The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.[113]
Diabetes is suspected based on symptoms. Urine tests and blood tests can be used to confirm a diagnose of diabetes based on the amount of glucose found. Urine can also detect ketones and protein in the urine that may help diagnose diabetes and assess how well the kidneys are functioning. These tests also can be used to monitor the disease once the patient is on a standardized diet, oral medications, or insulin.
People with diabetes can benefit from education about the disease and treatment, good nutrition to achieve a normal body weight, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.[83][84]

Oral medications are available to lower blood glucose in Type II diabetics. In 1990, 23.4 outpatient prescriptions for oral antidiabetic agents were dispensed. By 2001, the number had increased to 91.8 million prescriptions. Oral antidiabetic agents accounted for more than $5 billion dollars in worldwide retail sales per year in the early twenty-first century and were the fastest-growing segment of diabetes drugs. The drugs first prescribed for Type II diabetes are in a class of compounds called sulfonylureas and include tolbutamide, tolazamide, acetohexamide, and chlorpropamide. Newer drugs in the same class are now available and include glyburide, glimeperide, and glipizide. How these drugs work is not well understood, however, they seem to stimulate cells of the pancreas to produce more insulin. New medications that are available to treat diabetes include metformin, acarbose, and troglitizone. The choice of medication depends in part on the individual patient profile. All drugs have side effects that may make them inappropriate for particular patients. Some for example, may stimulate weight gain or cause stomach irritation, so they may not be the best treatment for someone who is already overweight or who has stomach ulcers. Others, like metformin, have been shown to have positive effects such as reduced cardiovascular mortality, but but increased risk in other situations. While these medications are an important aspect of treatment for Type II diabetes, they are not a substitute for a well planned diet and moderate exercise. Oral medications have not been shown effective for Type I diabetes, in which the patient produces little or no insulin.
A defect in the thirst mechanism, located in a person's hypothalamus, causes dipsogenic diabetes insipidus. This defect results in an abnormal increase in thirst and liquid intake that suppresses vasopressin secretion and increases urine output. The same events and conditions that damage the hypothalamus or pituitary—surgery, infection, inflammation, a tumor, head injury—can also damage the thirst mechanism. Certain medications or mental health problems may predispose a person to dipsogenic diabetes insipidus.
A. Diabetes is the inability of the body to ‘produce insulin - type 1 diabetes’ or ‘proper use of insulin - type 2 diabetes, gestational diabetes and pre-diabetes’. Diabetes is often goes undiagnosed because many of the symptoms of diabetes seems harmless. The causes of diabetes continues to be a mystery, pancreas it the organ whose defect causes diabetes.
^ Kyu HH, Bachman VF, Alexander LT, Mumford JE, Afshin A, Estep K, Veerman JL, Delwiche K, Iannarone ML, Moyer ML, Cercy K, Vos T, Murray CJ, Forouzanfar MH (August 2016). "Physical activity and risk of breast cancer, colon cancer, diabetes, ischemic heart disease, and ischemic stroke events: systematic review and dose-response meta-analysis for the Global Burden of Disease Study 2013". BMJ. 354: i3857. doi:10.1136/bmj.i3857. PMC 4979358. PMID 27510511.
Ketoacidosis, a condition due to starvation or uncontrolled diabetes, is common in Type I diabetes. Ketones are acid compounds that form in the blood when the body breaks down fats and proteins. Symptoms include abdominal pain, vomiting, rapid breathing, extreme lethargy, and drowsiness. Patients with ketoacidosis will also have a sweet breath odor. Left untreated, this condition can lead to coma and death.

observations The onset of type 1 diabetes mellitus is sudden in children. Type 2 diabetes often begins insidiously. Characteristically the course is progressive and includes polyuria, polydipsia, weight loss, polyphagia, hyperglycemia, and glycosuria. The eyes, kidneys, nervous system, skin, and circulatory system may be affected by the long-term complications of either type of diabetes; infections are common; and atherosclerosis often develops. In type 1 diabetes mellitus, when no endogenous insulin is being secreted, ketoacidosis is a constant danger. The diagnosis is confirmed by fasting plasma glucose and history.
Constant advances are being made in development of new oral medications for persons with diabetes. In 2003, a drug called Metaglip combining glipizide and metformin was approved in a dingle tablet. Along with diet and exercise, the drug was used as initial therapy for Type 2 diabetes. Another drug approved by the U.S. Food and Drug Administration (FDA) combines metformin and rosiglitazone (Avandia), a medication that increases muscle cells' sensitivity to insulin. It is marketed under the name Avandamet. So many new drugs are under development that it is best to stay in touch with a physician for the latest information; physicians can find the best drug, diet and exercise program to fit an individual patient's need.
Diabetes mellitus has been recorded in all species but is most commonly seen in middle-aged to older, obese, female dogs. A familial predisposition has been suggested. It is possible to identify two types of diabetes, corresponding to the disease in humans, depending on the response to an intravenous glucose tolerance test. Type I is insulin-dependent and comparable to the juvenile onset form of the disease in children in which there is an absolute deficiency of insulin—there is a very low initial blood insulin level and a low response to the injected glucose. This form is seen in a number of dog breeds, particularly the Keeshond, Doberman pinscher, German shepherd dog, Poodle, Golden retriever and Labrador retriever.
The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves.[32] Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness.[32] Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that diabetics visit an eye doctor once a year.[33] Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation.[32] Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes.[32] The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
a broadly applied term used to denote a complex group of syndromes that have in common a disturbance in the oxidation and utilization of glucose, which is secondary to a malfunction of the beta cells of the pancreas, whose function is the production and release of insulin. Because insulin is involved in the metabolism of carbohydrates, proteins and fats, diabetes is not limited to a disturbance of glucose homeostasis alone.
When an adult is diagnosed with diabetes, they are often mistakenly told that they have type 2 diabetes. This is because there is still a lack of an understanding in the medical community that type 1 diabetes can start at any age. It can also be tricky because some adults with new-onset type 1 diabetes are often not sick at first. Their doctor finds an elevated blood sugar level at a routine visit and starts them on diet, exercise and an oral medication. On the other hand, there are people who look like they have type 2 diabetes—they may be Latino or African American and/or overweight, but they have type 1 diabetes after all. This can be difficult for even the brightest doctor to diagnose. 
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose.[70] people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[71] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).[72]
FASTING GLUCOSE TEST. Blood is drawn from a vein in the patient's arm after a period at least eight hours when the patient has not eaten, usually in the morning before breakfast. The red blood cells are separated from the sample and the amount of glucose is measured in the remaining plasma. A plasma level of 7.8 mmol/L (200 mg/L) or greater can indicate diabetes. The fasting glucose test is usually repeated on another day to confirm the results.
Hypoglycemia, or low blood sugar, can be caused by too much insulin, too little food (or eating too late to coincide with the action of the insulin), alcohol consumption, or increased exercise. A patient with symptoms of hypoglycemia may be hungry, cranky, confused, and tired. The patient may become sweaty and shaky. Left untreated, the patient can lose consciousness or have a seizure. This condition is sometimes called an insulin reaction and should be treated by giving the patient something sweet to eat or drink like a candy, sugar cubes, juice, or another high sugar snack.
Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[63] 

Endocrinology A chronic condition which affects ±10% of the general population, characterized by ↑ serum glucose and a relative or absolute ↓ in pancreatic insulin production, or ↓ tissue responsiveness to insulin; if not properly controlled, the excess glucose damages blood vessels of the eyes, kidneys, nerves, heart Types Insulin dependent–type I and non-insulin dependent–type II diabetes Symptoms type 1 DM is associated with ↑ urine output, thirst, fatigue, and weight loss (despite an ↑ appetite), N&V; type 2 DM is associated with, in addition, non-healing ulcers, oral and bladder infections, blurred vision, paresthesias in the hands and feet, and itching Cardiovascular MI, stoke Eyes Retinal damage, blindness Legs/feet Nonhealing ulcers, cuts leading to gangrene and amputation Kidneys HTN, renal failure Neurology Paresthesias, neuropathy Diagnosis Serum glucose above cut-off points after meals or when fasting; once therapy is begun, serum levels of glycosylated Hb are measured periodically to assess adequacy of glucose control Management Therapy reflects type of DM; metformin and triglitazone have equal and additive effects on glycemic control Prognosis A function of stringency of glucose control and presence of complications. See ABCD Trial, Brittle diabetes, Bronze diabetes, Chemical diabetes, Gestational diabetes, Insulin-dependent diabetes, Metformin, MODY diabetes, Nephrogenic diabetes insipidus, Non-insulin-dependent diabetes mellitus, Pseudodiabetes, Secondary diabetes, Starvation diabetes, Troglitazone.

The three primary types of diabetic medication include oral diabetes medication, insulin, and other types of injectable diabetes medicine. Within these broad groups, diabetic medication can be classified more specifically as belonging to certain classes. The following article provides a list of diabetic medication broken down by type and class of medicine.
A person's body regulates fluid by balancing liquid intake and removing extra fluid. Thirst usually controls a person’s rate of liquid intake, while urination removes most fluid, although people also lose fluid through sweating, breathing, or diarrhea. The hormone vasopressin, also called antidiuretic hormone, controls the fluid removal rate through urination. The hypothalamus, a small gland located at the base of the brain, produces vasopressin. The nearby pituitary gland stores the vasopressin and releases it into the bloodstream when the body has a low fluid level. Vasopressin signals the kidneys to absorb less fluid from the bloodstream, resulting in less urine. When the body has extra fluid, the pituitary gland releases smaller amounts of vasopressin, and sometimes none, so the kidneys remove more fluid from the bloodstream and produce more urine.
Type 2 diabetes begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[2] As the disease progresses, a lack of insulin may also develop.[12] This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes".[2] The most common cause is a combination of excessive body weight and insufficient exercise.[2]
You may still feel hungry even after you’ve had something to eat. This is because your tissues aren’t getting enough energy from the food you’ve eaten. If your body is insulin resistant or if your body doesn’t produce enough insulin, the sugar from the food may be unable to enter your tissues to provide energy. This can cause your muscles and other tissues to raise the “hunger flag” in an attempt to get you to eat more food.
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