Diabetes 2

Diabetes type 2
The "Type 2 diabetes," or "non-insulin dependent diabetes (NIDDM) (also called" insulin-resistant diabetes or "diabetes of middle age") is a metabolic disease affecting glucose metabolism leading term diabetes mellitus.

Diabetes type 2 is characterized by microvascular lesions and macroangiopathic due to the effect of glucose in the blood (glucose) on the bodies. The greater the amount of glucose in the blood is high (hyperglycemia) and for a long period, more lesions may be numerous and severe. The boundary between a normal glucose levels and a potential risk of allowing the development of lesions is unclear. To standardize the study protocols and allow therapeutic treatment, a glucose threshold was chosen to define the type 2 diabetes. The ADA in 1997, the WHO in 1998 and the former ANAES in 1999 chose a fasting glucose greater than or equal to 1.26 g / L at two different samples.

On the pathophysiology, non-insulin dependent diabetes is characterized by insulin resistance of the organism and reactive hyperinsulinemia. The pancreas produces more insulin to exhaustion and if the amount of insulin is not enough to counter the resistance, the glucose level becomes abnormally high.

The type 2 diabetes is generally asymptomatic for many years, its detection and diagnosis based on laboratory test of fasting glucose or after stimulation by ingestion of sugar (glucose or postprandial glucose tolerance).

The type 2 diabetes is polygenic and environmental origin. It should not be confused with diabetes as in secondary hemochromatosis and after taking certain medications (eg, prolonged use of steroids). It typically occurs in adults over 40 years of age in 60% of cases, obesity or at least overweight. There is also a strong genetic factor in the etiology of this disease have family members (especially first degree) suffering from type 2 diabetes is a major risk factor for developing one too. The majority of patients with type 2 diabetes are obese - obesity leads to chronic increased resistance to insulin that can evolve into diabetes [This last sentence is just a guess. It is perfectly conceivable that obesity is a consequence of insulin resistance. Insulin is a hormone effect in triggering fat storage, and excess insulin results in weight gain. An insulin resistance is likely to gain weight. Furthermore, diabetes type 2 also affects thin people (about 40% of patients), which contradicts the theory that places the overweight as a trigger of this disease].

Diabetes type 2 is more likely to occur if physical inactivity, a diet rich (fat, carbohydrates with high glycemic index, ie raising acutely). It was found in the U.S. and Europe a clear correlation between overweight and diabetes. The increase of childhood obesity raises fears of a rise in type II diabetes.

A low weight at birth may promote the occurrence of type 2 diabetes.

Shorter nights or rather longer than the average appear to increase the risk of type 2 diabetes or impaired glucose tolerance (2.5 times). It is not clear whether this is a risk factor or disorder associated with the cause of diabetes.

The type 2 diabetes affects about two million people in France, which are added 600 000 who are unaware of their disease. It may change for 9 to 12 years without any symptoms.

In developed countries, diabetes is the leading cause of blindness in 20-65 years.

Diagnostic criteria
The diagnostic criteria for diabetes change regularly based on epidemiological studies the most significant. It is generally biological criteria based on the risk of microvascular lesions appear:

* Random blood glucose ≥ 200 mg / dl with symptoms (polyuria, polydipsia, polyphagia ...)
* Fasting blood glucose ≥ 126 mg / dl (when blood sugar is lower, we can offer to make a test in Oral Glucose Tolerance (Ttog))
* Blood glucose ≥ 200 mg / dl two hours after oral glucose overload (SOG) generated with 75 grams of sugar.

Namely, it must have these results twice.

* Glycated hemoglobin greater than 7%.

There is an entity that is called the impaired fasting glucose when fasting glucose is between 1.10 and 1.26 g / l. It can be interpreted as pre-diabetes and this population increased cardiovascular risk.

At the onset, insulin production by the pancreas is normal. The weight gain by stimulating the patient's muscle cells to preferentially use fatty acids to make energy. It is said that the cells of the body responsible for capturing and using glucose become insensitive to insulin. Glucose can not enter cells, beta cells of islets of Langerhans in the pancreas will produce more insulin to force glucose uptake by cells. As to measure the progress of the disease, the beta cells are exhausted, that is to say that their production of insulin will decrease until it disappears. The rate of blood sugar (glucose) will increase.

The small but repeated elevation of blood sugar in the blood leads to a glucotoxicite. This glucose toxicity causes insulin resistance and direct destruction of beta cells of islets of Langerhans. A vicious circle is created where insulin resistance and decreased insulin secretion worsens diabetes with elevated blood glucose.

Diabetes Type II is one of the factors of cardiovascular risk: it greatly increases the probability of having an atherosclerotic artery, resulting in a decreased blood flow, or stop by obstruction of the infusion of a body.

Treatment Preventive
It is based primarily on weight loss and exercise.

Some drugs have been tried with some efficacy in pre-diabetic subject, resulting in decreased progression to diabetes authentic: they are

* Metformin which is better than placebo and less than the weight loss without reducing mortality,
* The ascarbose
* Ramipril
* Rosiglitazone, which has reduced the incidence of diabetes without reducing mortality or cardiovascular complications.
* Rimonabant.
* Pioglitazone.

Their actual use in that one goal is not currently indicated.

Read also Diabetes mellitus