Volume 01 · Issue 01 · 2009

Yichou spring to rain add flowers, flowers move all over the mountains are fragrant; The February issue comes to the heart to control ink, and the ink dance benevolence adds a glorious chapter. In February 2009, the Chinese Diabetes Journal, which carries the infinite expectations of Chinese diabetes workers, was launched!

In the history of medical development, people's understanding of hyperglycemia first began from its association with poor health status (such as "thirst disorder" described in ancient China). In the history of modern medicine, the most typical disease state represented by hyperglycemia is undoubtedly type 1 diabetes. Before insulin was applied to the clinic, the main cause of death in patients with type 1 diabetes was ketoacidosis, which "originated from the same source" (absolute insulin deficiency) as hyperglycemia, in addition to hyperglycemia. Therefore, although the carbohydrate intake of type 1 diabetes patients was severely restricted at the time to alleviate the symptoms of hyperglycemia, uncontrollable ketoacidosis ultimately claimed the lives of patients in a short time.

gestational diabetes mellitus (GDM) is the first condition of decreased carbohydrate tolerance during pregnancy, accounting for about 80% to 90% of pregnancy complicated with diabetes. Although most patients with gestational diabetes can regain normal glucose tolerance after delivery, increased gestational blood glucose is easy to cause macrosomia, neonatal respiratory distress syndrome, hypoglycemia, hypocalcemia, polycythemia, hyperbilirubinemia, etc., which significantly increases perinatal complications of fetuses and newborns; At the same time, follow-up studies have found that nearly 50% of GDM patients will develop dominant diabetes in the next 20 years, and the risk of vascular disease and obesity and diabetes in their offspring will also increase significantly^[1]。 Therefore, gestational diabetes is a disease state that seriously endangers the health of mother and child in the near and long term. In view of this, more and more studies have focused on gestational diabetes, a "temporary" pathological condition.

More than 30 years ago, with the discovery of pancreatic islet cell antibody (ICA), Irvine et al^[1]The presence of islet autoantibodies also in clinically diagnosed patients with type 2 diabetes has been reported for the first time. Since then, this type of diabetes has been given various names, including type 1.5 diabetes, type 2 diabetes with islet autoantibodies, slow-progressing insulin-dependent diabetes, etc. However, the most widely used name so far is LADA (latent autoimmune diabetes in adults), which was proposed by Professor Mackay of Australia in 1993^[2,3]。 In 1998, the World Health Organization (WHO) Committee of Experts on Diabetes considered LADA to be, in fact, a slow-progressing type 1 diabetes. in 2005, the Immunology of Diabetes Society (IDS) proposed ADA (autoimmune Diabetes in adults) Name, and report its diagnostic criteria, that is, those who meet three conditions simultaneously (age over 30 years, positive islet autoantibodies, and do not need insulin therapy within 6 months after the discovery of diabetes) can be diagnosed as LADA^[3]。

The main purpose of diabetes treatment is to delay the occurrence and development of chronic complications, reduce the mortality and disability rate, and improve the quality of life of patients. In addition to lowering blood sugar and blood pressure, regulating blood lipids, antiplatelet therapy, and weight control, attention has been paid in recent years to "blood sugar fluctuations", another manifestation of glucose metabolism disorders, and is believed to be associated with chronic complications of diabetes.

To analyze the correlation of oxidative stress activation and acute glucose fluctuations in subtypes of impaired glucose intolerance by continuous glucose monitoring system (CGMS).

From January to July in 2008, assessed by repeated oral glucose tolerance test (OGTT), 30 individuals were divided into 2 groups: normal glucose tolerance (NGT, n=13), impaired glucose regulation (IGR, n=17). Thirty–six type 2 diabetes (T2DM) were chosen randomly in outpatients in our hospital. And their blood glucose (BG) levels were monitored by CGMS for 72 h. Intraday glycemic fluctuation were assessed by mean amplitude of glucose excursions(MAGE); From 48 h to 72 h during CGMS period, 24 h urine samples were collected and free 8–iso prostaglandin F_2α(8–isoPGF_2α) were measured by ELISA to evaluate oxidative stress. Repeated CGMS were given after three months insulin Lispro 25 intensive interventions in T2DM group. Periodical interview included life style intervention and insulin regulations. Glucose excursions and other metabolic readouts before and after intervention were compared by one–way ANOVA. Possible factors effected on the activations of oxidative stress and glucose excursions were analyzed by Pearson correlation coefficient and multivariate stepwise regression.

(1)Mean(SD) urinary excretion rates of 8–isoPGF_2α(1706±477)pg/mg of creatinine in T2DM group significantly increased by 690% and 534% compared with it in IGR group ((216±65) pg/mg) and NGT group ((269±60) pg/mg)(F=27.304, P<0.05). And levels of MAGE(6.04 mmol/L ) in T2DM group also elevated by 124% and 249% compared with those in IGR group ((2.7±1.2) mmol/L) and NGT group ((1.7±0.5) mmol/L)(F=67.729, P<0.05). (2) With insulin intensive interventions in T2DM group, urinary excretion rates of 8–isoPGF_2α, MAGE, glycosylated hemoglobin (HbA1c) and triglyceride(TG) readouts decreased by 34.53%, 31.81%, 18.50% and 28.79% respectively(F value equal to 6.108, 18.378, 39.322, 5.942 respectively, all P<0.05). Moreover, the level of systolic blood pressure(SBP), diastolic blood pressure(DBP), fasting blood glucose(FBG) and 2 h postprandial blood glucose (2 h PBG) also significantly decreased(F value equal to 7.879, 11.684, 38.952 and 61.207 respectively, all P<0.01). (3)Pearson correlation analysis: urinary excretion rates of 8–isoPGF_2α was positively correlated with MAGE(r=0.593, P<0.01), FBG(r=0.415, P<0.01), 2 h PBG(r=0.472, P<0.01), high density lipoprotein cholesterol(HDL–C) (r=–0.307, P<0.01), TG(r=0.296, P<0.01) and SBP(r=0.268, P<0.05). However, no significant correlation were found between HbA1c and urinary excretion rates of 8–isoPGF_2α(r=0.186, P>0.05). (4)Using urinary excretion rates of 8–isoPGF_2α as dependent, and positive correlation factors above–mentioned as independent, multivariate stepwise regression analysis showed MAGE and HDL–C entered final two models (r² value was 0.354 and 0.346 respectively, all P<0.01); and same results were found by Partial correlation analysis.

(1) With the deterioration of glucose regulation, the blood glucose excursions become increasingly fluctuant and oxidative stress become more activity. (2)The activation of oxidative stress in T2DM is positively correlated with glucose fluctuations and some lipoprotein metabolism. (3) With insulin intensive treatment, both glucose excursions and oxidative stress are improved obviously.

To analyze metabolic features and pregnancy outcomes of pregnant women with hyperglycemia.

One hundred and thirty pregnant women were enrolled between August 2005 and December 2006 and divided into the normal glucose tolerance group (NGT group, n=26), impaired glucose tolerance group (IGT group, n=42), and gestational diabetes mellitus group (GDM group, n=62) based on 75 g oral glucose tolerance test. Serum fasting glucose and insulin, HbA1c, lipid spectrum, and C–reactive protein were measured. Pre–pregnant BMI, ratio of advanced age pregnant women, HOMA–IR, HOMA–B, and ISI were calculated. Family history of diabetes and adverse pregnancy outcomes were recorded. ANOVA , χ ² test, and Logistic regression analysis were used for data analysis.

Among three groups of GDM, IGT and NGT, serum fasting glucose((5.1±1.0), (4.7±1.0), and(4.0±0.5)mmol/L, respectively) and insulin((9±4), (9±4), and(6±4)mU/L, respectively), HbA1c((5.67±0.76)%, (5.62±0.61)%, and (4.03±0.27)%, respectively), total cholesterol((5.5±1.3), (5.1±1.2), and(4.2±1.1)mmol/L, respectively), LDL–C((3.1±1.0), (2.8±0.8), and(2.3±0.8)mmol/L, respectively), C–reactive protein(2.7, 3.8, and 1.8 mg/L, respectively), HOMA–IR(1.9, 1.8, and 0.9, respectively), pre–pregnant BMI((24.4±4.0), (24.3±2.8), and (22.2±2.8)kg/m², respectively), the rate of cesarean delivery(71.0%, 52.4%, and 19.2%, respectively), infant birth weight((3304±608), (3345±463), and (2988±672)g, respectively), maternal complication rate (69.4%, 54.8%, and 23.1%, respectively), and neonatal complication rate(29.0%, 28.6%, and 3.8%, respectively) were increased in the GDM and IGT groups, although ISI(0.023, 0.024, and 0.052, respectively) was significantly decreased.HOMA–B(295.75, 168.76, and 126.25, respectively) was significantly different between the three groups. Family history of diabetes was more commonly seen in the GDM group(38.7%) than the NGT group(11.5%). Logistic analysis showed that adverse maternal–infant pregnancy outcomes were significantly related with pre–pregnant BMI, age and HbA1c.

Severe insulin resistance, β cell dysfunction, increased pre–pregnant BMI, lipid disorders, and hereditary susceptibility may be the main metabolic features of women with pregnant hyperglycemia. Pre–pregnant BMI, maternal age and HbA1c could be the risk factors of adverse maternal–neonatal complications.

To investigate the diagnostic value of insulin autoantibody(IAA) for latent autoimmune diabetes in adults (LADA).

Sera of 1003 phenotypic type 2 diabetes mellitus (T2DM) patients from the Second Xiangya Hospital of Central South University were screened for IAA with micro–plate radioimmuneassay. Autoantibodies to glutamic acid decarboxylase (GADA) and autoantibodies to protein tyrosine phosphatase(IA–2A) were analyzed with radioligand assay. Four patients with IAA positive alone were clinically followed up for 4 years. Comparisons between autoantibody status groups used two–sample t tests, or Wilcoxon signed–rank tests for non–normally distributed data. All statistical tests were performed by SPSS 13.0.

The positivity rate of IAA (3.39%, 34/1003)in clinic–based, phenotypic T2DM patients was higher than that of healthy controls (0.95%, 3/317)(3.39% vs 0.95%, χ ²=5.3, P<0.05), but lower than that of type 1 diabetes mellitus (T1DM) (21.82%, 24/110)(3.39% vs 21.82%, χ²=68.2, P<0.01). The positivity of combining three antibodies was 10.47%(105/1003), higher than 6.58% (66/1003) of GADA alone, 2.79% (28/1003) of IA–2A alone, 3.39% (34/1003) of IAA alone(χ²=9.2, 37.8 and 46.2, respectively, all P<0.05). Combined IAA measurement increased 2.39% of LADA. The IAA positivity decreased year on year during the peroid of follow–up. During that time, 2 out of 4 patients accompanied by GADA. Average descending rate of fasting insulin levels in IAA positive group was 15.37%, compared with 5.29% of its matched group, and without significant difference(t=1.7, P=0.059).

IAA can be used to screen LADA in penotypic T2DM in Chinese population. Combined IAA, GADA, and IA–2A testing can improve identifying LADA.

To enhance the understanding of fulminant type 1 diabetes (FT1DM).

Clinical and laboratory data of 3 patients diagnosed as FT1DM in our hospital from January 2007 to March 2008 were retrospectively analyzed.

(1)All of 3 cases were males aged from 29 to 43 years old with body mass index ranged from 21.5 to 23.3 kg/m². (2)They were developed to ketoacidosis rapidly after the appearance of diabetic symptoms in 2–4 days. One case had a cardiac arrest. (3) At the stage of onset, the plasma glucose level were above 38 mmol/L, glycosylated hemoglobin ranged from 6.2% to 6.3% and serum glycated albumin ranged from 15% to 24%. (4) Serum glutamic acid decarboxylase antibody and protein tyrosine phosphatase antibody were negative. (5) Their β–cell functions were extremely poor confirmed by a standard test meal and arginine stimulation test. (6) Serum hemodiastase (263–2319 U/L) and lipase (812–859 U/L) were high. Ultrasound and computed tomography showed a normal pancreas. (7) Serum creatinekinase level (1283–12 239 U/L) was extremely high. One case had rhabdomyolysis confirmed by biopsy at gastrocnemius muscle. Serum liver enzyme and myocardial enzyme pedigree were risen significantly. (8) Case 1 was treated with multiple daily insulin injections (MDI) when he was discharged. Case 2 was treated with continuous subcutaneous insulin infusion (CSII). Case 3 was treated with MDI at the beginning of the therapy and transferred to CSII later. Comparing glycemic parameters of continuous glucose monitoring, not only mean level of 24 h blood glucose and intra–day glycemic variability (mean amplitude of glycemic excursions and Schlichtkrull's M–value) but also day–to–day glycemic variability (absolute means of daily differences) were indicated case 2 < case 3 (CSII) < case 1<case 3 (MDI).

(1) FT1DM patients had clinical feathers of abrupt onset, serious metabolic disorders, serious impaired islet β–cell function, complicated with multiple organ impair, which required special attention by all medical practitioners. (2) FT1DM patients had a great glycaemia excursion and were subject to hypoglycaemia. Maybe long–term CSII regimen was needed to improve the prognosis.

To investigate serum omentin–1 levels in overweight and obese population in Nanjing and the relationship between serum omentin–1 concentration and body mass index(BMI), waist circumference(WC) and adiponectin.

Forty–two overweight or obese subjects and fifty–five normal–weight subjects were enrolled, BMI, WC, fasting insulin, fasting blood glucose, lipids, serum omentin–1, adiponectin were measured and waist–to–hip ratio(WHR), insulin resistance index were calculated. All of the statistical analyses were performed using the SPSS 15.0.

The serum concentration of serum omentin–1(μg/L) and adiponectin(mg/L) were 0.024±0.012 and 7.7±2.4 in normal–weight subjects, 0.016±0.007 and 6.4±3.1 in overweight or obese subjects. The serum omentin–1 and adiponectin levels in the overweight or obese subjects were significantly lower than those of the normal–weight subjects(allP<0.05), and serum omentin–1 concentration was negatively correlated with BMI(r=–0.321, P<0.05), WC(r=–0.312, P<0.05), WHR (r=–0.243, P<0.05), TG(r=–0.220, P<0.05) and positively correlated with adiponectin(r=0.232, P<0.05).

Serum omentin–1 levels in overweight and obese Nanjing population are significantly lower than those of the normal–weight subjects, and serum omentin–1 is positively correlated with adiponectin, and omentin might be intimately related to obesity, insulin resistance and type 2 diabetes.

To investigate the influence of oxidative stress on expression and secretion of adiponectin, leptin, resisitin and visfatin in adipocytes.

In vitro culture 3T3–L1 preadipocyte, induce the cell differentiation and maturity. Adding glucokinase into high–glucose culture media to make oxidative model. The cultured cells were divided into four groups for experiment, Group A: the expression of adiponectin, leptin, resistin and visfatin were examined in different concentration of glucokinase; Group B: the expression of above mentioned 4 adipocytokines were examined after against oxidative stress in different concentration of N–acetyl cysteine(NAC); Group C: the effect of different time period of NAC against the oxidative stress; Group D: oxidative stress with or without antagonistic effect on the above 4 adipocytokines.

(1)With the increase of glucokinase concentration, concentration–dependent inhibition of expression were observed with adiponectin, leptin, visfatin and resistin. Among these, adiponectin and leptin seems to be more obvious (adiponectin (6.94±0.07)ng/L & leptin(0.64±0.11)ng/L with glucokinase concentration of 25 U/L, all P<0.01 compared with control). (2) With the extension of NAC incubation duration, the expression of adiponectin, leptin, resistin and visfatin were increased (adiponectin (19.22±0.27)ng/L & leptin (2.95±0.22)ng/L with NAC incubation of 16 h, allP<0.01 compared with control). (3)With the same concentration of glucose oxidase (25 U/L), concentration–dependent increase of adipokine expression were observed with the increase of NAC concentration(adiponectint=6.88, leptin t=6.96, resistin t=4.52, visfatin t=3.15 with NAC concentration of 25 mmol/L, all P<0.05) .(4) Compared with the blank control, the expression of adiponectin, leptin, visfatin and resistin in NAC group were increased significantly, the expression of the adipokines were decreased significantly in glucokinase group.

Oxidative stress has significant influence on adiponectin, leptin, resistin and visfatin expression in adipocytes. Anti–oxidative can improve this effect. The influence of oxidative stress on adipokines maybe one of the mechanisms of insulin resistance and metabolic dysfunction pathogenesis.

To investigate the effects of rosiglitazone on fatty acid metabolism and expression and activity of AMP–activated protein kinase (AMPK) α in skeletal muscles in insulin resistance rats.

Forty male Wistar rats aged 4 to 5 months were randomly assigned into the normal control group (n=16; basic feeding) and the fat–rich diet group (n=24; fat–rich feeding). After feeding for 4 weeks, whole–body insulin sensitivity was determined using hyperinsulinemic–euglycemic clamp (8 from each group). The results showed that 4 weeks' fat–rich feeding resulted in insulin resistance. Then 16 rats in the fat–rich diet group were further randomly assigned into the fat–rich diet subgroup (n=8) and the rosiglitazone treatment subgroup (n=8). Rats in both groups were fed with fat–rich diet as before, and rosiglitazone was administered orally in the rosiglitazone treatment subgroup (3 mg·kg^–1·d^–1). Skeletal muscle triglyceride was extracted and measured by an automated biochemistry analyzer. mRNA expression of AMPKα1 and AMPKα2 was determined by real–time quantitative reverse transcription polymerase chain reaction (RT–PCR). Protein expression of AMPKα1, AMPKα2 and P–AMPKα was measured using sodium dodecyl sulfate–polyacrylamide gel electrohoresis (SDS–PAGE) and Western blot techniques. All data were analyzed by one–way ANOVA using SPSS software.

At the 8 weeks, glucose infusion rate was reduced in the fat–rich diet subgroup than that in the normal control group ((19.3±3.7) and (30.4±4.2) mg·kg^–1·min^–1, respectively; P<0.01), and glucose infusion rate was higher in the rosiglitazone treatment subgroup compared with the fat–rich diet subgroup((25.8±1.6)and(19.3±3.7)mg·kg^–1·min^–1, respectively; P<0.05). Skeletal muscle triglyceride was higher in the fat–rich diet subgroup than that in the normal control group((4.4±1.2) and (2.0±0.5)μmol/g, respectively;P<0.01), and was lower in the rosiglitazone treatment subgroup than that in the fat–rich diet subgroup((3.3±1.1)and(4.4±1.2)μmol/g, respectively;P<0.05). No difference in mRNA or protein expression of AMPKα1 was detected between groups (P>0.05). Compared with the normal control group, AMPKα2 mRNA and protein expression of AMPKα2 and P–AMPKα were decreased in the fat–rich diet subgroup, while rosiglitazone treatment increased these parameters (allP<0.05).

Fat–rich diet may result in lipid accumulation in skeletal muscles and insulin resistance in rats. Rosiglitazone intervention could increase the expression of AMPKα2 and improve the activity of AMPKα, leading to decreased lipid accumulation in skeletal muscles and increased insulin sensitivity in insulin resistant rats.

To study the effect of high–fat diet and rebaudioside(RA) intervention on the function of β cell and lipid metabolism of SD rats.

Ten–week–old male SD rats were randomly divided into 3 groups, i. e., the normal group (NC, n=10), the high–fat diet group (HF, n=10), and the high–fat diet plus RA intervention group (HF+ R, n=10). Rats in HF+ R group was administered RA 30 mg·kg^–1·d^–1 by intra–peritoneal injection, while rats in HF group was injected same volume of saline.Intraperitoneal glucose tolerance test (IPGTT) were carried out after eight weeks of feeding. Triglycerides (TG) content in liver and in muscle was calculated. The mRNA expression of genes involved in fatty acid metabolism was measured by using reverse transcription and real–time PCR.

(1) At the 30 min of the IPGTT, the insulin levels in NC, HF, HF+ R group were (16.0±6.1), (5.4±0.8) and (23.9±7.1) μg/L, respectively ( F=3.77, all P<0.05); the blood glucose at the 30 min in rats of HF+ R increased significantly as compared with NC group and HF group(F=3.83, P<0.05). (2)TG content of muscle and liver in HF and HF + R group increased significantly than NC group (F=4.39, P<0.05 in muscle,F=5.97, P<0.01 in liver). (3)The expression of acetyl coenzyme A carboxylase –2 (ACC–2) in rat muscle of HF group and HF+ R group was 1.74 fold and 19.97 fold higher than that in NC group, respectively (F=13.48, P<0.01); Compared with the NC group, the muscle carnitine acyltransferase 1(M–CPT–1) was increased only in HF group .

RA preserved early phase insulin secretion in rats feeding with high–fat diet, however, the blood glucose level was higher. The increased TG contents and the change of gene expression in muscle may account for the increased glucose level.

To study the effect of advanced glycated end products (AGEs) on the secretion of extracellular matrix metalloproteinase inducer (EMMPRIN) and the activity of matrix metalloproteinase–2 (MMP–2) in cultured mouse embryo/fetus calvaria osteoldasts (MC3T3–E1).

The AGEs–BSA was prepared by incubating bovine serum albumin (BSA) with glucose. The cultured MC3T3–E1 was added with AGEs–BSA (50, 100, 200, and 400 mg/L) for 24 h or 200 mg/L AGEs–BSA for 12, 24, and 48 h, respectively, taking DMEM and BSA as negative control. The concentration of EMMPRIN in the supernatant was quantified by ELISA. The activity of MMP–2 in MC3T3–E1 was determined by gelatin enzymogram method. MC3T3–E1 was cultured in the presence of DMEM and AGEs–BSA (50 mg/L) with or without Anti–EMMPRIN antibody. The activity of MMP–2 in MC3T3–E1 was determined by gelatin enzymogram method. All statistical analyses were carried out with the SPSS 13.0. Statistical analysis was done by one–way analysis of variance (ANOVA).

In different dose of AGEs group, the concentration of EMMPRIN in the supernatant ((7.34±0.11), (10.86±0.07), (14.48±0.14), and (15.43±0.23) μg/L) was higher than BSA group ( q was 3.111, 3.090, 2.921, and 4.387; P<0.05) and the activity of MMP–2 ((225.12±5.01), (305.83±5.21), (363.04±8.04), and (410.63±16.84)INT·mm²)was significantly increased than BSA group( q was 3.109, 3.545, 5.912, and 5.895; P<0.05). In different time of AGEs group, the concentration of EMMPRIN in the supernatant ((12.41±0.02), (17.88±0.35), and (18.88±0.36) μg/L) was higher than BSA group (q was 5.522, and 7.462, 7.323, P<0.05) and the activity of MMP–2 ((222.18±14.53), and (246.53±5.96) INT·mm²) was increased compared to BSA group (q was 4.159, and 4.321; P<0.05). The activity of MMP–2 was significantly decreased in anti–EMMPRIN antibody–blocking group compared to the control groups ((543.21±67.90) and (867.95±113.46) INT·mm², q=6.354, P<0.05) and 50 mg/L AGEs group ((127.63±11.36) and (160.76±17.45) INT·mm², q=7.742, P<0.05).

The AGEs could stimulate the expression of EMMPRIN and the activity of MMP–2 in cultured MC3T3–E1, which may be partially inhibited by anti–EMMPRIN antibody. These findings suggest that EMMPRIN might mediate the role of AGEs in the development of osteoporosis by MMP–2.

At present, the understanding of diabetes as a clinical entity is: (1) diabetes is a substance metabolism disease with chronic blood glucose (hereinafter referred to as blood glucose) level increased as the main clinical feature; (2) Severe acute metabolic disorders can occur in diabetic patients, and chronic metabolic abnormalities can also lead to more specific structural abnormalities involving almost all body tissues and organs accompanied by functional dysfunction, and can also promote the occurrence and development of atherosclerotic cardiovascular and cerebrovascular diseases; (3) The ultimate pathological mechanism of hyperglycemia in diabetics is that there must be a functional defect of insulin secretion by pancreatic islet β cells, and the sensitivity to insulin of tissues such as skeletal muscle, liver and/or fat that rely on insulin for substance metabolism may be reduced; (4) The etiology of diabetes is extremely heterogeneous. So far, hundreds of clinical conditions are known to cause diabetes. Nowadays, the understanding of the clinical manifestations and prevention and treatment of diabetes and its complications or complications is relatively sufficient, and the understanding of the final pathophysiological pathway of its onset has made great progress, while the understanding of the etiology of diabetes is still relatively shallow.

In 2008, the announcement of the results of several large-scale clinical studies caused unprecedented disturbance in the global academic community. The debate has started since the early suspension of the Action to Control Cardiovascular Risk in Diabetic Patients (ACCORD) study at the beginning of this year. The cause is that the ACCORD Safety Monitoring Committee found that 257 patients died in the intensive hypoglycemic treatment group, while only 203 died in the standard treatment group. The average annual difference between the two groups was 0.3% over 4 years^[1]。 Such results have surprised and confused clinicians. At the annual meeting of the American Diabetes Association (ADA) in June 2008, the results of ACCORD, the Intensified Blood Glucose Control and Diabetes Vascular Outcome Action (ADVANCE), and the American Veterans Diabetes Trial (VADT) were announced, which heated the subsequent discussion. Up to now, ACCORD investigators have not identified the exact cause of the increase in mortality in the intensive hypoglycemic group. Fortunately, the intensive group of ADVANCE study did not increase the mortality of patients. However, for macrovascular events, the ADVANCE study enhancement group also failed to achieve statistical benefits. The same is true of the VADT study results.

Recently, many scholars at home and abroad have confirmed that glucagon-like peptide-1 (GLP-1), as an insulin secretion promoter and insulin sensitizer, can effectively reduce blood glucose level^[1]。 Foreign studies have found that the secretion of GLP-1 in patients with type 2 diabetes is reduced compared with normal controls^[2]。 Accordingly, we suggest that the decrease of GLP-1 level and its dysfunction play an important role in the pathogenesis of type 2 diabetes. However, there are few studies on plasma GLP-1 levels in patients with different course of type 2 diabetes. In this study, we measured the changes of GLP-1 levels at fasting, 30 min and 120 min postprandial in patients with different courses of type 2 diabetes, and the results are reported below.

Blood glucose control has always been the most important issue in the treatment of diabetes. A number of large-scale trials such as the British Diabetes Prospective Study (UKPDS) and the Diabetes Control and Complications Trial (DCCT) have confirmed that blood glucose control is closely related to the occurrence and development of diabetic complications. At the same time, these large-scale studies have also confirmed the direct relationship between reducing glycosylated hemoglobin (GHb) and reducing the risk of diabetic complications, and the correlation between mean blood glucose level and GHb^[1,2]。 As currently the best indicator for assessing long-term glycemic status, GHb helps to determine therapeutic goals to reduce the risk of chronic complications of diabetes^[3]。 Because the increase of GHb represents a chronic increase in blood glucose, more and more scholars have recently advocated the use of this index in the diagnosis of diabetes^[4]。

A 41-year-old female was admitted to the hospital on 16 January 2008 due to "9 years of weight loss, elevated blood glucose and hepatosplenomegaly for 5 years". Nine years ago, the patient experienced general emaciation without obvious inducement, especially the face and trunk. Five years ago, it was found that my blood sugar increased, and my fasting blood sugar exceeded 11.1 mmol/L for many times. I have taken "metformin + glibenclamide" for 1 year, Chinese medicine (details unknown) for 1 year, and "gliclazide 80 mg, twice/d". So far, my fasting and 2 hours postprandial blood sugar is about 16 mmol/L, and there is no symmetrical numbness and pain in the limbs, no blurred vision, loss of vision, edema, etc. Physical examination 1 month ago found blood pressure increased by up to 180/80 mm Hg (1 mm Hg =0.133 kPa). There is no family genetic history.

At present, the Diabetes Branch of Chinese Medical Association is organizing and promoting the 2007 edition of the Guidelines for the Prevention and Treatment of Type 2 Diabetes in China nationwide^[1]In order to facilitate the wider readers to deepen their understanding and use of the guide, this article makes some supplements to the purpose and content of the guide. It is important to note that although the results of a number of large evidence-based medicine studies were reported internationally in 2008, the basic ideas of this guideline are still applicable.

Because of their unique mechanism of action and β-cell protection, incretin drugs have become a hot spot in recent years. Long-acting glucagon-like peptide-1 analogs such as liraglutide only need to be injected once a day, which is more convenient than short-acting formulations, but their safety and efficacy have not been determined.

Medical nutrition therapy is an important basic treatment of diabetes. Medical nutrition therapy is an essential component of a healthy lifestyle, according to the American Diabetes Society. A number of clinical studies have shown that medical nutrition therapy can make HbA_1cReduce by 0.25% to 2.9%. However, at present, the optimal proportion of the three major nutrients intake by diabetic patients is still inconclusive.

There are undoubtedly significant medical and socioeconomic benefits in predicting the risk of developing type 2 diabetes in a population. The pathophysiological basis of type 2 diabetes is the progressive decline of pancreatic islet β cell function and insulin resistance, while the former is the central link in the pathogenesis and progression of type 2 diabetes. Because the oral glucose tolerance test is complex and time-consuming, the current diabetes prediction model is mainly based on fasting blood glucose.

Clinical diagnostic criteria for metabolic syndrome are useful for understanding the relationship between insulin resistance and cardiovascular disease, but whether it can predict the risk of cardiovascular disease or type 2 diabetes is unclear. To this end, Sattar et al. analyzed 4,821 people aged 70 to 82 years without diabetes at baseline in the "Prospective Study of Pravastatin in High-Risk Elderly Patients (PROSPER Study)" and 2,737 non-diabetic people aged 60 to 79 years in the "British Regional Heart Study (BRHS Study)". The researchers followed the metabolic syndrome criteria established by the third guideline of the National Cholesterol Education Program Adult Treatment Expert Group (obesity indicator: BMI ≥30 kg/m was used in the PROSPER study²The BRHS study, with waist circumference ≥102 cm), analyzed the relationship between baseline levels of each component of metabolic syndrome and the onset of fatal and non-fatal cardiovascular disease and type 2 diabetes during follow-up. The PROSPER study was followed up for 3.2 years, during which 772 cases of new cardiovascular disease and 287 cases of new diabetes, and metabolic syndrome could not predict the risk of cardiovascular disease (HRwas 1.07, 95%CI0.86 to 1.32), but was associated with the risk of diabetes mellitus (HR4.41, 95%CI3.33-5.84), especially closely related to fasting blood glucose (HR18.4, 95%CI13.9-24.5). The BRHS study was followed up for 7 years, during which 440 cases developed cardiovascular disease and 105 cases developed diabetes, and metabolic syndrome was slightly associated with the risk of cardiovascular disease [RR1.27 (1.04-1.56)], and was significantly associated with the risk of diabetes mellitus [RR7.47 (4.90-11.46)]. In both studies, body mass index, waist circumference, triglycerides, and glucose cut-off point were not associated with the risk of cardiovascular disease but with the risk of new-onset diabetes. Accordingly, the researchers believe that no cutting point of metabolic syndrome that can predict the risk of cardiovascular disease and diabetes at the same time has been found, so cutting point standards for predicting the risk of these two diseases should be established separately. – – Translated from Can metabolic syndrome usefully predict cardiovascular disease and diabetes? Outcome data from two prospective studies. Lancet, 2008, 371:1927 – 1935.

Vildagliptin is a potent selective dipeptidyl peptidase IV inhibitor that can increase the response ability of islet β and α cells to glucose through incretin hormone-mediated action, thereby improving the blood sugar control level of patients with type 2 diabetes. Some studies have pointed out that vildagliptin does not affect insulin secretion and blood glucose level in individuals with normal glucose tolerance, but whether it can improve the blood glucose control level of patients with impaired glucose tolerance (IGT) with mild impairment of incretin hormone needs to be further studied.

Subclinical inflammation is associated with type 2 diabetes progression. Epidemiological data show that this relationship is more closely associated with women. Although some small-scale clinical studies have found that short-term high-dose aspirin has obvious hypoglycemic effects, there are still no randomized trials to directly evaluate the efficacy of conventional dose aspirin in the prevention of diabetes. To this end, the researchers selected 38,716 non-diabetic women over 45 years old from the "Women's Health Study" subjects from 1992 to 1995 and randomly assigned them to a low-dose aspirin group or a placebo group (median follow-up time was 10.2 years). The results showed that the low-dose aspirin group (n=19 326) 849 developed type 2 diabetes, and the placebo group (n=19 340) 847 developed type 2 diabetes, and there was no statistically significant difference in the incidence of diabetes between the two groups (RR1.01; 95%CI0.91-1.11). A stratified analysis of risk factors for diabetes (including age, body mass index, family history of diabetes, physical activity, HbA1c and high-sensitivity C-reactive protein) did not affect any of the variables; Analysis of the length of treatment also did not reveal any beneficial effects. The above data show that long-term use of low-dose aspirin in healthy women cannot effectively prevent the occurrence of type 2 diabetes. – – Translated from A randomized trial of low-dose Aspirin in the prevention of clinical type 2 diabetes in women. Diabetes Care, 2009, 32: 3 – 8.

One of the important pathophysiological changes in the early stage of type 1 diabetes is that the body produces an autoimmune response to insulin molecules, which in turn damages beta cells. Individuals with genetic susceptibility can detect insulin autoantibodies at 6 to 12 months after birth, so theoretically inducing immune tolerance to insulin can be used as a secondary preventive measure for type 1 diabetes.

Statin therapy reduces the risk of occlusive vascular events in diabetic patients, but whether its effect on reducing all-cause death and macrovascular disease in diabetic patients is related to type of diabetes, lipid type, or other factors is inconclusive.LancetA published meta-analysis sought to answer this question.

At least 246 million people in the world have diabetes. Epidemiologically, poor dietary structure and population aging are the main reasons for the increase of type 2 diabetes patients. Type 2 diabetes is a metabolic disorder characterized mainly by insulin resistance and insufficient insulin secretion. The goal of modern diabetes treatment is to make blood sugar control of diabetic patients close to the level of healthy people, so as to reduce the risk of complications. Experts recommend starting insulin early in treatment to ensure good blood sugar control [glycosylated hemoglobin (HbA1c)<7%] and maintain beta cell function.