Volume 02 · Issue 03 · 2010

With the rapid development of economy, acute infectious diseases are no longer the main cause of death of patients in China, but tumors, cardiovascular and cerebrovascular diseases, chronic obstructive pulmonary disease and diabetes have become the main causes of death of patients in China. According to our survey, the prevalence of diabetes in adults over the age of 20 in China has reached 9.7%, while the prevalence of prediabetes (impaired fasting blood glucose and impaired glucose tolerance) has reached 15.5%^[1]。 The results were shocking and triggered a review of diabetes prevention strategies, as well as some readers questioning the results^[2]。 In the 2002 National Nutrition Survey, the prevalence of diabetes was only 2.6%^[3]It has increased four-fold in 6 years. It is difficult to directly compare different surveys due to the inconsistency of methodology, but we must acknowledge the reality that the prevalence of diabetes has increased substantially and has become one of the main chronic diseases that threaten the physical health of our people. In this paper, the reasons for the rapid rise of diabetes in China are briefly analyzed, and the influence of different epidemiological investigation methods and statistical treatment on the estimation of diabetes prevalence is discussed.

To investigate the relationship between prognosis and blood glucose level in patients with acute coronary syndrome (ACS).

Data were collected from medical records concerning 1756 patients with diagnosis of ACS admitted to department of cardiology of two tertiary public hospitals in Beijing from January 2003 to December 2006, for whom at least 10 glucose measurements were available in no less than 3 days of hospital stay. Of the total cohort, mean age was (61±9) years, 1270 were male, 596 had a history of diabetes. Coefficient of variation of blood glucose(GluCV) and mean blood glucose(MBG)during hospitalization were calculated for each patient. Total cohort, diabetic cohort and non-diabetic cohort were divided into four groups according to their quartiles of MBG or GluCV respectively. The association between glucose indics and adverse in-hospital outcomes(including major adverse cardiovascular events(MACEs) and in-hospital death) was assessed for these three cohort. Multivariate logistic regression with in-hospital death as the dependent variable was performed to evaluate the independent risk facotr of in-hospital death.

Considering overall population, both MACEs and in-hospital death significantly increased in patients with GluCV >13.33% or MBG>(8.4±2.0) mmol/L compared with those with lower GluCV or MBG( P<0.05). For nondiabetic ACS patients, MACEs and in-hospital death occurred more frequently when MBG>(7.0±2.4)mmol/L (P<0.05) , MACEs were seen more common when GluCV >10.47%, in-hospital mortality significantly increased when GluCV> 19.99% (P<0.05). For diabetic ACS patients, MACEs occurred more frequently when MBG was above (11.01±3.1) mmol/L(P<0.05)or GluCV above 30.16%(P<0.05), in-hospital death was more common when MBG>(8.7±1.5) mmol/L, but there were no significant differences in-hospital mortality among GluCV quartiles. Independent predictors of in-hospital mortality were history of hypertension, GluCV, history of diabetes, MBG and HDL-C, GluCV was a stronger predictor of in-hospital death than MBG(OR, 1.479; OR, 1.165).

Both MBG and GluCV are independent predictor for in-hospital death. Decreasing variability of blood glucose concentration might be helpful for management of ACS patients, especially for those without preexisting diabetes.

To investigate the effect of glycosylated hemoglobin A1c (HbA1c) on carotid atherosclerosis in relatively healthy elderly Chinese people.

A total of 1863 relatively healthy Chinese people (≥50 years old) were randomized enrolled from the Guangzhou Biobank Cohort Study (GBCS). Personal general historiy was collected before the study in all object. The blood pressure, fasting glucose, lipids, HbA1c and common carotid artery intima-median thickness (CCA-IMT) were measured respectively. After adjustment relevant confounding factors, analysis of convariance was used for continuous variable analysis.

(1)After adjusting for age, sex and fasting glucose, mean CCA-IMT were increased significantly with the increase of HbA1c level in all participant (P=0.005). The results of linear regression models show that, HbA1c levels was positively associated with mean CCA-IMT after adjusting for age, sex, smoking, physical activity, waist circumference, systolic and diastolic blood pressure, triglyceride, high-density, low-density lipoprotein cholesterol and fasting glucose (regression coefficient t=0.014, P=0.03). Compared to the optimal group (HbA1c <6.5%), adjusted odds ratios (95% confidence interval) for carotid atherosclerosis in the satisfactory group (HbA1c 6.5%-7.5%) and unsatisfactory group (HbA1c>7.5%) were 1.62(1.10, 2.38)and 1.76(0.86, 3.63)respectively( P for trend=0.01).

Increasing HbA1c level is an independent risk factor for carotid atherosclerosis; that HbA1c-lowering treatment may be an important means for preventing the progression of carotid atherosclerosis.

To investigate the association of obstructive sleep apnea hypopnea syndrome (OSAHS) and type 2 diabetes mellitus.

This study was conducted from May 2008 to December 2009 from the subjects diagnosed at the Sleep Center of the First Affiliated Hospital of Nanjing Medical University. Based on polysomnography examination, 104 habitual snorers were assigned to the simple snorer group (control group) and the OSAHS group which was further assigned to the mild OSAHS group and the moderate-to-severe OSAHS group according to the apnea hypopnea index (AHI) during sleep to compare the incidence of type 2 diabetes mellitus. Parameters among different groups were compared with Chi-square test and analysis of variance respectively. Spearman correlation analysis and Logistic regressive analysis were used to evaluate the correlation among AHI, minimal SaO₂ (mini-SpO₂), mean SaO_2, fasting blood glucose, true insulin, proinsulin, HOMA index, body mass index (BMI), waist circumference (WC) and neck circumference (NC).

Type 2 diabetes mellitus was found in 15.3%(13/85) of all the OSAHS patients. The incidence of type 2 diabetes mellitus in moderate-to-severe OSAHS group (25.7%(9/35)) was significantly higher than that in the control group (5.3%(1/19), χ ²=4.942, P=0.026) and in the mild OSAHS group (8.0% (4/50), χ ²=4.011, P=0.045). Spearman correlation analysis indicated that HOMA index and PI were negatively correlated with nocturnal mini-SpO₂ and mean SpO₂. There was no statistically significant correlation of HOMA index and PI with AHI. Mini-SpO₂ and mean SpO₂ were negatively correlated with BMI, WC, and NC. Univariate logistic regression analysis suggested that the HOMA index and PI were risk factors of severe OSAHS (odds ratio was 1.924 (1.302 to 2.847; P<0.01) or 1.714 (1.175 to 2.507;P<0.01)).

There is an association between OSAHS and type 2 diabetes mellitus. Insulin resistance may play an important role in the coexistence of OSAHS and type 2 diabetes mellitus. The OSAHS patients with a lower SpO₂ can be more susceptible to type 2 diabetes mellitus.

To observe the effects of nateglinide treatment on insulin secretion and dynamic glucose change in newly diagnosed type 2 diabetic patients.

A total of 36 newly diagnosed type 2 diabetic patients were enrolled in this study. According to the levels of fasting plasma glucose (FPG), all the subjects were divided into group A (FPG 5.0-6.9 mmol/L; n=12), group B (FPG 7.0-8.9 mmol/L; n=12), and group C (FPG 9.0-11.1 mmol/L; n=12). All the subjects underwent continue glucose monitor (CGM) for 72 hours within 3 days after the oral glucose tolerance-insulin release test (OGTT-IRT). After 24 hours of CGM, the participants underwent the nateglinide-oral glucose tolerance-insulin release test (NAT-OGTT-IRT), and received single 10-minute preprandial nateglinide (120 mg) during the test and after that. Data in the same group before and after the intervention were compared by matched pair t test, while one-way ANOVA was used for the comparison between groups.

Compared with the group C, the increase of the ratio of insulin increase and glucose increase 30 minutes after glucose load(ΔI₃₀ /ΔG₃₀)was significantly raised in the group A and group B ((9.6±2.1), (5.2±1.7), and (0.6±0.4) U/mol, respectively; F=7.431, P<0.01). Compared with that in the first day of CGM, the amplitude of glycemic excursions (AGE) of the three groups showed a significant decrease in the third day ((4.9±1.5) mmol/L vs (10.5±2.1) mmol/L, (4.9±1.6) mmol/L vs (10.2±1.9) mmol/L, (8.6±1.6) mmol/L vs (10.4±2.2) mmol/L, respectively;P<0.01) . The AGE was decreased more significantly in the group A and group B compared with the group C (F=24.950, P<0.01). Compared with that in the first day, there were a longer duration when plasma glucose achieved the target level after taking nateglinide in the third day of CGM in the group A and group B ((16.5±1.2) h vs (21.3±0.4) h, (11.3±1.6) h vs (17.7±1.2) h, respectively;t values were -12.782 or -11.296, P<0.01). However, no significant difference was found in the group C.

Nateglinide can stimulate insulin release, decrease glycemic fluctuation and prolong the duration that plasma glucose achieves the target level in the newly diagnosed type 2 diabetic patients. Moreover, nateglinide may exert more effective role in type 2 diabetic patients with lower FPG levels.

To investigate the polymorphism of the interleukin-6 promoter -572C/G and its relationship with type 2 diabetes mellitus(T2DM) complicated with vascular disease of lower extremities.

Two hundreds and eighty hospitalized T2DM patients from the Department of Endocrinology in General Hospital of Tianjin Medical University were recruited from February 2008 to January 2009. One hundred and thirty cases were male in (58.7 ± 0.8) years and 150 cases were female (mean age (58.1 ± 0.5) years). Based upon the ultrasound test of the lower extremities, the participants were divided into vascular disease of lower extremities(VDLE) group, vascular and neuropathic disease of lower extremities (VNDLE) group, neuropathic disease of lower extremities(NDLE) group and non-complications group(NC). Seventy people for health care were non-randomly recruited as healthy control group. By PCR-RFLP technique, the polymorphism of the human IL-6 gene -572C/G in 70 health controls and 280 type 2 diabetic patients was evaluated.The genotype and allele frequency in different groups was evaluated by χ ² test. The measurement data in different groups was evaluated by analysis of variance.

The IL-6 promoter -572C/G had polymorphism. The frequency of genotype GG and CG, as well as allele G, had statistics difference between T2DM group and healthy control group (χ² =12.649, 12.054, respectively, all P<0.05). And so did they in T2DM patients who complicated with different vascular disease of the lower extremities compared with healthy control group (χ²=22.015, 20.471, respectively, all P<0.05). The genotype and allele frequency was also higher in T2DM patients complicated with vascular disease of lower extremities than those without the complications(χ²=6.399, 5.752, respectively, all P<0.05).

The genotype GG and CG and the allele G of the Interleukin-6 promoter -572C/G might be the susceptibility gene of the T2DM complicated with vascular disease of the lower extremities. The polymorphism of the Interleukin-6 promoter -572C/G might has great correlation with T2DM complicated with vascular disease of the low extremities.

To investigate the role of different risk factors on glomerular filtration rate(GFR) in prediabetic patients.

A total of 165 prediabetic patients were undergone 75 g oral glucose tolerance test (OGTT) in the out-patient at department of endocrinology from January 2007 to July 2009, and were classified into 3 groups: isolated impaired fasting glucose group(IFG group, 42 cases), isolated impaired glucose tolerance group(IGT group, 56 cases) and combined glucose intolerance group(CGI group, 64 cases). In addition, 30 participants with the normal glucose tolerance (NGT group) were chosen as control group.fasting glucose(Gluc₀), fasting insulin(Ins₀), 2 h postprandial glucose (Gluc₁₂₀), and glycosylated hemoglobin A1c(HbA1c) were measured in all participants. Insulin resistance indices(HOMA-IR) and insulin secretion function indices (HOMA-B%) early stage of insulin secretion indices (ΔI₃₀/ΔG₃₀) and second phase insulin secretion indices (AUC₁₂₀) were calculated at baseline or after glucose load.Pearson linear correlation and multiple linear stepwise regression analysis were used for statistical treatment.

(1)GFR values were increased progressively from NGT group, IFG group, IGT group to CGI group, and the significant difference were found among all groups(GFR was (103±12, 113±13, 133±16, 143±14)ml/min respectively, P<0.05); (2)The correlation analysis indicated that BMI, HOMA-IR, Gluc₁₂₀ and AUC₁₂₀ were positively related with GFR(r=0.571, 0.842, 0.606, 0.788, 0.528, P<0.01), and ΔI₃₀/ΔG₃₀ was negatively correlated with GFR(r=-0.628, P<0.01); (3) Multiple linear stepwise regression analysis showed that HOMA-IR, Gluc_120, ΔI ₃₀/ΔG₃₀ and AUC₁₂₀ were the risk factors of GFR(β=0.631, 0.343, -0.198, 0.248,P<0.05).

It is considered that elevated GFR is caused by increased HOMA-IR, Gluc_120, AUC₁₂₀ and decreased ΔI ₃₀/ΔG₃₀ in prediabetic patients; To prevent the occurrence of diabetic nephropathy, both of control blood glucose, reduce insulin resistance and improve islet beta cell function is important.

To investigate the effect small interfere RNA of TGF-β inducible early gene to the negative feedback factor Smad7 in the Smad signal pathway and collagen Ⅳ which is the primary composition of deposition of extracellular matrix in the kidney of diabetic rats.To provide a new target spot for diabetic nephropathy treatment.

15 male SD rats(weight 200-300 g) were randomly assigned to 3 groups. Ten Sprague-Dawley rats injected with streptozotocin (STZ) were ramdomly devided into TIEGsi-R group and TIEGsi-C group, Other five normal rats were used as control. Each of the TIEGsi-R group and TIEGsi-C group were injected with TIEGsi-R and TIEGsi-C respectively via the tail vein. 4 weeks after the treatment, TIEG expression levels were determined by fluorescence quantitative PCR.The expression of Smad7 protein was detected by immunohistochemistry and western blotting, and CollagenⅣ protein was detected by immunohistochemistry only. Renal fibrosis was also assessed by Masson staining .All the datas were expressed in mean± standard deviation. We used one way ANOVA when compared between groops, Kruskal-Wallis rank test when there was heterogeneity of variance.

Compared to TIEGsi-C group, TIEGsi-R group effectively increased expression of Smad7 protein which was detected by immunohistochemical semi-quantification ((3.2±0.2)% vs(4.8±0.4)%)and western-blot method(F=7.934, P=0.006), and downregulated expression of Collagen Ⅳ protein((3.7±0.4)% vs (4.8±0.4)%)and alleviated fibrosis which was detected by MASSON staining semi-quantification results.All the differences had statistical significance (P<0.01).

TIEGsiRNA may be useful in preventing the progression of diabetic renal fibrosis through upregulating negative feedback factor Smad7 in the Smad signal pathway .

To indicate the mechanism of podocyte injury in diabetic nephropathy (DN) patients by identifying the urinary podocytes and observe the situation of detached podocytes in glomeruli ; to discuss the correlation between the urinary podocyte excretion and the proteinuria, blood glucose(FBG), serum creatinine (SCr)in DN patients by detection of theses items in different phases.

The DN patients were divided into five groups according to the CKD phases, and were divided into three groups according to the volume of proteinuria, namely small, medium and large-volume-proteinuria group. Urinary podocytes and the podocalyxin (PCX) expression state of podocytes in glomeruli were identified and observed by indirect immunofluorescent method. The urinary podocytes of every group were caculated respectively. Then the podocyte number were calculated respectively. Meanwhile, the 24 h proteinuria, FBG and the SCr of DN pateints were tested. The correlation among the proteinuria, SCr, FBG and the urinary podocyte number of DN pateints was analyzed statistcally.

Urinary podocytes were found in 88 percent of patients with DN, whereas 0 of patients with MCD and healthy cases. The absence of expression of PCX was found in DN patients.In contrast, PCX was expressed integrally in MCD patients.The podocytes in small-volume-proteinuria group was (1.5±1.0)/ml, medium-volume-proteinuria group (2.2±0.7)/ml and large-volume-proteinuria group (3.5±1.3)/ml, respectively.The difference from small and medium groups were not signifficent statistically, the others were all significant. The podocyte number increased according to the proteinuria. The correlation between urinary podocyte number and proteinuria, SCr of CKD Ⅰ to Ⅲ DN patients and urinary podocytes number were positive statistically. However, the correlation between SCr of CKD Ⅳ to Ⅴ patients and urinary podocyte number , FBG and urinary podocyte number were not significant statistically.

the mechanism of the podocyte injury in DN patients is present.The podocyte injury in DN may positively correlate to the proteinuria and SCr of CKD Ⅰ to Ⅲ patients, but the FBG and SCr of CKDⅣ-Ⅴpatients may not correlate to the urinary podocyte number.

To investigate the effect of rosiglitazone on the expression of pigment epithelium-derived factor (PEDF) and transforming growth factor-β₁ (TGF-β₁) in the kidney of diabetic rats.

A total of 42 healthy male SD rats (180 to 200 g) were randomly assigned to the normal control (NC) group (n=14), diabetes mellitus (DM) group (n=14), and rosiglitazone (RSG) treatment group (n=14). Diabetes was induced by an intraperitoneal injection of 55 μg/g streptozotocin. The rats in the RSG group were given rosiglitazone sodium 5 μg·g ^-1·d^-1. At the end of 12 weeks, fasting blood glucose, kidney mass, kidney/body mass, 24-hour urinary albumin excretion (UAE), serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), high-density lipoprotein cholesterol (HDL-C), BUN, SCr and PEDF were measured. The expression of TGF-β₁ and PEDF in the kidney was determined by immunohistochemical analysis and Western blot. Statistical analysis was performed using two-tail Student’s t test.

Compared with the NC group, the DM group was characterized by the glomerular hypertrophy, mesangial expansion and glomerular basement membrane thickening; the protein expression of TGF-β₁ was significantly increased (immunohistochemical analysis: 4.60±0.14 vs 1.57±0.14, t=3.052, P<0.01; Western blot: 1053±64 vs 462±70,t=2.817, P<0.01), whereas the protein expression of PEDF was significantly decreased (immunohistochemical analysis: 1.53±0.12 vs 3.96±0.18,t=2.845, P<0.01; Western blot: 228±275 vs 698±120,t=3.152, P<0.01) in the DM group. Compared with the DM group, the glomerular hypertrophy, mesangial expansion and glomerular basement membrane thickening were significantly ameliorated in the RGS group; the protein expression of TGF-β₁ was significantly lower (immunohistochemical analysis: 2.79±0.16 vs 4.60±0.14, t=2.964, P<0.01; Western blot: 753±81 vs 1053±64,t=2.884, P<0.01), whereas the protein expression of PEDF was significantly higher (immunohistochemical analysis: 2.64±0.32 vs 1.53±0.12,t=2.347, P<0.05; Western blot: 473±127 vs 228±275,t=2.334, P<0.05) in the RSG treatment group.

Renoprotection of rosiglitazone on diabetic rats may be mediated by decreased expression of TGF-β₁ and increased expression of PEDF.

To investigate the alteration of ultrastructure and protein expression profile in hippocampus of early diabetic rats, and to explore the possible mechanism of brain damage caused by diabetes.

15 male SD rats(6-8 week-old, 200-250 g) were randomly divided to control group and diabetes group. Diabetic rat model was established by peritoneal injection of STZ 55 mg/kg. After 5 weeks of treatment, ultrastructure of hippocampus were observed by transmission electron microscope(TEM); two-dimensional gel electrophoresis(2-DE) technology was applied to isolate proteins in hippocampus, MALDI-TOF-MS was used to identify the differentially expressed protein.

Pyknosis of nuclei and obvious swelling in end foot of astrocytes were noted in hippocampus of diabetes group under TEM. Eight differential proteins were identified by MALDI-TOF-MS: Cytochrome b-c1 complex subunit, mitochondrial, 14-3-3 proteinβ/α, GFAP and Guanine nucleotide-binding protein G(0) subunit α were up-regulated and ATP synthase subunit d mitochondrial, Thioredoxin-dependent peroxide reductase mitochondrial, and ERP29 were down-regulated in diabetic rat; Endophilin-A1 was only expressed in control group.

Pathological changes found in hippocampus of early diabetic rats may be related to abnormal energy metabolism caused by oxidative stress, and proteins related to aging and degenerative diseases are probably involved in the pathology.

Insulin resistance is one of the main pathophysiological bases of type 2 diabetes. In recent years, it has been found that some important transcription factors are also involved in the occurrence of insulin resistance, such as peroxisome proliferator-activated receptor (PPAR), liver X receptor, sterol-regulatory element binding protein-1c (SREBP-1c), etc. SREBP-1c, a subtype of nuclear transcription factor SREBPs, is an important transcriptional regulator in fat metabolism, and plays a very important role in maintaining the balance of lipid metabolism. Inappropriate expression of SREBP-1c will cause lipid metabolism disorders, resulting in non-adipose tissue lipid accumulation, thus causing metabolic diseases. Therefore, it is believed that SREBP-1c may be the junction point of lipid metabolism disorders, insulin resistance and metabolic syndrome^[1,2]。 Moreover, the expression of SREBP-1c is regulated by various hormones and nutrients such as insulin, glucose and leptin^[3,4]Part of the mechanism is still unclear. In this study, a rat model of insulin resistance was established by feeding high-fat diet, and the expression of SREBP-1c mRNA in the liver of insulin resistant rats and its relationship with adipocytokines such as leptin and tumor necrosis factor-α (TNF-α) were observed. The relationship between SREBP-1c and insulin resistance and its regulatory mechanism were preliminarily discussed.

Several epidemiological studies have shown that the high incidence of diabetes in Asia is related to the rapid economic development and rapid improvement of nutritional level, suggesting that environmental factors may play an important role in the epidemic of diabetes in Asia. Growth inhibition caused by nutrient deficiency can produce compensatory rapid growth phenomenon after nutrient recovery, which is called catch-up growth. Study found that catch-up growth is closely related to insulin resistance and type 2 diabetes^[1]。 Epigenetics is the study of stable and heritable changes in gene function that occur in the absence of DNA sequence alterations. Studies have shown that epigenetic changes are involved in the occurrence of islet β cell function damage and insulin resistance in catch-up growth. The epigenetic mechanism of catch-up growth is expected to become a new field to study the pathogenesis of metabolic diseases such as type 2 diabetes. This paper reviews the progress of catch-up growth and epigenetics.

Type 2 diabetes is a progressive disease characterized by insulin resistance and progressive decline in pancreatic beta cell function. It is well known that good glycemic control is essential for reducing and controlling complications of type 2 diabetes. To reduce the serious consequences of poor glycemic control, the American Diabetes Association recommends a HbA1c control target of less than 7%^[1]。 In the early stages of diagnosis, patients can generally effectively reduce blood sugar by changing their diet, lifestyle, and oral hypoglycemic treatment. However, due to the characteristics of progressive development of the disease, most diabetic patients need to start insulin therapy within 6 years of diagnosis, while patients with poor blood sugar control often need continuous intensive therapy to achieve the blood sugar control goal^[2]。

American Diabetology Association (ADA) 2010 Guidelines^[1]The criteria for diagnosing diabetes were revised. In addition to the past fasting blood glucose (FBG) ≥7.0 mmol/L, or postprandial blood glucose and random blood glucose ≥11.1 mmol/L, it was proposed that glycosylated hemoglobin (HbA1c) ≥6.5% could be included in the diagnostic criteria of diabetes, and HbA1c ranging from 5.7% to 6.1% could be used as a high-risk marker of possible diabetes. It is believed that HbA1c can make up for some shortcomings of the above diagnostic criteria and is a convenient and accurate method, which is undoubtedly a breakthrough in the diagnostic criteria of diabetes. The following will introduce the background of promoting glycosylated hemoglobin screening and diagnosis of diabetes.

The main clinical concerns for insulin therapy to optimize glycemic control are hypoglycemic events and weight gain. Insulin detemir is a new long-acting insulin analogue. Previous studies have shown that it effectively controls blood glucose while rarely occurring hypoglycemic events, especially nocturnal hypoglycemic events, and less weight gain^[1]。 Here, the application of insulin detemir in patients with type 2 diabetes is described as follows.

It has long been recognized that oral glucose stimulates insulin secretion in a significantly greater amount than the insulin release caused by intravenous glucose, a phenomenon known as the "incretin" effect^[1]。 Both glucagon-like polypeptide-1 (GLP-1) and glucose-dependent insulin-releasing peptide (GIP) belong to incretin, but GIP has no effect on islet alpha cells and the islet beta cells of type 2 diabetes patients respond to GIP significantly decreased, thus limiting the clinical application of GIP. GLP-1 is an intestinal peptide hormone. Its physiological functions mainly include: promoting insulin synthesis and secretion, inhibiting β cell apoptosis, promoting β cell proliferation and regeneration, inhibiting glucagon secretion, reducing food intake, delaying gastric emptying, enhancing glucose utilization in peripheral tissues, reducing liver glucose output, etc^[2]。 The physiological effects of GLP-1 and the decrease of GLP-1 secretion in patients with type 2 diabetes suggest that it can be used as a new weapon in the treatment of type 2 diabetes. However, natural GLP-1 has a short half-life, which makes it difficult to directly use it to treat diabetes. Liraglutide is a GLP-1 analog formed by replacing lysine at position 34 with arginine, and adding a 16-carbon palmitoyl fatty acid side chain at position 26. It is 97% homologous to natural GLP-1, and has a half-life of about 12~14 h. It can play a good hypoglycemic effect when administered once a day^[3]。 At the same time, liraglutide can improve beta cell function, significantly reduce blood sugar and systolic blood pressure, and reduce body weight and the incidence of hypoglycemia.

For critically ill patients, accurate real-time blood glucose monitoring may be a safe and effective way to achieve blood glucose standards. The aim of this study was to evaluate the effect of real-time ambulatory blood glucose monitoring on blood glucose control and the risk of hypoglycemia in critically ill patients.

There is a high incidence of depression in diabetic patients. Recent antidepressant studies have shown that 70% of non-diabetic patients respond poorly to initial medication. The aim of this study was to evaluate the effect of initial antidepressant therapy in diabetic patients.

Relatives of patients with type 1 diabetes are at high risk of diabetes. The aim of this study was to investigate the onset pattern of hyperglycemia in relatives of type 1 diabetic patients and the evolution of insulin sensitivity and islet beta cell function in the development and development of diabetes mellitus.

This study aimed to prospectively evaluate the association between the duration of lactation and the incidence of metabolic syndrome in women of childbearing age.

Patients with type 2 diabetes have a greatly increased risk of developing breast cancer, and hyperinsulinemia has been proven to be a major cause of type 2 diabetes and breast cancer. This study hypothesized that reducing high insulin levels by drugs could slow the progression of breast tumors associated with type 2 diabetes.

This study aimed to clarify the secondary failure rate and its predictors of metformin alone therapy in clinical work.

It has been shown that iron deficiency in late pregnancy in non-diabetic women increases glycated hemoglobin, while glycated serum proteins are not affected. This study aimed to verify whether iron deficiency in diabetic women during the third trimester of pregnancy also contributes to the elevation of glycosylated hemoglobin, which is of great significance for the determination of blood glucose monitoring indicators in diabetic women during pregnancy.

The purpose of this study was to determine the effect and extent of ramipril and/or rosiglitazone on pancreatic islet β cell function in patients with impaired fasting blood glucose or impaired glucose tolerance, and to clarify whether these two drugs can prevent or delay the occurrence of diabetes in people at high risk of type 2 diabetes.

It has been reported that glycated serum albumin/glycated hemoglobin in patients with type 2 diabetes is significantly higher than that in patients with type 1 diabetes, suggesting that glycated serum albumin may be more sensitive than glycated hemoglobin, and its mechanism may be related to the obvious blood glucose fluctuation caused by low insulin release in patients with type 1 diabetes. This study aimed to clarify whether endogenous insulin release affects glycated serum albumin and glycated hemoglobin levels in patients with type 2 diabetes.