The first simple exam should be performed is the fasting glucose. If the value exceeds 126 mg/dl, repeated measurements, different days you can make a diagnosis of diabetes. If the value is between 110 and 126 mg/dl, it is necessary to deepen the investigation with further testing. The most commonly used is the glucose tolerance test (oral glucose load), an examination to assess the body's ability to contain the blood glucose within usual after administration of oral glucose load of 75 g (standard dose). As we said, the main indication for a curve by oral glucose load is a glycaemia of between 110 and 126 mg/dl, but there are also other conditions under which the case to investigate thoroughly the existence of other risk factors: family history, obesity, neurological events with young subjects, atherosclerotic coronary, retinopatiche, of which the cause is unclear. The dosage of insulin (insulinemia) is another, very important because it allows you to establish directly the functionality of the beta cells of the pancreas. The measurement made during glucose tolerance test makes us see "live" the body's ability to produce insulin circulating under the stimulus induced by glucose. The doctor, according to the criteria recognized by the World Health Organization (who), will interpret the combined results of blood glucose and insulin, indicating the State of normality, a reduced glucose tolerance or diabetes mellitus case found. Another survey of easy implementation and which can also be done from the same patient is urine examination. With it you can identify the presence of glycosuria (glucose in the urine) and chetonuria (presence of ketones in the urine). If there is glucose in the urine means as stated that the blood glucose is over 180 mg/dl because only over this concentration the kidney removes the glucose in the urine (the renal threshold for glucose). The glycosuria must be carried out throughout the day between meals and to detect any increases in blood glucose that aren't obvious to fasting but only after meals. Ketonuria is always an expression of severe metabolic decompensation. C is a peptide fragment of the original molecule from which to form insulin. As seen in the figure below, when the initial molecule produces the insulin itself is released even peptide C.
  Sequence of activation of insulin and C-peptide release From the pre-molecule of calves before the signal peptide, then formed the disulfide (S-S) among two peptide sequences (of). All the intermediate between the two chains connected by disulfide bonds, C-peptide, calves and remains the active insulin molecule.
In patients who do therapy with insulin secretory capacity to test the beta cell cannot directly take the insulinemia, because that would be measured also administered as a drug. We can then assess the concentration of C-peptide (which is not contained in the drug insulin), particularly in patients with recent onset diabetes mellitus, to check the capacity residual beta cell to produce endogenous insulin. Since the type 1 diabetes at onset often the formation of antibodies against various elements involved in diabetic disease (pancreatic beta cells, insulin) you use blood tests to reveal some of these antibodies. These tests are usually performed to diagnose the early stages of diabetes type 1, or to identify people at risk of developing this type of diabetes. These antibodies are present in more than 95% of cases of diabetes type 1 in the initial phase and then tend to shrink until their disappearance. We tend to ascribe to a predictive role for these antibodies in the onset of diabetes: it was seen that the 50% of first degree relatives (parents, siblings, children) of persons with diabetes and people without ICA antibodies have developed diabetes within 9 years of highlighting. The predictive value is even higher (63%) if the subject had in blood insulin antibodies (IAA). These antibodies may appear in the circle before clinical onset of diabetes and are associated with an increased risk of disease in first degree relatives of patients with type 1 diabetes. Both have an inverse correlation with age and the duration of the preclinical stage: higher levels of IAA, seems to be the most rapid progression to disease, therefore I am predicting a valid marker of the disease only in individuals under the age of 10 years. It was observed a significant positive association between autoantibody and the presence of HLA DR4.
  These antibodies are important for the IAA are two orders of reasons. First of all, have been found in many subjects considered at risk for diabetes and that feedback is often parallel those of ICA described above, increasing the risk factor for the disease. Moreover, they were at the root of the therapeutic difficulty when not used insulin synthesis. Administering insulin induced the formation of these antibodies that are tied to it and it would block the action. Could however happen that insulin, unpredictably, freed from this bond and could induce hypoglycemia crisis, anytime of the day. These antibodies were then responsible for severe instability of the disease. With the advent of synthetic recombinant insulin identical to humans, these antibody reagents are missing. These antibodies are more sensitive and more specific than the ICA. In humans there are two isoforms of GAD, which differ in molecular weight (65kD and 67kD), to derive gene and tissue distribution. The GAD65 represents the predominant isoform in the pancreatic islets, in which it is expressed by cells to both b cells and seems localized to the level of synaptic microvescicole. It is coded by a gene located on chromosome 2 and has a 65% homology with GAD67. 65 and antiGAD67 antiGAD autoantibodies have been reported in patients both before and wing time of diagnosis of diabetes, however the GAD65 seems to rappresentar the dominant isoform. Have been demonstrated in patients with type 1 diabetes before and at the time of the clinical onset of the disease are autoantibodies that react with two island of 37kD proteins (IA2) and 40kD (IA2b). They are highly predictive of future appearance of the disease in 1 degree relatives of patients with type 1 diabetes. Glycosylated hemoglobin is a very useful parameter for assessing the patient's glycemic control. In fact, while the glucose gives us a picture "snapshot" of the situation, the glycemia is glycated hemoglobin as a "movie" that indicates if the blood glucose has been well controlled in 3 months earlier. This measurement is based on the following principle: hemoglobin, which serves to carry oxygen to the tissues, is contained in red blood cells, which have an average life span of 120 days. When the blood glucose in diabetic patient rises, a part of glucose irreversibly binds to hemoglobin (glycosylation) forming precisely glycated hemoglobin (HbA1). This form of hemoglobin is stable, until the red blood cells do not complete their life cycle and are destroyed. Let's say that in this protein, in the event of an increase in blood glucose, remains an indelible trace of what has happened. Then the HbA1 is an index of metabolic control in diabetics that must not exceed 6-7%.


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