Health Worlds

Overof diabetes directory causes of editing term clinical complications of diagnostic tests treatment options to prevent editing of this paragraph is an overof diabetes, the interaction of genetic and environmental factors cause common diseases, high blood sugar as the main clinical signs, symptoms more common to drink, polyuria, polyphagia, and weight loss, etc., if the lack of effective treatment of diabetes, the body can cause multi-system damage. Caused by inadequate secretion of insulin and the absolute or relative insulin sensitivity of target cells reduced, causing the protein, fat, water and electrolytes and a series of metabolic syndrome disorders, one of the main signs of high blood sugar. Typical clinical cases, there may be polyuria, polydipsia, polyphagia, weight loss, such as performance, that is "a little" symptoms. Edit this paragraph etiology etiology
According to etiology can be divided into primary and secondary two categories: primary, accounting for the vast majority of unknown etiology and pathogenesis, secondary accounted for a minority, such as acromegaly, the pituitary diabetes, Cushing's syndrome steroid diabetes and so on.
(A) the characteristics of various types of diabetes are as follows:
1. Insulin-dependent diabetes (IDDM, type) is characterized as follows: more acute onset; typical cases seen in children and adolescents, but the disease can be any age; plasma insulin and C peptide levels low, the serving post-glucose secr


etion continued to show a low and flat curve; must rely on insulin therapy based, once the arrest is ketoacidosis, a life-threatening; inheritance was an important incentive, performance at HLA on chromosome 6, the positive rate of increase or decrease of certain antigens ; islet cell antibodies (ICA) always positive, especially in the early onset of 2 to 3 years, sometimes for several years before the onset of regular has shown a positive response, recent studies indicate that the identification of patients with type , glutamic acid decarboxylase antibody (anti-GAD) positive for ICA more meaningful than that, especially in the course of the disease longer, slower development of patients.
2. Non-insulin-dependent diabetes (NIDDM, type) is characterized as follows: slow onset; typical cases seen in middle-aged adults, occasionally in the child care; plasma insulin level is only a relatively decreased, and was delayed after the glucose release, fasting plasma insulin in obese patients and sometimes the base value may be high, insulin-stimulated glucose was also higher than normal, but lower than the same weight as the lower non-diabetic obese; genetic factors are also important causes, but are negative for HLA; ICA negative; insulin effects are often very poor; oral anti-diabetic drugs alone generally can control blood sugar, not fat according to body weight and obesity can be divided into two types, without fat in NIDDM, in fact, also include a number of autoimmune lesions of patients with type very slow, and its initial clinical presentation resembles NIDDM while the MIDDM treatment, long after the last show progressively the full features of type , insulin must be free from ketoacidosis, it is the time of diagnosis, age often large, anti-GAD positive results was significantly higher than NIDDM, 76%: 12%, can be termed that as from late autoimmune diabetes (LADA), was also known as type 1.5 diabetes, and recent reports of mitochondrial DNA mutations at home and abroad diabetes, was not because of its typical clinical features of NIDDM: early onset and no obesity, duration of treatment and often need to use insulin more impaired -cell function, associated with nerve deafness with fashion, it is likely that one belongs to LADA species, currently ongoing in-depth understanding of mitochondria in diabetes.
NIDDM in, there are a class of disease before the age of 25, in 5 years will be able to control high blood sugar without insulin, generally do not ketoacidosis, as young people, middle-aged diabetes mellitus (MODY), an autosomal dominant multi- , and its microvascular complications in NIDDM with the same general common, but less macrovascular complications.
3. And malnutrition-related diabetes is characterized as follows: This type mostly found in Asia, Africa, South America and other Third World countries, in tropical or subtropical regions, it is also known as the of tropical pancreatic diabetes, named variety, later named by the WHO and malnutrition-related diabetes; age of onset was mostly young people (15 to 30 years old); body weight loss, malnutrition; many cases to be treated with insulin, and sometimes larger doses; but ketosis is rare; this type and can be divided into the following two subtypes:
pancreatic stones fiber type: pathology in chronic pancreatic fibrosis, pancreatic body and narrow pancreatic duct expansion of calcification within the stone, so that both exocrine and endocrine involvement; onset in young people, male to female ratio was 3:1; with chronic recurrent abdominal pain, diarrhea, dyspepsia, nutritional deficiencies and other chronic disease characterized by pancreatic; blood sugar can sometimes be very high, up to 400 ~ 600mg/dl (22 ~ 33mmol / L); insulin therapy to be about 80% ; But even withdrawal, ketosis rare; Most of the patients died in 40 to 50 years old, also showed a variety of chronic complications of diabetes; cause is unknown at present, there are believed to be more food derived from cassava poisoning caused by chronic CN, this disease, also known as Z-type, as first seen in 1955, Zuidema, similar to the case, I have seen one case of hospital, with autopsy confirmed.
lack of protein-based: This type also known as J-or M-type, as first seen in 1955, Jamaica, characterized by: onset in young people aged 15 to 25; has a long history of protein and energy malnutrition, resulting in extreme weight loss , BMI usually <19; moderately elevated blood glucose, insulin therapy required; ketosis rare; Asia the disease to female ratio was 2 to 3:1, the African men and women are equal, more women of West Indian Zeyi; cause unknown, probably due to chronic malnutrition, cell number and dysfunction caused by, but with IDDM different, there are still C peptide after glucose release.
4. Secondary and other
pancreatic: Because pancreatic resection, pancreatitis, pancreatic cancer, blood diseases such as caused by insufficient insulin secretion.
endocrine: pituitary diabetes, due to excessive secretion of growth hormone found in acromegaly or gigantism; steroid diabetes, excessive secretion of the hormone cortisol found in Cushing's disease or syndrome; pancreatic l tumor-induced blood glucose without diabetes, the islet A ( ) cell tumor of excessive glucagon secretion; diabetes caused by pancreatic somatostatin cell tumor, due to pancreatic islet D ( ) over cell adenoma somatostatin secretion wait.
drug-induced and chemical properties: a variety of drugs, chemicals can affect glucose metabolism, such as thiazide diuretic antihypertensive drugs meters, corticosteroids, female oral contraceptives, analgesic antipyretic (aspirin, indomethacin, etc.) , tricyclic anti-inhibitor in Miami for the forest, to Jiabing imipramine are largely caused by impaired glucose tolerance only.
insulin receptor abnormalities: another point: receptor itself, congenital defects of fat nutritional abnormalities (congenital lipodystrophy) and acanthosis nigricans with masculine women; insulin receptor antibody-induced resistance to diabetes.
hereditary syndrome with diabetes mellitus: a variety of: metabolic disorders such as type glycogen calcinosis, acute intermittent porphyria Blood, hyperlipidemia, etc.; hereditary neuromuscular diseases such as diabetes, optic atrophy with diabetes insipidus and deafness; progeria syndrome; secondary to obesity, glucose intolerance, such as Prader-Willi syndrome syndrome.
(B) impaired glucose tolerance (impaired glucose tolerance, referred to as IGT) according to the diagnostic criteria for this group of fasting blood glucose of <140mg/dl (7.8mmol / L) 2 hours after meal <200mg/dl (11.1mmol / L) but higher than normal by oral glucose tolerance test (OGTT) curve between diabetes and also between the upper limit of normal, this group features are: high blood sugar, but not diabetes standards of diabetes candidate system can be divided into obese and non-fat type, if not timely intervention of such an object about 2 / 3 can be transformed into diabetes, diet and exercise intervention can reduce morbidity, it is important for the prevention of diabetes one of the objects.
(C) gestational diabetes (gestational diabetes mellitus, referred to as GDM) is limited in this group occurred in women with gestational IGT and DM, it is not known diabetes in pregnancy is this group, most patients in the follow-up OGTT return to normal after delivery, Only 30% of patients in the 5 to 10 years follow-up into a true diabetes (according to WHO standards), this group of patients met all the pregnant women in the 1% to 2%.
Pathogenesis
Most of the absolute lack of insulin seen in type (IDDM), are mostly found in the relative lack of type (NIDDM) patients, the absolute lack of evidence the following points: fasting plasma insulin levels low, generally <4 U/ml (normal is 5 ~ 20 U/ml), or even undetectable; blood and 24-hour urine C peptide were very low, often can not be measured; with glucose or glucagon stimulated plasma insulin and C peptide was still low, showed a flat curve; ineffective treatment of sulfonylurea; pathological insulitis on the show, early infiltration of lymphocytes, etc.; post- cells were hyaline degeneration, fibrosis, cells, and only 10% of the original, and the relative lack of insulin secretion expressed in fasting plasma insulin and glucose stimulated insulin release test were lower than the corresponding weight concentration of the non-diabetes, but diabetes, obesity, type base value or plasma insulin concentrations than normal controls after stimulation peak was higher than the corresponding weight is only diabetes rather than low and the peak was delayed, normal glucose-stimulated insulin peak after oral administration of glucose found in 30 to 60 minutes, type the patient's peak of about 30 to 45 minutes delay appears in Figure .
Figure 1 insulin release test in normal, non-diabetic obese and obese people with type diabetes mellitus type diabetes mellitus compared plasma insulin concentration
Note: normal fasting plasma insulin concentration of 5 ~ 20 u/ml, significantly increased after oral administration of 100g of sugar, about 45 minutes and reached peak insulin concentration 250 u/ml more than 3 hours, not back to normal.
obesity (Non-diabetic) fasting plasma insulin levels higher than normal, after oral administration of 100g of sugar was 90 to 120 minutes a peak, but lower than normal.
type diabetes, fasting plasma insulin levels slightly lower than normal, after oral administration of 100g of sugar was 90 to 120 minutes a peak, but lower than normal.
obese diabetic fasting plasma insulin than normal or normal, oral administration of 100g of sugar reached a peak after 2 hours, significantly higher than normal, but not obesity, diabetes, compared with the corresponding weight is lower.
The data on insulin secretion of diabetes than normal-weight corresponding to low, and the peak was delayed, suggesting that the relative lack of insulin secretion, diabetes mellitus (juvenile, thin persons) less secretion of
Type patients at least daily insulin secretion, fasting glucose, after the base value and the peak was significantly lower than normal, indicating that the absolute secretion, normal-weight patients with type lower than normal insulin secretion, and glucose peaks after low and delayed, but the secretion of obese people with diabetes greater than normal, and the base value and the fasting glucose was significantly higher than normal after the peak, but was delayed, suggesting that the relative lack of insulin secretion and release of slow, as insulin secretion the cause of lack of the following factors:
(A) the number of genetic factors in patients with positive family history, in our hospital 922 cases of 8.7%, foreign reports about 25% to 50%, regardless of genetic factors in type or type than positive, according to research modern twin children, dominant type of CPC was 50%, the rest is environmental factors; type CCP more than 90% dominant, the study of human chromosomes are known from the type patients on the short arm of chromosome VI stereotypes compatibility leukocyte (HLA) allele point increase or decrease the frequency, suggesting that genetic susceptibility is a tendency rather than the disease itself, and with race and ethnic-specific, a large number of HLA studies concluded that the HLA D and DR antigens associated with type is most important, especially DW3-DR3 DW4-DR4 and susceptibility to type diabetes mellitus, and finally found DQ chain variants, and the relationship between type diabetes mellitus more closely than DR4, DQ 57 DQ 52 non-aspartic acid and arginine can significantly increase the susceptibility to type diabetes mellitus, but its impact is far less significant white, HLA type of patients is no special signs.
(B) of the patients with autoimmune type is closely related to the autoimmune response to pancreatic islets mainly via molecular simulation may (Mimicry) due process, such as chemistry and composition of an antigen and -cell type resembles, the antigen antibodies will also launch immune attacks against cells, antigen could be a virus, the virus can also be outside, as the virus infection, cell destruction and severe diabetes doctrine, as in the popular way and serological studies there are still inconsistent results and found that islet cells from the damage to between onset of symptoms has a long incubation period when such facts are that still need to re-valuation.
diabetes susceptibility gene with the individual, such as with cells resembles the foreign antigen (twin antigen), phagocytes that MHC class United bind tightly in the IL in cooperation with and , the After the secondary T cell recognition, the launch of the strong and sustained antigen immune response against the original production of specific antibodies and immune cells, cells resembles the foreign antigen, and thus the attack by antibodies, and antibodies against foreign antigens -cell binding, to attract phagocytes, complement and natural killer cells, phagocytes will own the information passed to the secondary antigen T cells, which further expand the immune response against self antigens.
Type diabetic patients evidence of cellular and humoral immunity are: patients may be associated with a variety of other immune diseases, such as Graves disease, Hashimoto's thyroiditis, pernicious anemia, primary chronic adrenal cortex hypofunction psychosis; can associated with organ-specific antibodies, including thyroid, gastric parietal cell antibodies and anti-adrenal; more acute onset and death within 6 months who have inflammation of pancreatic islets; including T lymphocytes, NK cells and K cell infiltration ; leukocyte migration inhibition test was positive; islet cell antibodies (ICA) immunofluorescence determination of positive cases in the incidence of type 1 to 2 years up to 85% (normal positive rate was only 0.5% ~ 1.7%), decreased gradually after; later found that islet cell surface antibodies (ICsA), complement fixation islet cell antibodies (CF ICA), islet cell cytotoxic antibodies (Cytotoxic-ICA), 64K and 38K immunoprecipitation and antibodies, which ICsA, CF ICA and immunoprecipitation antibody selection role in cells, recent years found that patients with type antigens for islet cell antibodies, glutamic acid de-identified, Department of carboxylic acid (GAD), in patients with recent onset of type The positive rate of 69% in the incidence of 3 to 42 years, 59% of patients still positive rate than dura 3 years in patients with type , ICA, the positive rate was high; inhibitory function of T lymphocytes and decreased, K increased cell number and activity of , pathogenesis of patients with type shown in Figure .
Figure 2 Pathogenesis of insulin-dependent diabetes mellitus
(C) insulin resistance and other hormones, according to Unger emphasized that the pathogenesis of diabetes, high blood sugar not only because of the relative and absolute lack of insulin, while glucagon must be relative or absolute excess, normal pancreas when blood sugar is too high glycemic inhibition of factors, but diabetes is not suppressed, especially in ketoacidosis, the insulin treatment restored the rear, not in proper control of diabetes are often higher, so? bang bird species of ape pry deficient Di Huang rate Tam partridge call-sac gun brake bran Huan Cheng Hau hammer Xiu Wei nger dualism and other theories proposed that the pathogenesis of diabetes is not only the relative and absolute lack of insulin, but is still accompanied by glucagon is too high relative or absolute, but the exact cause is unknown.
Islet D ( ) cells secrete somatostatin (GHRIH, SS) on pancreatic B ( ) cells to secrete insulin and A ( ) cells was inhibited by glucagon and glucagon to inhibit dominant , it can prevent the removal of insulin-induced IDDM diabetic ketoacidosis, according to Unger and Orci speculate that in normal human cells in these three was next to the secretion of three hormones regulate each other, so that the normal range of blood glucose was maintained at , when B or D cell dysfunction and low secretion of glucagon may promote excessive lead to high blood sugar and diabetes (Three of doctrine); but Felig so that the pathogenesis of diabetes is still in relative or absolute deficiency of insulin as the main pathophysiological basis of the role of glucagon to enhance high blood sugar or only a secondary factor for the slave.
(D) diabetes mechanism of the pathogenesis of type patients with type different, not because of autoimmune destruction of cells caused by genetic defects primarily on the basis of the existence of barriers to insulin resistance and insulin secretion in two areas, the majority of scholars believe that insulin resistance Department of Primary anomaly, but it may be both need to be there but the performance has, uneven it can be divided into three phases: the first, with insulin resistance and hyperinsulinemia, plasma glucose to maintain normal; s two, increased insulin resistance, although hyperinsulinemia, but the insulin the higher the less sensitive receptors, creating a vicious special, although hyperinsulinemia, postprandial hyperglycemia is still there; the third phase, insulin resistance still exist, but decreased insulin secretion, resulting in fasting hyperglycemia, islet secretion can be due to toxic effects of sustained high blood sugar further deterioration of the pancreas in patients with type found in amyloid deposition, the Department of 37 amino acid peptide said amylin (amylin), normal co-amylin and insulin stored in secretory granules, agents in insulin secretion and insulin also stimulated secretion in animal studies, amylin can lead to insulin resistance, in a small Island in the accumulation of amylin may patients when insulin secretion in the late failure.
NIDDM patients with type or three levels of performance by insulin resistance.
1. Insulin receptor level before such mutation was found in 1979, Tager insulin (mutant insulin) caused by diabetes, in the first 25 amino acids Lin B (Phe) is replaced by leucine and failure, and later found that B-chain the first 24 amino acids (phenylalanine) is also replaced by serine, A chain of the first three amino acids (valine) is replaced by leucine and failure are caused by diabetes, suggesting that the biosynthesis of insulin gene mutations the formation of abnormal structure and biological activity decreased insulin lead to diabetes, similar to the situation in the first 65 amino acid linker (Arg) is replaced by histidine, but also because enzymes may be defective linker can not make insulin (proinsulin) decomposition to the formation of C peptide of insulin, resulting in excessive circulating insulin and insulin deficiency, leading to diabetes, but such abnormal insulin in the etiology of diabetes caused by only a tiny minority.
2. The level of insulin receptor insulin receptor is a transmembrane glycoprotein macromolecules, composed of two subunits and two subunits, located on chromosome 19, the insulin receptor gene encoding the wall, containing 22 exons and in exon 2 -subunit of insulin specific binding and cell configuration after change, leading to insertion in the subunit of the intracellular tyrosine kinase activity, which is to play its role in insulin modified the first step of intracellular insulin receptor gene mutations way affect the receptor through a variety of functions: reduced rate of receptor biosynthesis; receptor into the cell membrane during abnormal; decreased affinity of insulin receptors; tyrosine kinase activity decreased; receptor degradation accelerated, now more than 30 Insulin-like receptor gene point mutation or deletion associated with severe insulin resistance, has also been found in several clinical syndrome and insulin receptor gene mutations, such as the fairy disease, diabetes, fatty atrophy.
3. Receptor level of insulin binding to its receptor subunit, subunit tyrosine kinase activation, a series of cellular changes is not yet clear, inside the cytoplasm or cell substrate phosphorylation and de- phosphorylation, depending on the characteristics of the target tissue and a different key enzymes and insulin to promote glucose transport organizations and glycolysis, liver and muscle glycogen synthesis, gluconeogenesis and glycogenolysis inhibition, the process is dependent on glucose, insulin GLUT4 transported out of the body and many of the key enzymes such as glucose (G) kinase, glycogen synthase, phosphofructokinase, pyruvate kinase and pyruvate dehydrogenase activity, in which, GLUT4, and G kinase's role in insulin resistance recent years has been in-depth study, GLUT4 insulin-dependent rotation G, which activates GLUT4 and to promote its cell microsomes by the translocation to the cell membrane, thus promoting G into the cell, which has been found to obesity and type diabetes GLUT4 gene expression in fat cells decreased content decreased, resulting in reduced insulin action and insulin resistance, G kinase in the process of glucose metabolism is the first key enzyme, catalytic G into 6 - phosphate - glucose, specifically in the liver and cells expression, and many family survey research shows young people in adult-type? value raised ants arrived in the school was Chu kinase gene linkage disequilibrium, and found that mutations in certain genes, leading to insulin resistance, and NIDDM pathogenesis of Figure 3, the main is integrated in the genetic basis of the consequences of a variety of factors, including post-receptor defect with insulin or insulin resistance and pancreatic cell function as well as the main obstacle link.
.
Figure 3 pathogenesis of diabetes mellitus and NIDDN Edit this paragraph have the clinical diagnosis of typical cases of the disease prompted more than three disease groups, mild asymptomatic diagnosis entirely on tests, often in the health examination or by accident due to other diseases and found that many patients first found that complications, and then back and the disease, but regardless of symptoms or complications, the key is to first consider the possibility of this disease and the urine, blood sugar screening, be confirmed.
(A) of the urine test results to determine diabetes should pay attention to the following situations, determine the results of urine diagnostic reference purposes only, and diagnosed with diabetes need to rely on blood glucose.
1. If a small or micro diabetes, and those who occasionally appear in the postprandial blood glucose and oral glucose tolerance test should be conducted, and noted the spot's Department of copper sulfate solution is reduced to a carbohydrate such as reaction of copper oxide into the sky, many drugs such as morphine, salicylic acid, chloral hydrate, amino aspirin, ammonia acid, a large number of citric acid, uric acid and many other sugars may also occur the original copper sulfate false positive results, it is now widely used in glucose The urine glucose oxidase test strip is made to avoid false positive results.
2. Clinical signs of diabetes and urine sugar or a suspect repeatedly negative, should be noted that fasting and postprandial 2 h blood glucose, except for the case of increased renal glucose threshold.
(B) blood glucose determination methods commonly used in three ways: venous plasma glucose (VPG), capillary whole blood glucose (CBG) and venous whole blood glucose (VBG), in which the two most commonly used previously, measured in different ways slightly different results, VPG method results measured 10% higher than the CBG, about 15% higher than the VBG, analysis reports and pay attention to blood glucose levels caused by higher than other cases, such as the injection of sugar, the various endocrine disorders brain disease and stress and so on, will be addressed later, especially in mild or early type patients and normal fasting blood glucose can not be easily exception must be made 2 hours after meal blood sugar or glucose tolerance test.
(C) fasting blood glucose tolerance test for normal or slightly higher and the occasional diabetic patients or patients with suspected diabetes (if positive family history or repeated miscarriage, premature birth, stillbirth, giant baby, childbirth, abortion The maternal, or repeated hair carbuncle swollen boils, etc.), to carry out glucose tolerance test, but significantly higher fasting blood glucose are diagnostic of heavy dominant cases have been able to identify a large number of glucose can increase the burden should be exemption.
1. Oral glucose tolerance test (oral glucose tolerance test, OGTT) the most commonly used in the past adults with a 100g, in recent years, WHO recommended 75g (or whether adults or children per kg standard body weight 1.75g, total no more than 75g) oral law, before and after oral glucose in 1 / 2, 1,2,3-hour venous blood sugar test, urine check and collect urine specimens.
Results: The normal (age 15 to 50 years) fasting blood glucose was 70 ~ 100mg/dl (real sugar, glucose oxidase method), glucose absorption peak seen at 30 to 60 minutes (more than 50 years after the shift), not more than 170mg/dl, 2-hour glucose levels returned to normal range, 3 hours can be reduced to normal the following, negative urine sugar, 100g and 75g is not very different method compared, only the latter an early return to normal blood glucose, glucose tolerance is often over 50 years of age physiological reduced peak at 1 hour and 10-year-old elevated blood sugar increases every 10mg/dl.
Diagnostic criteria: At present, most made by WHO in 1985, the interim standards are as follows:
diabetes symptoms, any time, venous plasma glucose 200mg/dl (11.1mmol / L), and fasting venous plasma glucose 140mg/dl (7.8mmol / L) can be diagnosed as diabetes.
If the result doubtful, should be carried out OGTT (oral glucose adults 75g), children per kg body weight 1.75g, total no more than 75g), 2 hour glucose 200mg/dl (11.1mmol / L) can be diagnosed as diabetes, blood glu 140mg / dl ~ <200mg/dl as impaired glucose tolerance (TGT).
without symptoms of diabetes, in addition to the above two diagnostic criteria, plus a target yet to help diagnose, that is, the curve in OGTT 1 or 2 blood glucose 200mg/dl or another fasting blood glucose 140mg/dl.
gestational diabetes can also use this diagnostic criteria.
Diagnostic criteria above can be summarized as Table Table 1 The World Health Organization (WHO) provisional diagnosis of diabetes standards
Oral glucose tolerance test (OGTT) plasma glucose mg / dl (mmol / L) whole blood and venous plasma capillary whole blood of diabetes (DM) fasting and (or) after glucose loading 2h 120 (6.7) 200 (11.1) impaired glucose tolerance (IGT) fasting and after glucose loading 2h 120 (6.7)Impact of diagnosis of diabetes than the glucose tolerance must fashion a variety of factors, including the anterior pituitary, adrenal cortex, hyperthyroidism and other endocrine diseases, obesity, liver disease, a variety of drugs (such as thiazide diuretics, female contraceptives, glucocorticoids , phenytoin, chlorobenzene, a thiadiazine, etc.), stress (such as fever, infection, acute myocardial infarction, surgery, etc.), loss of potassium.
2. Postprandial blood glucose 2h glucose consumption is equivalent to 100g of carbohydrate foods such as bor rice and two after 2 2h glucose, such as more than 140mg/dl were reduced to tolerance, 200mg/dl those with diabetes.
Because low-sugar diet or impaired glucose tolerance allow hunger, so try to adjust your diet before the 3d should be noted that the carbohydrate intake of not less than 250g / d, only to get reliable results.
Some patients had to estimate the -cell function or glycemic control, the can still make the following determination:
1. Fasting plasma insulin measured by radioimmunoassay in our hospital fasting plasma insulin normal range of 5 ~ 20 u/ml, -type patients are often in the 5 u/ml the following, sometimes as low as undetectable, -type normal plasma insulin concentrations , a few who have low, obese patients often higher than normal, was increased significantly by hyperinsulinemia, suggesting insulin resistance, metabolic syndrome which is an integral, can be considered a risk factor for coronary heart disease, concern in recent years, insulin and insulin-immune cross-cutting the original, so can the general radioimmunoassay for the measure, while the adverse cardiovascular effects of insulin could be worse than insulin, proinsulin has been the determination of applications clinical.
2. Insulin release test in the oral glucose tolerance test for the simultaneous determination of plasma insulin levels to reflect the function of pancreatic -cell reserve, -type patients than the low level of fasting, the glucose stimulated insulin levels remain low, showing low flat curve , in particular, is to calculate both the glucose (G) and insulin (IRI) ratio, (IRI) / G, prompt insulin secretion is low (normal is 25 u/mg), -type patients may be normal or high fasting levels and stimulate was delayed after the release, such as insulin stimulation of glucose no significant rise or low-lying water, indicating that -cell dysfunction.
3.C Peptide release from islet -cells by insulin after insulin by the liver and kidney enzymes can destroy the surrounding blood 80% of each cycle will be destroyed, and its half-life of only 4.8 minutes, so the blood concentration of only on behalf of its very small portion of the total secretion, C peptide and insulin system formed from a split proinsulin peptide molecules of matter, can not destroy the liver enzyme, subject only to the role of renal excretion, and its half-life of 10 ~ 11 minutes, so the blood levels to better reflect the function of islet -cell reserve to determine when the C peptide from the interference of insulin antibodies, and determination of non-insulin cross-immune response, but the impact of insulin injections from outside, so in recent years has been measured using the blood concentration of C peptide or 24-hour urinary excretion to reflect cell function.
Determination of serum C peptide concentration : 2 immunosorbent assay using radio normal fasting serum C peptide was 1.0 0.23mg/dl, when the oral glucose peak after 60 minutes to see a concentration of 3.1ng/ml, measured according to Block, etc. , 100g oral glucose in normal human serum C peptide from 1.3 0.3ng/ml in 60 minutes and then increased to 4.4 0.8ng/ml, type diabetes rose by only 2 hours after 2.3ng/ml, the other 5 cases of type disease who had treatment with insulin for more than 5 years the low level of C peptide, both fasting and after stimulation were not detected.
24-hour urine C peptide measurement: normal 24-hour urine C peptide was 36 4 g, -type disease in only 1.1 0.5 g, -type patients was 24 7 g, the daily discharge is about the equivalent of C peptide of insulin secretion the amount of 5%, while only 0.1% of insulin excretion.
Determination of the C peptide of insulin treatment in type disease process may identify -cell function, currently only for research, clinical also often used.
4.HbA1c normal fasting blood glucose determination of blood glucose fluctuations may reflect the past 2 to 3 month blood glucose, normal HbA1c6%, HbA1 was 8%, diabetes often higher than normal.
5. Fructosamine serum fructosamine normal 2.13 0.24mmol / L (plasma low-0.3mmol / L), can reflect the past 1 to 4 weeks blood glucose and HbA1c parallel, regardless of diabetes type , type were increased, especially in type is high.
In short, the diagnosis of diabetes can be the root history, clinical manifestations, combined with the urine, blood glucose and OGTT determined, in addition, it has yet to identify a variety of complications and associated disorders, and estimate its severity, type, stage of development and major organ function status, the treatment of this disease and the prognosis is very important.
TCM diabetes
Medicine on the pathogenesis of this disease more detailed discussion that was mainly due to ferrite Yin, five internal organs, soft, complex due to improper diet, excessive eating Feigan, emotional disorders, like excessive labor, which led to kidney yin deficiency, lung and stomach heat; focus on the pathogenesis deficiency hot flashes, and the deficiency-oriented, hot as the standard; disease delay the course of time, sinister and yang, yin and yang, both virtual; Yin hot, burning liquid consumption of subsidized the blood viscosity, blood Shibuya lag from stasis; sinister and Yang, Yang Hanning, can lead to blood stasis within the yang.
1. Ferrite ferrite lead Yin Yin reasons: deficiencies: "Lingshu five Pandemic" said: "The five internal organs are weak and are, good elimination hate disease" refers to inadequate maternal child care, loss over the day after tomorrow: evil, such as drug abuse, loss of Yin-chun, lack of s: the internal organs, such as chemical and biological damage to Yin-chun, no sex fluid chemical and biological weapons, such as "Taiwan Miyao Diabetes door", said: "Consumers thirsty, the original of its launch, this is due to kidney deficiency, which each made to the sweet urine, " yin and yang relationship between the organs imbalance and finally sinister too much sun will Piansheng, Too Yang is addressed to the" consumer " such as "Medical Laws by edema door," said: "Secretary for opening and closing of kidney, kidney yang is from the open sun Too close is not the whole family, compared with consumption of water straight down," Kang yang side, so stomach heat Sheng and Consumers Valley Bulimia.
2. Diet, body fat over the long-term eating sweet Atsumi, so that injury of the spleen, stomach Ji Zhi, Yun heat of the dry, Shangyin consumption of Tianjin, but also to the stomach hot flashes, increased consumer Valley Bulimia such as "Yin and Yang Su Wen Another " said: "Two positive statement that the consumer," the second Yang Ming Yang refers to the stomach and hand-foot Yangming large intestine, is the stagnation of the gastrointestinal heat, stomach heat and the consumption Valley Bulimia, on Thermal evil smoked in the lungs, the Hyperactivity-chun injury, there polydipsia polydipsia, colon constipation heat in the poor, phlegmatic for fat people, phlegm of the heat, but also loss Yin-chun, Yin-chun, but also chemical and biological weapons lack of heat, hot flashes will Shangyin complex vicious cycle that occurred Diabetes.
3. Emotional disorders, liver qi stagnation conditions fail to materialize due to the long Shu, Yu Zhi heat, of dry Shangyin; or because of anger, leading to liver failure be reached; air-block, but also of dry heat, and Consumer Shuo lung and stomach yin chun, leading to lung and stomach heat, thirst, polydipsia occurs, consumers Valley Bulimia, Yin hot course of time, will inevitably lead to Qi and Yin Deficiency, Diabetes patients before the deficiency heat, and see more polydipsia, polyuria, good hunger, both a long time, the emergence of sinister and Yang Qi Yang micro phenomena, such as body drowsiness, fatigue, difficulty of eat less, loose stools thin, dry mouth and do not want to drink, nocturnal enuresis and daytime anti-less , thin weak pulse, pale tongue, thin white or yellow fur, which is due to the lung, stomach, kidney yin deficiency by three, yang is suppressed the emergence of yin and yang syndromes. Edit this paragraph laboratory examination items (a) of the urinary
1. Diabetes often have severe cases of diabetes before treatment, but only in the early dinner or a mild infection, stress, a lot of chronic illness are due to renal glucose threshold increased, although without diabetes high blood sugar, urine sugar can be from trace to more than 10g%, generally about 0.5% ~ 5g%, even up to 15g% or more of sugar per day can be lost from the micro to hundreds of grams, generally speaking, conditions in the quantitative loss of sugar diet and disease proportional to the severity, and blood sugar have a high degree of relationship, the decision whether the amount of diabetes and urine sugar of three factors: blood glucose levels, glomerular filtration rate, tubular glucose absorption rate of return, normal renal glucose threshold of 160 ~ 180mg/dl; such as inulin clearance was 125ml/min, tubular to the glomerular filtrate back to glucose absorption 250 ~ 300mg/min, so the blood sugar normal urine, but many of the patients with advanced renal arteriosclerosis, glomerular sclerosis and other diseases, renal blood flow reduction in glomerular filtration rate and tubular back to the absorption of sugar to reduce the function of the relative is still good, despite the high blood glucose levels without diabetes, clinically known as renal glucose threshold increased, and vice versa, such as the function of renal tubular reabsorption of sugar fell 120mg/min the following, the blood glucose concentration, although there is still around in 100mg/dl diabetes, clinically known as lower renal glucose threshold, seen in renal diabetes, disease-oriented