Autonomic changes involving cardiovascular control (eg, heart rate, postural responses) have been described in as many as 40% of children with diabetes. Cardiovascular control changes become more likely with increasing duration and worsening control. [18] In a study by 253 patients with type 1 diabetes (mean age at baseline 14.4 y), Cho et al reported that the prevalence of cardiac autonomic dysfunction increases in association with higher body mass index and central adiposity. [19]
Rosiglitazone, a thiazolidinedione, has not been found to improve long-term outcomes even though it improves blood sugar levels.[93] Additionally it is associated with increased rates of heart disease and death.[94] Angiotensin-converting enzyme inhibitors (ACEIs) prevent kidney disease and improve outcomes in those with diabetes.[95][96] The similar medications angiotensin receptor blockers (ARBs) do not.[96] A 2016 review recommended treating to a systolic blood pressure of 140 to 150 mmHg.[97]
Insulin resistance is the most common cause of type 2 diabetes, but it is possible to have type 2 and not be insulin resistant. You can have a form of type 2 where you body simply doesn’t produce enough insulin; that’s not as common. Researchers aren’t sure what exactly keeps some people from producing enough insulin, but that’s another thing they’re working hard to figure out.
Know Your Numbers: Knowing your ABCs—A1c, blood pressure, and cholesterol—are important in reducing your risk for diabetes and keeping your diabetes in good control. If you are someone with diabetes who has elevated blood pressure or cholesterol, you are increasing your risk of heart attack and stroke. Your physician will give you your A1c, blood pressure, and cholesterol targets. Make sure you pay attention to them and understand what they mean and why they are important.
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.[53]
Most pediatric patients with diabetes have type 1 diabetes mellitus (T1DM) and a lifetime dependence on exogenous insulin. Diabetes mellitus (DM) is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, an anabolic hormone. Insulin is produced by the beta cells of the islets of Langerhans located in the pancreas, and the absence, destruction, or other loss of these cells results in type 1 diabetes (insulin-dependent diabetes mellitus [IDDM]). A possible mechanism for the development of type 1 diabetes is shown in the image below. (See Etiology.)
Jump up ^ Santaguida PL, Balion C, Hunt D, Morrison K, Gerstein H, Raina P, Booker L, Yazdi H. "Diagnosis, Prognosis, and Treatment of Impaired Glucose Tolerance and Impaired Fasting Glucose". Summary of Evidence Report/Technology Assessment, No. 128. Agency for Healthcare Research and Quality. Archived from the original on 16 September 2008. Retrieved 20 July 2008.
The diabetic patient should learn to recognize symptoms of low blood sugar (such as confusion, sweats, and palpitations) and high blood sugar (such as, polyuria and polydipsia). When either condition results in hospitalization, vital signs, weight, fluid intake, urine output, and caloric intake are accurately documented. Serum glucose and urine ketone levels are evaluated. Chronic management of DM is also based on periodic measurement of glycosylated hemoglobin levels (HbA1c). Elevated levels of HbA1c suggest poor long-term glucose control. The effects of diabetes on other body systems (such as cerebrovascular, coronary artery, and peripheral vascular) should be regularly assessed. Patients should be evaluated regularly for retinal disease and visual impairment and peripheral and autonomic nervous system abnormalities, e.g., loss of sensation in the feet. The patient is observed for signs and symptoms of diabetic neuropathy, e.g., numbness or pain in the hands and feet, decreased vibratory sense, footdrop, and neurogenic bladder. The urine is checked for microalbumin or overt protein losses, an early indication of nephropathy. The combination of peripheral neuropathy and peripheral arterial disease results in changes in the skin and microvasculature that lead to ulcer formation on the feet and lower legs with poor healing. Approx. 45,000 lower-extremity diabetic amputations are performed in the U.S. each year. Many amputees have a second amputation within five years. Most of these amputations are preventable with regular foot care and examinations. Diabetic patients and their providers should look for changes in sensation to touch and vibration, the integrity of pulses, capillary refill, and the skin. All injuries, cuts, and blisters should be treated promptly. The patient should avoid constricting hose, slippers, shoes, and bed linens or walking barefoot. The patient with ulcerated or insensitive feet is referred to a podiatrist for continuing foot care and is warned that decreased sensation can mask injuries.

A person of Asian origin aged 35 yr or more with two or more of the above risk factors, should undergo a screening test for diabetes. An oral glucose tolerance test (OGTT) is commonly used as the screening test10. Fasting and 2 h post glucose tests can identify impaired fasting glucose (IFG) (fasting glucose >110 - <125 mg/dl), impaired glucose tolerance (IGT) (2 h glucose >140-<200 mg/dl) and presence of diabetes (fasting > 126 and 2 h glucose >200 mg/dl). If a random blood glucose value is > 150 mg/dl, further confirmation by an OGTT is warranted. Recently, glycosylated haemoglobin (HbA1c) has been recommended as the test for diagnosis of diabetes (>6.5%). Presence of pre-diabetes is indicated by HbA1c values between 5.7 - 6.4 per cent11.

Pre-clinical diabetes refers to the time during which destruction of pancreatic insulin-producing cells is occurring, but symptoms have not yet developed. This period may last for months to years. Normally, 80-90% of the pancreatic beta cells must be destroyed before any symptoms of diabetes develops. During this time, blood tests can identify some immunological markers of pancreatic cell destruction. However, there is currently no known treatment to prevent progression of pre-clinical diabetes to true diabetes mellitus.


Because people with type 2 diabetes produce some insulin, ketoacidosis does not usually develop even when type 2 diabetes is untreated for a long time. Rarely, the blood glucose levels become extremely high (even exceeding 1,000 mg/dL). Such high levels often happen as the result of some superimposed stress, such as an infection or drug use. When the blood glucose levels get very high, people may develop severe dehydration, which may lead to mental confusion, drowsiness, and seizures, a condition called hyperosmolar hyperglycemic state. Currently, many people with type 2 diabetes are diagnosed by routine blood glucose testing before they develop such severely high blood glucose levels.

Insulin inhibits glucogenesis and glycogenolysis, while stimulating glucose uptake. In nondiabetic individuals, insulin production by the pancreatic islet cells is suppressed when blood glucose levels fall below 83 mg/dL (4.6 mmol/L). If insulin is injected into a treated child with diabetes who has not eaten adequate amounts of carbohydrates, blood glucose levels progressively fall.
Hypoglycemic reactions are promptly treated by giving carbohydrates (orange juice, hard candy, honey, or any sugary food); if necessary, subcutaneous or intramuscular glucagon or intravenous dextrose (if the patient is not conscious) is administered. Hyperglycemic crises are treated initially with prescribed intravenous fluids and insulin and later with potassium replacement based on laboratory values.

Metformin (Glucophage, Glucophage XR, Glumetza, Fortamet, Riomet) belongs to a class of drugs called biguanides. Metformin is first-line therapy for most type 2 diabetics. It works to stop the liver from making excess glucose, and has a low risk of hypoglycemia. Hypoglycemia, or very low blood sugar can cause symptoms such as sweating, nervousness, heart palpitations, weakness, intense hunger, trembling, and problems speaking. Many patients lose some weight taking metformin, which is also helpful for blood sugar control.


People with type 2 diabetes have insulin resistance, which means the body cannot use insulin properly to help glucose get into the cells. In people with type 2 diabetes, insulin doesn’t work well in muscle, fat, and other tissues, so your pancreas (the organ that makes insulin) starts to put out a lot more of it to try and compensate. "This results in high insulin levels in the body,” says Fernando Ovalle, MD, director of the multidisciplinary diabetes clinic at the University of Alabama in Birmingham. This insulin level sends signals to the brain that your body is hungry.
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