Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells).
Studies in type 1 patients have shown that in intensively treated patients, diabetic eye disease decreased by 76%, kidney disease decreased by 54%, and nerve disease decreased by 60%. More recently the EDIC trial has shown that type 1 diabetes is also associated with increased heart disease, similar to type 2 diabetes. However, the price for aggressive blood sugar control is a two to three fold increase in the incidence of abnormally low blood sugar levels (caused by the diabetes medications). For this reason, tight control of diabetes to achieve glucose levels between 70 to120 mg/dl is not recommended for children under 13 years of age, patients with severe recurrent hypoglycemia, patients unaware of their hypoglycemia, and patients with far advanced diabetes complications. To achieve optimal glucose control without an undue risk of abnormally lowering blood sugar levels, patients with type 1 diabetes must monitor their blood glucose at least four times a day and administer insulin at least three times per day. In patients with type 2 diabetes, aggressive blood sugar control has similar beneficial effects on the eyes, kidneys, nerves and blood vessels.
Target organ damage occurs through multiple mechanisms in metabolic syndrome. The individual diseases leading to metabolic syndrome produce adverse clinical consequences. For example, hypertension in metabolic syndrome causes left ventricular hypertrophy, progressive peripheral arterial disease, and renal dysfunction.  However, the cumulative risk for metabolic syndrome appears to cause microvascular dysfunction, which further amplifies insulin resistance and promotes hypertension. 
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^ 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.
Especially severe cases of hypertension, or hypertensive crises, are defined as a BP of more than 180/120 mm Hg and may be further categorized as hypertensive emergencies or urgencies. Hypertensive emergencies are characterized by evidence of impending or progressive target organ dysfunction, whereas hypertensive urgencies are those situations without progressive target organ dysfunction. 
Daily exercise: Being fit is a key part of blood pressure control. All kids with hypertension should exercise and play sports for 1 hour each day — with some activity (like jogging) most days and higher levels of activity (like running) 3 times a week. Usually, exercise is restricted only when hypertension is very severe. Kids with severe hypertension should not do any weight- or power-lifting, bodybuilding, or strength training until their blood pressure is under control and a doctor says it's OK.
Weight loss surgery in those with obesity and type two diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.
^ Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC (October 2009). "Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity" (PDF). Circulation. 120 (16): 1640–45. doi:10.1161/CIRCULATIONAHA.109.192644. PMID 19805654.
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The best way to prevent metabolic syndrom is to adopt heart-healthy lifestyle changes. Make sure to schedule routine doctor visits to keep track of your cholesterol, blood pressure, and blood sugar levels. Speak with your doctor about a blood test called a lipoprotein panel, which shows your levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides.
The exact cause of metabolic syndrome is not known. Many features of the metabolic syndrome are associated with "insulin resistance." Insulin resistance means that the body does not use insulin efficiently to lower glucose and triglyceride levels. Insulin resistance is a combination of genetic and lifestyle factors. Lifestyle factors include diet, activity and perhaps interrupted sleep patterns (such as sleep apnea).
According to the Mayo Clinic, doctors may use other tests to diagnose diabetes. For example, they may conduct a fasting blood glucose test, which is a blood glucose test done after a night of fasting. While a fasting blood sugar level of less than 100 milligrams per deciliter (mg/dL) is normal, one that is between 100 to 125 mg/dL signals prediabetes, and a reading that reaches 126 mg/dL on two separate occasions means you have diabetes.
Emerging data suggest an important correlation between metabolic syndrome and risk of stroke.  Each of the components of metabolic syndrome has been associated with elevated stroke risk, and evidence demonstrates a relationship between the collective metabolic syndrome and risk of ischemic stroke.  Metabolic syndrome may also be linked to neuropathy beyond hyperglycemic mechanisms through inflammatory mediators.