Volume 06 · Issue 12 · 2014

Traditional diabetes diagnosis and screening methods include measurement of fasting blood glucose (FPG), randomized blood glucose and 2 h blood glucose (2 h PG) after oral glucose tolerance test (OGTT) stress. Due to the shortcomings of high individual variability, poor repeatability, greater influence by meals and physical activity, and the need for timing, the further improvement of diabetes diagnosis and screening efficiency is limited. Glycosylated hemoglobin (HbA_1c) is the product of the non-enzymatic glycosylation reaction between glucose and hemoglobin free amino groups in blood, reflecting the average blood glucose level 2 to 3 months before detection. Since 1968 Rahbar first discovered HbA in red blood cells of diabetic patients_1cIt has been more than 40 years, after repeated exploration, research and practice, people have been interested in HbA_1cIncreasingly in-depth and comprehensive understanding, at present HbA_1cThe clinical application has gradually expanded to the screening, diagnosis and prediction of diabetes.

World Health Organization Recommendation 2011: Use glycosylated hemoglobin (HbA) in areas where conditions are permitted_1c) Diagnosis of diabetes. HbA_1cAchieving the standard is the target of diabetes blood sugar control and the standard for evaluating the effectiveness of diabetes treatment programs. It is an index that has been gradually popularized and applied internationally since the mid-1990s. At present, in a considerable number of countries and regions, HbA_1cIt is the first choice diagnostic indicator of diabetes, China's new version of type 2 diabetes prevention and treatment guidelines (2013 edition)^[1]Suggestions: "It is not recommended to use HbA in China for the time being_1cAs a cutoff point for diabetes diagnosis, but for hospitals with standardized testing methods and strict quality control, with normal reference values between 4.0% and 6.0%, HbA_1c≥6.5% can be used as a reference for the diagnosis of diabetes. "Therefore, it is guaranteed that HbA_1cDetermining quality is very important.

Diabetes is a global epidemic in the 21st century, and haemoglobin A_1c, HbA_1c) Achieving the standard is not only the blood glucose control goal of diabetic patients, but also an effective index to evaluate the blood glucose management treatment plan. HbA_1cIt is also the first diagnostic indicator of diabetes recommended by the World Health Organization (WHO) and many national diabetes societies^[1,2]。 Compared with the traditional diagnostic measure of diabetes, blood glucose, HbA_1cIt has the characteristics of small biological variability, not easily affected by blood sugar fluctuation, no need to take blood on fasting or at a specific time, and little instability before analysis. It is an index that has been gradually popularized and applied internationally since the mid-1990s.

To investigate and analyze the current situation on reference interval and cut- off value of glycated hemoglobin A_1c(HbA_1c).

Thirty- one provinces across the country were covered in this survey, wherein every one of the 1 250 clinical laboratories attending the 2014 external quality assessment program of HbA_1c testing received an online questionnaire. Information regarding the upper/lower limits, cut-off values, data resources, method principles, instruments and reagents of the HbA_1c testing were submitted and collected via the internet, and the cut-off values of HbA_1c were further grouped by testing systems and geographic regions. One-way ANOVA based on data resources, upper/lower limits and cut-off values were conducted utilizing SPSS 19.0 and Microsoft excel 2007, while LSD test were adopted for comparison between groups.

A total number of 953 labs submitted their results. The dominant resources for reference intervals came from manufacturers' instructions (≈70%), National Guide to Clinical Laboratory Procedures (≈17%) or were determined by individual laboratories (7%). The minimums and maximums between upper/lower limits and cut- off values showed notable discrepancies, whereas the medians were approximate to the averages. Cases occurred where the upper limit overlapped with the lower limits, while the P_2.5 and P_97.5 varied significantly amongst subgroups by different testing systems. The range of the lower limits, upper limits and the cut-off value of HbA_1c was 0-6.4%, 5.2%-18.5% and 5.1% -17.0%, respectively. The averages of cut-off values between subgroups by distinct instruments or geographic regions had no statistical differences (P>0.05).

More than 40% of the laboratories set their reference intervals for HbA_1c at 4.0% to 6.0%, with the cut- off value at 6.5%, despite the lack of a nationwide consensus. It is essential to establish a uniformed reference interval and cut- off value for HbA_1c that is adaptable for the major regions as well as prevailing testing systems, which should provide a reference for the standardization of HbA_1c testing.

To evaluate the efficacy and safety of two dose levels of gliclazide MR (30 mg/d and 60 mg/d)in the treatment of Chinese patients with newly diagnosed type 2 diabetes mellitus (T2DM), and its effects on insulin resistance and β-cell function.

A total of 120 subjects with newly diagnosed T2DM were randomized to receive 30 mg/d (Group 30 mg)or 60 mg/d (Group 60 mg)of gliclazide MR in the proportion of 1 to 1 according to random number table for 16 weeks. Glycated hemoglobin A_1c (HbA_1c)was measured as major efficacy index, and secondary indices such as fasting plasma glucose (FPG), two-hour postprandial plasma glucose (2 h PG), 7-point glucose profile, area under curve of insulin (AUC_INS), insulin sensitivity index (SEN) and the indices of the β-cell secretory function [including early insulin secretion index (ΔI ₃₀/ΔG₃₀) , basic insulin secretion index (HOMA-β)and modified β- cell function (MBCI)]. Safety was assessed by adverse events (AEs), and so on. The difference of the measurement data was compared with thet test. The Wilcoxon test was used to assess the statistical difference among the groups.

At 16 weeks, the change from baseline in HbA1c was -1.2%±1.1% in the Group 30 mg and -2.2%±1.4% in the Group 60 mg, intergroup comparison with baseline HbA_1c as a covariate showed that the descent range in the Group 60 mg was more significant (F=4.2, P=0.04). There was no intergroup difference in the change from baseline of FPG, 2 hPG and 7-point glucose profile. Also, no intergroup difference was noted in the change from baseline of AUC_INS and ΔI ₃₀/ΔG₃₀. After treatment, the index of HOMA-β had a significant increasing amplitude in the Group 60 mg compared to that in the Group 30 mg (t=1951.0, P=0.04). The incidence of hypoglycemia related to study drug was 10.5% (6/57)in the Group 30 mg and 16.1%(9/56) in the Group 60 mg. To the end of follow-up, no significant difference in the body mass index was found between the two groups[(24.8±2.6) kg/m² in Group 30 mg and (24.2±2.5) kg/m² in Group 60 mg, t=1.09, P>0.05].

The dose regimen of gliclazide MR 60 mg/d is superior to 30 mg/d in the improvement of HbA_1c and β-cell function for Chinese patients with newly diagnosed T2DM; however, dosage of 60 mg/d increases the incidence of slight hypoglycemia events. Thus, for patients with newly diagnosed T2DM, selection of initial therapy dose should be patient- tailored, based on clinical features of β cell function and hypoglycemia risks.

To investigate the association of sex hormone with the severity of diabetic foot ulcer (DFU) and its effect on prognosis of DFU in postmenopausal women.

From January 2012 to January 2013, clinical data from 158 postmenopausal women with DFU and 162 postmenopausal women with high risk of DFU admitted to Diabetic Foot Center of Ruijin Hospital were collected. The severity of DFU was evaluated on admission. Serum concentration of sex hormone, included follicle stimulating hormone (FSH), lutenizing hormone (LH), prolactin (PRL), estradiol (E2), progesterone (P), testosterone (T), free testosterone (FT), dehydroepiandrosterone (DHEAS), androstenedione (AD) and sex hormone-binding globulin (SHBG) were tested within 48 hours after admission. The association between sex hormone and the severity of DFU was analyzed by using multiple linear regression. All these patients with DFU were followed up for 6 months to observe their outcomes including ulcer healing, recurrence, and non-fatal cardiovascular and cerebrovascular events. Logistic regression was used to analyze the impact of sex hormones on the outcome of DFU.

Serum concentrations of E2, T, FT increased (t=4.47, 2.03, 2.16 respectively;P=0.0001, 0.0410, 0.0350 respectively for trend) with the Wagner grades of DFU in postmenopausal women. Similarly, serum concentration of E2 increased (t=2.41;P=0.02 for trend) with the severity of infection. The level of E2 was positively correlated with the occurrence of non- fatal cardiovascular and cerebrovascular events (OR=1.109, 95%CI:1.002-1.037, P<0.05).

Serum concentration of E2 and T/FT were associated with the severity of DFU in postmenopausal women. The change of E2 might imply the occurrence of non-fatal cardiovascular and cerebrovascular events.

To study the effects of forkhead transcription factor O1 (FoxO1) on the podocyte injury in diabetic rats.

90 Streptozotocin-induced diabetic rats were divided into three groups: diabetic rats (DM,n=30), rats transfected with blank lentiviral vectors (DM plus LV-pSC-GFP group, designated LV- NC,n=30) and rats which were transfected with lentiviral vectors carrying constitutively active FoxO1 (DM plus LV- CA- FoxO1 group, designated LV- CA,n=30). The rats which received an injection of diluent buffer served as normal control (NG,n=30). At 2, 4, and 8 weeks after transfection, the levels of urine albumin, blood glucose, blood urea nitrogen and serum creatinine were measured. Real-time PCR and Western blotting were performed to measure the mRNA and protein levels of FoxO1, podocalyxin (PCX) and nephrin in the renal cortex. Moreover, light microscope and electron microscope were used to observe the structure changes of glomerulus and podocytes. One-way analysis of variance was used for data analysis.

Compared with the LV-NC and DM groups, in the LV-CA group, there was a significant increase in the mRNA and protein levels of FoxO1 ( F_8w were 10 919.75, 3 867.34, respectively, both P< 0.05), and a distinct decrease in the levels of urine albumin, blood urea nitrogen and serum creatinine of rats (except at the two-week time point) ( F_8w were 132.72, 187.68, 503.69, respectively, all P<0.05), the mRNA and protein levels of PCX and nephrin all increased ( F_8w of mRNA were 778.94, 478.10, respectively, both P< 0.05; F_8w of protein were 393.64, 255.79, respectively, both P<0.05) and pathological changes in kidney were also ameliorated, larger renal glomeruli, proliferated mesangial cells, thickened glomerular basement membrane and fused foot processes all were improved.

Up-regulating the expression of FoxO1 by transfecting with constructed lentiviral vectors can definitely improve the podocyte injury in diabetic rats.

To investigate the influence of overexpression of Chemerin on 3T3- L1 adipocyte constructed by recombinant lentiviral on glycometabolism and the potential mechanism.

Rat Chemerin expression of recombinant lentivirus was constructed. This recombinant lentivirus and control lentivirus transfected 3T3-L1 cells respectively. The expression of chemerin in 3T3-L1 cells was detected by real-time reverse transcriptase-polymerase chain reaction (RT-PCR). 3T3-L1 preadipocytes were induced into mature adipocyte by insulin, IBMX and dexamethasone. Oil red O was used to identify the mature 3T3- L1 adipocytes. Recombination lentiviruses were added in culture medium at the eighth day of differentiation. The cells were continuously cultured for five days and then were harvested for series of determinations. Glucose oxidase method was used to test the glucose consumption. The mRNA expression of IRS1, IRS2, Akt1 and FoxO1 were detected by RT- PCR. The protein expression of chemerin, Akt, pAkt, FoxO1 and pFoxO1 were determined by western blotting. The measurement data were measured by mean ± _{standard deviation (}± s₎. Student'st- test was used for comparison of two groups.

Red fluorescence can be observed in 3T3-L1 cells after being infected with recombination lentivirus for 72 h. The expression of chemerin mRNA significantly increased (relative expression: (3.04±0.19)vs(1.01±0.11), t= 15.65, P<0.05) and glucose consumption decreased ((3.30±1.44)vs(6.07±1.15) mmol/L, t=-0.35, P<0.05) in over expression chemerin group comparing with empty- vector control group. There were no difference of IRS1and IRS2 mRNA between the two groups (all P>0.05). Compared to the empty-vector control group, the over expression chemerin group have higher FoxO1 mRNA and protein expression (relative expression: (1.53±0.30) vs (1.03±0.21), t=2.34, P<0.05; (1.04±0.09)vs(0.76±0.14) , t=-2.91, P<0.05), and lower Akt1 mRNA expression (relative expression: 0.76 ± 0.08 vs 1.07 ± 0.15, t=- 3.11, P<0.05), as well as lower Akt, pAkt and pFoxO1 protein expression(relative expression: (0.74±0.21) vs (1.23±0.20), (0.58±0.17) vs (0.92± 0.07), (0.61±0.13) vs (0.89±0.10) , t=2.81, 3.17, 2.93, all P<0.05 ).

Chemerin may reduce glucose consumption in 3T3-L1 by down regulation Akt1 mRNA expression.

To explore the specific mechanism of pancreatic kallikrein(PKK) renal disease in type 2 diabetic mice.

A total number of 20(4 week- old) db/db mice were randomly divided into 2 groups depending on their body weights and blood glucose. One group was treated with PKK (PKK group,n=10, 60 U·kg^-1·d^-1, intraperitoneal injection), while the other was given saline (DM group,n= 10, 1 ml/g, intraperitoneal injection). In addition, littermates db/m mice (NC group,n=8, 1 ml/g, intraperitoneal injection) were given saline as non- diabetic control group. Blood glucose and body weight were measured weekly, and both systolic and diastolic blood pressure were monitored monthly. After treated for 16 weeks, mice were sacrificed and kidney tissues were collected. Light microscopy and transmission electron microscope were used to examine the tubular pathological changes and the ultrastructure, respectively. Immunohistochemistry were performed to detect the expression of epithelial- cadherin (E- cadherin). Real- time PCR was applied to determine the gene expression of interleukin- 1β (IL- 1β) and fibronectin in the whole kidney.

(1) After 16 weeks,both blood glucose and body weight in DM and PKK group were significantly higher than NC group, and the kidney weight /body mass index was lower than NC group (blood glucose for NC,DM and PKK group were (5.4±0.6), (27.4±4.6), (26.9±3.0) mmol/L, expectively (F=86.35,P<0.01) ; Body weights were (24.3±3.1), (42.6±4.8), (41.5±2.6) g, expectively (F= 38.82,P<0.01) ; the kidney weight/body mass index were 12.52±2.53, 9.01±1.25, 9.83±1.18, expectively (F=7.27,P<0.01) ). However, there wasn' t any difference between DM and PKK group. Both systolic and diastolic blood pressures showed no differences between any two groups. (2)The results of transmission electron microscope showed that PKK treatment could significantly improve cellular mitochondrial swelling which was present in both the proximal and distal tubular epithelial cells in DM group. Meanwhile, PKK could also increase the number of mitochondria and ameliorate lipid metabolism disorders in proximal tubular cells as compared to DM group. (3) Compared with NC group, E- cadherin expression was significantly decreased in DM group, while the PKK treatment significantly increased the expression of E- cadherin. Quantitative PCR showed that PKK could significantly decrease the gene expression of IL-1β and fibronectin as compared with DM group.

PKK has protective effects on tubules of db/db mice, which was independent of improvements in blood pressure and blood glucose. The renoprotective effect of PKK might be mediated by reducing inflammation, anti- fibrosis and decreasing the epithelial to mesenchymal transition.

To explore the relationship between phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) and diabetic macroangiopathy, and the intervention effect of atorvastatin.

Total of 25 healthy male Wistar rats (4 weeks old) were randomly divided into experiment group (EX,n=19) and normal control group (NC,n=6) with random number table, the rats were fed with standard rodent chow diet or high- fat, high- sugar diet in the control and EX group. The rates in EX group were injected intraperitoneally with 1% streptozotocin(STZ) (30 mg/kg) and blood glucose≥7.8 mmol/L was considered as DM. The well- estabolished DM rats model were then randomly divided into two subgroups: diabetic control group (DM group,n=7) and atorvastatin-treated diabetic group (ATR group,n=8). The rats in ATR group were given intragastric administration of atorvastatin (10 mg · kg^-1·d^-1) for 8 weeks, and DM group was given drinking water in the same way. Body weight was measured weekly. The expression of phosphorylated p38 MAPK, neuclear factor(NF)-κB, and monocyte chemoattractant protein-1(MCP-1) in the thoracic aorta and blood lipids, intercellular cell adhesion molecule- 1(ICAM- 1), vascular cell adhesion molecule- 1(VCAM- 1) were measure by immunohistochemistry. The data were analyzed with SNK-q and Pearson correlation analysis.

Structural destructions in DM rat aorta tissue were observed by HE staining, which characterized by endothelia cells swollen and degeneration and intima thickness. Smooth muscle disorders and collagen fiber hyperplasia in tunica media were also found in DM rats when compared to NC animals. All these pathological alterations can be improved by atorvastatin treatment. The expression of p-p38MAPK, NF-κB and MCP-1 was significantly increased in DM rats when compared to those in NC group (Z= -3.466, -3.728, -3.832, P<0.05) and all these increasing were partly reversed by atorvastatin treatment( Z= -2.308, -2.160, -2.501, P< 0.05). The expression of NF-κB and MCP-1 were both found to be correlated with p-p38 MAPK levels(r=0.406, 0.310, both P<0.05). Compared with NC group, the levels of serum NF-κB, ICAM-1, VCAM-1, total cholesterol(TC), triglyceride(TG), and low-density lipoprotein(LDL) were significantly increased in DM group(t= -9.200, -5.586, -7.041, -8.788, -5.247, -5.142, all P< 0.05), whereas the level of high-density lipoprotein(HDL) decreased in DM group ( t=5.598, P<0.05). After 8 weeks of atorvastatin treatment, the serum levels of NF- κB, ICAM- 1, VCAM- 1, TG, TC, LDL were all significantly decreased compared to DM group( t=3.661, 3.360, 2.496, 4.348, 3.077, 3.446, all P<0.05).

Activation of p38 MAPK pathway plays an important role in the development of diabetic macroangiopathy. Atorvastatin may ameliorate diabetic macrovascular disease through activating p38 MAPK and decreasing vascular inflammation response.

To evaluate the efficacy and safety of liraglutide and neutral protamine hagedorn (NPH) in combination with metformin in newly diagnosed type 2 diabetic patients with continuous glucose monitoring system (CGMS). A total of 63 newly diagnosed type 2 diabetic patients were randomized into the liraglutide plus metformin group and NPH plus metformin group. They were treated for 12 weeks. Continuous glucose monitoring (CGM) was performed for 72 hours in both groups before and after treatment. The parameters of blood glucose fluctuations, blood lipid and BMI were measured and compared before and after treatment. Fasting plasma glucose (FBG), glycated hemoglobin A1c (HbA_1c) and mean blood glucose (MBG) were decreased in both groups after 12 weeks^, treatment, but there was no statistical difference in the comparison between the two groups (P>O.05). In the liraglutide group, the mean average glucose excursions (MAGE), large amplitude of glycemia excursion (LAGE), mean of daily differences (MODD), mean postprandial glucose excursion (MPPGE), T_PG≤3.0 mmol/L, body mass index (BMI), triglyceride (TG), total cholesterol (TC), low density lipoprotein- cholesterol (LDL- C) and systolic blood pressure (SBP) were significantly lower than those in the NPH group respectively(t=2.773,3.250,2.870,2.721,4.955,2.686,2.152, 2.310,2.342,2.048, P<0.05, respectively). The incidence of hypoglycemia episode in the liraglutide group was significantly lower than in the NPH group (χ²=4.14, P<0.05). Both groups have a good control of blood glucose for newly diagnosed type 2 diabetic patients. As compared with NPH, liraglutide can reduce the glucose fluctuation and have less hypoglycemia event, while liraglutide is superior in weight reduction, improvement of blood lipid and blood pressure.

Diabetes mellitus is one of the four major non-communicable diseases identified by WHO^[1]The survey shows that there are currently 280 million people with diabetes worldwide, and the number is expected to double by 2025, with the Asia-Pacific region accounting for 30% of all diabetes patients^[2]。 The prevalence of diabetes among people over 20 years old in China has reached 9.7%, and the prevalence of pre-diabetes has reached 15.5%^[3]。 Diabetic retinopathy is the most serious and common ocular complication in diabetic patients^[4]The prevalence was 27.0% to 43.1%^[5,6,7,8]。 The early symptoms of diabetic retinopathy are insidious, with only a small amount of retinal microangioma and hemorrhage. The patient has no self-conscious symptoms, but the prognosis of the late stage of the lesion is poor^[9]It brings a huge burden to patients, families and society. However, diabetic retinopathy can be prevented and treated, among which good awareness of diabetic retinopathy and regular follow-up of diabetic patients are crucial for clinical prevention and treatment, and timely and effective treatment can reduce severe visual loss of patients^[10]。 This study investigated the cognitive status of diabetic retinopathy among diabetic patients in Desheng Community, Beijing, which is reported below.

About 7% of the world's population carries hemoglobin variants, 1/3 of them have clinical symptoms, and some hemoglobin variants are life-threatening^[1]。 1,173 hemoglobin variants have been identified so far^[2]。 Hemoglobin variants as glycated hemoglobin (HbA_1c) A distracting factor for laboratory testing^[3]It has attracted widespread attention because of its possible impact on blood glucose assessment. In this paper, hemoglobin variants and HbA_1cThis paper summarizes the relationship between hemoglobin variants and the influence of hemoglobin variants on diabetic blood glucose monitoring, so as to be used for reference in daily clinical work.

Maturity onset diabetes of the young (MODY) is an early onset diabetes inherited within the family in an autosomal dominant manner. Patients with MODY are usually diagnosed with diabetes around the age of 10 to 45, without obesity or insulin resistance, often accompanied by mild hyperglycemia, and do not need to use insulin to control blood sugar for at least 2 years after diabetes diagnosis, and glutamate decarboxylase antibodies and tyrosine phosphatase antibodies are negative^[1]。 There are currently 11 known MODY-causing genes, among which glucokinase gene mutation diabetes mellitus (MODY2), hepatocyte nuclear factor-1 α gene mutation diabetes mellitus (MODY3), and hepatocyte nuclear factor-4 α gene mutation diabetes mellitus (MODY1) are more common. Others such as insulin promoter factor 1 gene mutation diabetes (MODY4), hepatocyte nuclear factor-1 β gene mutation diabetes (MODY5), neurogenic differentiation factor 1 gene mutation diabetes (MODY6), etc. are relatively rare^[2,3]。 Many studies have found that the types of gene mutations in MODY patients include: missense mutations, in-frame deletion mutations and other point mutations. In recent years, studies have found that they also include deletion and duplication of large gene fragments^{[4,5,6,7,8,9,10]}。 This paper mainly introduces the research progress of deletion and duplication of large fragments of MODY-related genes.

In recent years, the incidence of diabetes gradually tends to be younger, and the incidence of adolescents has increased significantly, especially the obese. The incidence of diabetes among Chinese adolescents is more than four times that of American adolescents of the same age, and the incidence of diabetes among Chinese adolescents aged 7-17 is 1.9%; 14.9% in prediabetes^[1]。 According to the etiological classification, juvenile diabetes mainly has the following types: Type 1 diabetes mellitus (T1DM) (further divided into immune-mediated and idiopathic), Type 2 diabetes mellitus (T2DM), maturity-onset diabetes of the young (MODY) and other types of diabetes. Juvenile diabetes is mainly T1DM^[2]In the past ten years, more and more reports show that with the increase of obesity incidence in adolescents, the incidence of T2DM also tends to increase^[3,4,5,6]。 In the past, T1DM was always considered more severe because of its insulin dependence and risk of hypoglycemia, so when adolescents were diagnosed with T2DM, clinicians and family members did not pay attention to it. However, some recent studies have shown that patients with T2DM have more complications and higher mortality than patients with T1DM with the same course of disease and similar blood sugar control. There are few studies on the outcome of type 1 and type 2 diabetes in adolescents in China, so this paper mainly refers to foreign literatures to compare the long-term outcome of T1DM and T2DM in adolescents.

A 20-year-old male with small testicles since childhood and no development after puberty, but an erection. Height 192 cm, weight 67 kg, blood pressure 145/95 mmHg (1 mmHg =0.133 kPa), childlike face, childlike voice, no Adam's apple, acceptable intelligence, no relevant eye signs, underdeveloped muscles, multiple depigmentation spots on the trunk and limbs, no hair loss, no beard, no axillary hair in both axils, soft body hair, and inverted triangular pubic hair. No cervical webs and cubitus valgus were observed, the thyroid gland was swollen and hard at second degree, the surface was not flat, the breast was slightly larger, the heart and lungs were not abnormal, and the liver and spleen were not swollen. There is no similar disease in the family, the parents are not close relatives, and the mother is 57 years old. Laboratory test: blood routine: white blood cells 4.1×10^-9/L (4~10), lymphocytes 52.51% (20~40), serum lactate dehydrogenase (LDH) 240 U/L (135~225), serum alkaline phosphatase (ALP) 147 U/L (40~129), serum creatine kinase (CK) 203 U/L (39~308), serum alanine aminotransferase (ALT) 62 U/L (5~40), serum gamma glutamyltransferase (GGT) 72 U/L (10~47), serum aspartate transferase (AST) 49 U/L (8~40), serum free triiodothyronine (FT3) 4.08 pmol/L (2.63~5.70), serum free thyroxine (FT4) 14.20 pmol/L (9.01~19.00), serum thyroid stimulating hormone (TSH) 2.14 mU/L (0.35~4.94), serum thyroid peroxidase antibody (TPOAb)>1 000 (0.00~5.61), thyroglobulin antibody (TGAb) 782 U/ml (0.00~4.11), fasting blood glucose (FPGAB) Insulin autoantibody (IAA), glutamate decarboxylase autoantibody (GADA) and islet cell autoantibody (ICA) were negative, and the insulin release curves at 0, 1 and 2 h were 4.54, 17.61, 25.16 ng/ml (4.1-4.6), ACTH 18.11 pg/ml (0-46), COR 295.6 mmol/L (85.3-459.6), serum free testosterone (F-test) 32.11 pmol/L (55.05-185.50), sex hormone binding globulin (SHBG) 24.20 μ mol/L (13.00~71.00), serum testosterone (TES) 9.33 nmol/L (9.08~55.23), serum androstenedione (AND) 13.90 nmol/L (1.05~11.52), serum dehydroepiandrosterone (DHS) 7.33 μ mol/L (2.117~15.20), serum luteinizing hormone (LH) 21.90 mU/L (0.80~7.60), follicle stimulating hormone (FSH) 39.00 (0.70~11.10) mU/L. Serum estradiol (E₂）<73.40 pmol/L (73.40-206.00), and serum prolactin (PRL) 127.20 mU/L (53.00-360.00). Semen test: Semen volume 3 ml, pH 7.1 (7.2~80), total sperm count 0. Testicular ultrasound: 2.29 cm ×0.88 cm on the right side and 2.20~0.91 cm on the left. Chromosomes were collected from peripheral blood, specimen number 44762, karyotype 47, XXY. Diagnosis: 47, XXY sex chromosome syndrome, congenital testicular dysplasia, diabetes, autoimmune thyroid disease, hypertension, vitiligo.

Lipoatrophy is a rare disease characterized by different degrees of adipose tissue loss causing lipodystrophy with significant hyperlipidemia, elevated basal metabolism without hyperthyroidism and insulin resistant diabetes with little ketosis tendency. A case of generalized lipoatrophy with adolescent onset and severe osteoporosis is presented.

Diabetic peripheral neuropathy (DPN) is one of the common diabetic complications in clinic. Most of them are presented as paresthesia and chronic mild to moderate pain, while acute severe painful insulin neuritis is relatively rare. A case of insulin neuritis is reported and the literature is further reviewed.

gestational diabetes mellitus (gestational diabetes mellitus, GDM)^[1]It refers to different degrees of abnormal glucose metabolism occurring during pregnancy, excluding diabetes already existing before pregnancy. Disputes about the diagnostic criteria and treatment of GDM have never stopped at home and abroad, which not only reflects the importance of GDM diagnosis, but also poses severe challenges to the treatment of GDM.

The 5th Forum of Young and Middle-aged Diabetes Physicians was held in Taiyuan, Shanxi Province on August 7-9. The conference was hosted by the Diabetes Branch of the Chinese Medical Association, hosted by the Youth Committee of the Diabetes Branch of the Chinese Medical Association, and supported by the Chinese Diabetes Journal. More than 400 young talents from all over the country attended the conference.

Studies have shown that C-type lectin domain family 16 member A (Clec16a; KIAA0350) is a susceptibility gene for type 1 diabetes, multiple sclerosis, and adrenal dysfunction diseases, but its function is unknown. Soleimanpour and others from the University of Pennsylvania Perelman School of Medicine found that Clec16a is a membrane-associated endosomal protein that interacts with E3 ubiquitin ligase Nrdp1 by using isotope random or targeted differentiated interaction technology (I-DIRT), mass spectrometry and co-immunoprecipitation methods. Clec16a deletion leads to upregulation of the Nrdp1 target Parkin, which is the primary regulator of mitophagy.

Loss of functional beta cell mass is a characteristic of type 1 and type 2 diabetes, and it is necessary to find ways to restore beta cells. The homologous domain transcription factor NK6 homeobox 1 (Nkx6.1) is required for β cell development. Overexpression of Nkx6.1 in rat pancreatic islet cells can cause β cell proliferation and enhance glucose-stimulated insulin secretion, but the molecular mechanism by which Nkx6.1 activates β cell proliferation is unclear. Nuclear Receptor Subfamily 4, Group A Orphan Nuclear Receptor Family (Nr4a) includes three members: Nr4a1/Nur77, Nr4a2/Nurr1, and Nr4a3/NOR1. Researchers such as Tessem from Duke University Medical Center in the United States found that Nkx6.1 regulates islet β-cell proliferation by regulating the genes of Nr4a1 and Nr4a3.

db/db leptin receptor mutant mice are animal models of type 2 diabetes. Do et al. of the University of Queensland, Australia, studied the nature of islet secretion defects through db/db mice. The researchers compared glucose tolerance between db/db mice and wild-type mice.

Encode ATP-sensitive K⁺Genetic mutations in the channel (KATP channel) decrease the sensitivity to ATP inhibition, which in turn decreases the sensitivity to ATP inhibition by inhibiting β-cell glucose-stimulated free calcium ([Ca²⁺] i) activity and insulin secretion, leading to neonatal diabetes. Gap junctions of connexin 36 (Cx36) also regulate islet cell electrical activity; Once the Cx36 gene was knocked out, at basal glucose levels, beta cells showed [Ca²⁺] elevation of i.

Betatrophin (also known as lipasin or angiopoietin-like protein 8) is a recently discovered protein secreted by the liver and white adipose tissue under the condition of insulin resistance. It can significantly stimulate the proliferation of insulin beta cells in mice, which may help to explore new methods for treating diabetes. Previous studies have shown that overexpression of liver betatrophin protein can increase beta cell replication in mice by 17-fold. However, whether betatrophin can stimulate replication of human beta cells is unknown. Jiao et al. from the University of Pennsylvania Perelman School of Medicine observed the effect of betatrophin on human beta cells by transplanting human pancreatic islets into immunodeficient mice whose livers overexpressed betatrophin.