Arousal of subjects in the GHB group sometimes even required a painful stimulus; this was not seen in the Triazolam or the Pentobarbital group. Fortunately, during this heavy sedation with GHB the subjects maintained normal respiration and blood pressure. This is often not the case with opioids as they will cause respiratory depression.

Treatment for lightheadedness depends on the cause or underlying problem. Treatment may include drinking plenty of water or other fluids (unless the lightheadedness is the result of water intoxication in which case drinking water is quite dangerous). If a sufferer is unable to keep fluids down from nausea or vomiting, they may need intravenous fluid. Sufferers should try eating something sugary and lying down or sitting and reducing the elevation of the head relative to the body (for example, by positioning the head between the knees).

Other simple remedies include avoiding sudden changes in posture when sitting or lying and avoiding bright lights.

Several essential electrolytes are excreted when the body perspires. When people are out in unusual or extreme heat for a long time, sweating excessively can cause a lack of some electrolytes, which in turn can cause lightheadedness.