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B‑cell lymphomas (BCLs) are malignant lymphoid tumours originating from the malignant proliferation and transformation of mature lymphocytes at various stages of differentiation and clonal expansion of the lymphatic and circulatory systems. Efforts to control or even eradicate BCLs are frequently hampered by the development of drug resistance. Autophagy is an evolutionarily conserved biological process of the energy metabolism. By degrading intracellular organelles and proteins, autophagy provides cells with biochemical reaction substrates for the maintenance of homeostasis under nutrient deprivation or other stressful conditions. Accumulating evidence indicates that autophagy plays an important role in chemotherapy resistance. S100A8 is an important member of the calcium‑binding protein family that plays an important role in regulating tumour resistance to chemotherapy, while the specific molecular regulatory mechanisms remain unclear. In the present study, by employing three BCL cell lines (Daudi, SUDHL‑4 and JeKo‑1), it was demonstrated that BCL cells with a strong drug resistance also exhibited active autophagy. In addition, S100A8 was found to be crucial for regulating drug resistance and promoting autophagy in BCL cells. Interference of S100A8 significantly downregulated Bcl‑2/adenovirus E1B 19‑kDa protein‑interacting protein 3 located in the mitochondria and endoplasmic reticulum to further inhibit autophagy. In addition, S100A8 interference markedly inhibited the formation of the BECN1‑PI3KC3 complex and promoted B‑cell lymphoma 2 expression, which collectively inhibited autophagy.

To investigate the effect of autophagy on the drug resistance of different human lymphoma cells.Human Burkitt's lymphoma cell Daudi, human B lymphoma cell SUDHL-4, and human mantle cell lymphoma cell JeKo-1 were taken as the research subjects. The expression of Atg5 was inhibited by the treatments of autophagy inhibitors or stable interference via lentivirus infection. The autophagy activity of B lymphoma cell was changed, and the changes of lymphoma cells to the drug resistance of ADR and VCR was observed.JeKo-1 cells showed the strongest resistance to ADR and VCR, followed by SUDHL-4, and Daudi cells showed the weakest resistance to ADR and VCR. At the same time, JeKo-1 cells showed the strongest autophagy activity, followed by SUDHL-4, and Daudi cells showed the weakest autophagy activity. After the treatments of autophagy inhibitors or stable Atg5 interference, the resistance of lymphoma cells to ADR and VCR was significantly weakened, and there was the positive correlation at the drug resistance and the autophagy activity of B lymphoma cell.The higher autophagy activity in lymphoma cells, the lower chemotherapy resistance of the lymphoma cells after autophagy was inhibited.自噬对B细胞淋巴瘤细胞耐药性的影响.探讨细胞自噬对不同种人源淋巴瘤细胞耐药性的影响.以人Burkitt′s淋巴瘤细胞Daudi、人B淋巴瘤细胞SUDHL-4和人套细胞淋巴瘤细胞JeKo-1为研究对象，通过自噬抑制剂处理细胞和慢病毒稳定感染干扰Atg5基因的表达，改变B细胞淋巴瘤细胞的自噬活性，并观察淋巴瘤细胞对ADR和VCR的耐药性的变化.JeKo-1细胞对ADR和VCR具有较强的耐药性，SUDHL-4次之，Daudi细胞对ADR和VCR的耐药性最弱。同时，JeKo-1细胞自噬活性也最强，SUDHL-4次之，Daudi细胞自噬活性最弱。自噬抑制剂处理或稳定干扰Atg5基因的表达后，淋巴瘤细胞对ADR和VCR的耐药性显著降低，且耐药性降低程度与淋巴瘤细胞本身自噬活性呈正相关.自噬可以增强淋巴瘤细胞Daudi、SUDHL-4和JeKo-1对ADR和VCR的耐药性，自噬活性越高，淋巴瘤细胞的耐药性越强.

Diffuse large B‑cell lymphoma (DLBCL) is the most common and aggressive form of non‑Hodgkin's lymphoma. Extracellular vesicles (EVs) derived from cancer cells are known to modify the tumor microenvironment. The aim of the present study was to investigate the role of miR‑125b‑3p carried by EVs in DLBCL in vitro and in vivo. TNFAIP3 expression in patient lesions was measured and the upstream miR that regulates TNFAIP3 was predicted using the starBase database. EVs were isolated from DLBCL cells and identified. DLBCL cells were transfected with pcDNA to overexpress TNFAIP3 or inhibit miR‑125b‑5p expression, incubated with EVs, and treated with rituximab to compare cell growth and TNFAIP3/CD20 expression. DLBCL model mice were administered EVs, conditioned medium, and rituximab to observe changes in tumor size, volume, and weight. TNFAIP3 was downregulated in patients with DLBCL and its levels further decreased in patients with drug‑resistant DLBCL. Overexpression of TNFAIP3 in DLBCL cells enhanced the inhibitory effect of rituximab and increased CD20 expression. miR‑125b‑5p targeted TNFAIP3. Inhibition of miR‑125b‑5p enhanced the inhibitory effect of rituximab in DLBCL cells. The EV‑carried miR‑125b‑5p reduced the sensitivity of DLBCL cells to rituximab, which was averted by overexpression of TNFAIP3. EVs reduced the sensitivity of DLBCL model mice to rituximab via the miR‑125b‑5p/TNFAIP3 axis. The study findings indicate that the tumor‑derived EVs carrying miR‑125b‑5p can enter DLBCL cells and target TNFAIP3, thus reducing the sensitivity of DLBCL to rituximab, which may provide a novel therapeutic approach for DLBCL.

Objective: To investigate the in vitro biological characteristics of side-population(SP) cells in mantle cell lymphoma(MCL).The SP cells in JeKo-1 cells were enriched by continuous culture and sorted by flow cytometry（FCM）, and the expression of CD19 and IgM were analyzed. The differences of gene expression and their self-renewal ability between SP cells and non-SP cells were estimated by qRT-PCR and colony-forming assay(CFA) respectively.SP cells in JeKo-1 cells could be enriched by continuous sorting and in vitro cultureing, and it was found that CD19JeKo-1 cell line of mantle cell lymphoma contains SP cells, which can be enriched by continuous sorting and culture for research. The SP cells in JeKo-1 contain four different cell populations with different immunophenotypes： CD19Jeko-1细胞株中边群细胞的免疫表型、干细胞基因和集落形成能力的生物学特点.初步探讨套细胞淋巴瘤中边群细胞的体外细胞生物学特性.利用流式细胞术分选结合连续培养富集JeKo-1细胞中的边群细胞，并对其进行CD19、IgM免疫表型分析；用qRT-PCR进行基因验证及集落形成实验了解边群细胞及非边群细胞基因表达及体外自我更新能力的差异.通过连续分选结合培养的方法可以富集JeKo-1细胞株中的边群细胞，且边群细胞中包含比例不同的4群细胞： CD19套细胞淋巴瘤JeKo-1细胞株含有边群细胞，该群细胞可通过连续分选及培养进行富集后用于研究；JeKo-1中的边群细胞具有更强的干性基因及体外自我更新能力，并含有4种免疫表型不同的细胞群体：CD19

To investigate the expression and significance of LncRNA RP11-513G11.1 in peripheral blood of patients with diffuse large B-cell lymphoma (DLBCL), and to analyze its correlation with clinicopathological features and prognosis of patients.The serum samples of 93 patients with DLBCL(DLBCL group) and 62 normal persons (control group) were collected from the Department of Hematology, Southwest Medical University. The expression of RP11-513G11.1 in serum samples was detected by real-time fluorescence quantitative PCR, the relationship between the RP11-513G11.1 expression with clinicopathological characteristics and prognosis was analyzed.Compared with normal control group, the expression of RP11-513G11.1 significantly increased in DLBCL patients (P0.001). The expression of RP11-513G11.1 not related with the age, sex, course of treatment and germinal center B-cell-like lymphoma(GCB) subtypes of the patients, but it related with the diameter of tumor,Ann Arbor stage,B symptoms,chemosensitivity and the international prognostic index(IPI) (P0.05). The progression-free survival time and overall survival time of patients, whom with high expression of RP11-513G11.1 were significantly shorter than those of RP11-513G11.1 low expression（P0.001）. The median progression-free survival time and overall survival time of chemotherapy-sensitive patients were significantly longer than those of chemotherapy-resistant patients (P0.001). Univariate analysis and multivariate Cox regression analysis showed that Ann Arbor stage, RP11-513G11.1 expression, IPI and chemosensitivity were also the independent factors affecting the prognosis of DLBCL patients（P0.05）.RP11-513G11.1 is highly expressed in patients with DLBCL, which is related with the prognosis of DLBCL patients.LncRNA RP11-513G11.1在弥漫大B细胞淋巴瘤患者外周血中的表达及意义.探讨LncRNA RP11-513G11.1在弥漫大B细胞淋巴瘤(DLBCL)患者外周血中的表达及意义.收集93例于西南医科大学血液科确诊为DLBCL（DLBCL组）患者和62例正常人（对照组）血清标本，采用实时荧光定量PCR法检测血清标本中RP11-513G11.1的表达，分析其表达与患者临床病理特征及预后的关系.RP11-513G11.1在DLBCL患者血清中的表达明显高于正常对照组（P0.001）；RP11-513G11.1的表达与患者的年龄、性别、治疗周期及生发中心B细胞淋巴瘤(GCB)亚型无关（P0.05），而与肿瘤大小、Ann Arbor分期、B症状、化疗敏感性及淋巴瘤国际预后指数（IPI）均显著相关(P0.05)；RP11-513G11.1高表达的患者无进展生存时间及总生存时间与低表达者比较，明显缩短（P0.001）。化疗敏感者的中位无进展生存时间及总生存时间与化疗耐药者比较，均明显延长（均P0.001）。单因素分析及多因素Cox回归分析发现，Ann Arbor分期、RP11-513G11.1表达水平、国际IPI指数及化疗敏感性均是影响DLBC患者预后的独立因素（P0.05）.RP11-513G11.1在DLBCL患者中高表达，且与DLBCL患者的预后相关.

Although metabolomics are desirable to understand the pathophysiology of gestational diabetes mellitus (GDM), comprehensive metabolomic studies of GDM are rare. We aimed to offer a holistic view of metabolites alteration in GDM patients and investigate the possible multimarker models for GDM diagnosis. Biochemical parameters and perinatal data of 131 GDM cases and 138 controls were collected. Fasting serum samples at 75 g oral glucose tolerance test were used for metabolites by ultra performance liquid chromatography-quadrupole-time of flight-mass spectrometry, ultra performance liquid chromatography-triple triple-quadrupole-mass spectrometry and gas chromatography- time-of- flight mass spectrometry platforms. Significant changes were observed in free fatty acids, bile acids, branched chain amino acids, organic acids, lipids and organooxygen compounds between two groups. In receiver operating characteristic (ROC) analysis, different combinations of candidate biomarkers and metabolites in multimarker models achieved satisfactory discriminative abilities for GDM, with the values of area under the curve (AUC) ranging from 0.721 to 0.751. Model consisting of body mass index (BMI), retinol binding protein 4 (RBP4), n-acetylaspartic acid and C16:1 (cis-7) manifested the best discrimination [AUC 0.751 (95% CI: 0.693-0.809), p < 0.001], followed by model consisting of BMI, Cystatin C, acetylaspartic acid and 6,7-diketoLCA [AUC 0.749 (95% CI: 0.691-0.808), p < 0.001]. Metabolites alteration reflected disorders of glucose metabolism, lipid metabolism, amino acid metabolism, bile acid metabolism as well as intestinal flora metabolism in GDM state. Multivariate models combining clinical markers and metabolites have the potential to differentiate GDM subjects from healthy controls.

To identify the appropriate visceral adipose tissue (VAT) cutoff values for the diagnosis of abdominal obesity in predicting diabetes and the corresponding waist circumference in the Chinese population.At baseline, 381 volunteers aged 35-75 years were enrolled without diabetes from the Shanghai urban area. Anthropometry and VAT area determined by magnetic resonance imaging were measured. During the average 7.8 years of follow-up, glucose tolerance was monitored. Receiver operating characteristic (ROC) curve analysis was used to define the optimal cutoff points for abdominal obesity.At the end of the study, 290 participants were followed up, in which 63 participants developed diabetes. Using ROC curve analyses in participants with normal glucose regulation, the appropriate VAT cutoff was 90 cm(2) for both genders to predict diabetes development. In logistic regression models, the relative risks (95% confidence intervals) of VAT value over 90 cm(2) were 3.35 (1.10-10.18, P=0.033) in men and 4.57 (1.73-12.07, P=0.002) in women after adjusted for age, impaired glucose regulation, hypertension and dyslipidemia. The optimal waist circumference cutoffs were 88 cm for men and 82 cm for women to indicate VAT value over 90 cm(2) in ROC analyses.VAT cutoff of 90 cm(2) is useful for defining visceral obesity in Chinese individuals. The appropriate waist circumference cutoffs for abdominal obesity are 88 cm for men and 82 cm for women in the Chinese population.

To explore the associations of the level of glycated albumin (GA) with coronary artery disease (CAD).A total of 306 patients undergoing coronary angiography (CA) were collected. There were 201 males and 105 females with an age range of 38-86 years. CA was the major diagnostic criteria of CAD. Metabolic syndrome was diagnosed according to the Guideline on PreventionTreatment of Blood Lipid Abnormality in Chinese Adults.(1) CAD was found in 227 patients (74.2%). The levels of 2 h postprandial glucose, GA and hemoglobin A1c in the CAD patients were higher than those in the non-CAD counterparts (all P0.05). (2) In the subgroup of normal glucose tolerance (NGR), the CAD patients had a higher level of GA than the non-CAD patients ((15.0 ± 2.1)% vs (13.3 ± 1.7)%, P0.01). And the level of GA was higher in the patients with 1-vessel ((14.8 ± 2.1)% vs (13.3 ± 1.7)%, P0.05) and multi-vessel lesions ((15.1 ± 2.1)% vs (13.3 ± 1.7)%, P0.05) than that in the non-CAD counterparts (all P0.05). Similar results were obtained in the hyperglycemia subgroup. (3) Logistic regression demonstrated that the level of GA was independently correlated with CAD after adjusting other traditional factors among all subjects, NGR and hyperglycemia subgroup.The serum level of GA becomes significantly elevated the CAD patients. And it is an independent risk factor of CAD in both hyperglycemic and NGR patients.

To explore the relationship between glycated albumin (GA) level and pancreatic β cell function in newly diagnosed type 2 diabetics.The subjects sought the confirmation of diabetes diagnosis or underwent diabetes screening tests in high-risk patients from January 2008 to October 2010. All of them underwent 75 g oral glucose tolerance test (OGTT) and insulin releasing test. The levels of GA and hemoglobin A1c (HbA1c) were analyzed by liquid enzymatic method and high performance liquid chromatography respectively. Homeostasis model assessment (HOMA) was used to evaluate the basal insulin resistance (HOMA-IR) and pancreatic β cell function (HOMA-β). ΔI30/ΔG30 was used to evaluate early-phase insulin secretion after a glucose load.(1) Among 500 type 2 diabetics according to the diagnostic criteria of WHO (1999), 279 were males and 221 were females. Average age was 56.3 ± 12.3, GA (21.1 ± 5.4)% and HbA1c (7.0 ± 1.3)%. (2) A significantly positive relationship was shown between HbA1c and GA (r = 0.691, P0.01). GA was also positively correlated with fasting plasma glucose (FPG), 0.5 hPG, 1 hPG, 2 hPG and 3 hPG after a glucose load of OGTT test (r = 0.511 - 0.627, P0.01). (3) GA was negatively correlated with body mass index (BMI) (r = -0.112, P0.01), HOMA-β (r = -0.350, P0.01) and ΔI30/ΔG30 (r = -0.263, P0.01). (4) Multivariant stepwise regression analysis showed that HbA1c, FPG, 3 hPG and ΔI30/ΔG30 were independent factors of GA level.Glycated albumin level is closely correlated with the function of early-phase insulin secretion in newly diagnosed type 2 diabetics.

To assess the validity of combined detection of hemoglobin A1c (HbA1c) and glycated albumin (GA) in diabetic screening.A total of 1480 subjects at our out-patient department from March 2007 to December 2009. Those suspected of diabetes or at a high risk of diabetes were enrolled. The study population included 677 males and 803 females with a mean age of 52.7 years. All subjects received an oral glucose tolerance test (OGTT) after a 10-hour fasting. Glycated albumin (GA) and hemoglobin A1c (HbA1c) were measured with liquid enzyme method and high pressure liquid chromatography respectively.(1) According to World Health Organization diabetes diagnosis criteria, there were 562 subjects with normal glucose tolerance (NGT), 411 subjects with impaired glucose regulation (IGR) and 507 subjects with newly diagnosed diabetes mellitus (DM). The level of HbA1c and GA had a rising tendency among NGT, IGR and DM groups (P0.01). (2) Pearson correlation analysis demonstrated that HbA1c had a positive association with GA (r = 0.75, P0.01). (3) Using OGTT as golden standard of diabetic diagnosis, receiver operator characteristic (ROC) curve indicated that HbA1c and GA were strong predictors of diabetes. The area under curve (AUC) was 0.882 and 0.881 respectively with no significant difference (P0.05). (4) The sensitivity of combined use of HbA1c and GA at optimal cut-off points of 6.1% and 17.1% was significantly higher than that of single use of HbA1c or GA in diabetic screening (94.7% vs 81.1%, 88.4%, P0.01).A combined detection of HbA1c and GA may improve the efficacy of diabetic screening. The subject with HbA1c ≥ 6.1% or GA ≥ 17.1% is recommended to undergo OGTT for confirming a diagnosis of diabetes.

To investigate the relationship of liver enzymes with hyperglycemia in a large population in Shanghai and identify the association between liver enzymes and insulin resistance.A total of 3 756 participants were enrolled. Each participant underwent an oral glucose tolerance test and completed a questionnaire. Anthropometric indices were recorded and serum samples were collected for measurement.Liver enzymes concentrations were independently associated with i-IGT, IFG+IGT, and diabetes. With the increase of ALT and GGT concentrations, ORs for i-IGT, IFG+IGT, and diabetes increased gradually. By comparing patients in the highest quartile of GGT concentrations or ALT concentrations with those in the lowest quartile (Q1), ORs for i-IGT, IFG+IGT, or diabetes was significant after adjustment. Both ALT and GGT concentrations were linearly correlated with HOMA-IR and independently associated with HOMA-IR [ALT OR (95% CI): 2.56 (1.51-4.34) P=0.00; GGT OR (95% CI): 2.66 (1.53-4.65) P=0.00].Serum ALT and GGT concentrations were closely related to pre-diabetes and diabetes in the Shanghai population and positively associated with insulin resistance.

1. Recent reports have described the role of osteocalcin in glucose metabolism and glycaemic variability has been proven to be associated with an increased risk of diabetes complications. However, the relationship between osteocalcin and glycaemic variability remains unclear. The aim of the present study was to examine the relationship between serum osteocalcin and glycaemic variability, as determined by a continuous glucose monitoring (CGM) system in patients with Type 2 diabetes mellitus (T2DM). 2. Fifty-nine T2DM patients with glycosylated haemoglobin (HbA1c) levels between 7.0% and 10.9% were recruited to the present study. Biochemical information and CGM parameters were collected at baseline and after 8 weeks of antihyperglycaemic therapy (either sulphonylurea, sulphonylurea + an α-glucosidase inhibitor or insulin + metformin combination therapy). 3. Compared with baseline, serum osteocalcin increased significantly (P = 0.014), whereas parameters related to glucose variability, including the mean amplitude of glycaemic excursions (MAGE) and the standard deviation of blood glucose values, decreased significantly (P0.001) after the 8 week treatment period. At baseline, there was a positive correlation between serum osteocalcin levels and fasting C-peptide levels (P = 0.004) and homeostatic model assessment of β-cell function (P = 0.048), but a negative correlation between serum osteocalcin levels and fasting plasma glucose (P = 0.023), HbA1c (P = 0.020), glycated albumin (P = 0.019) and 24 h mean blood glucose (P0.001). Multiple stepwise regression analysis indicated that baseline osteocalcin was the single parameter that best predicted the change in MAGE (β = -0.122; P = 0.039). 4. In conclusion, serum osteocalcin concentrations increased with improved glucose control. High initial osteocalcin levels were associated with subsequent improvements in glucose variability during glucose-lowering treatment.

1. The aim of the present study was to assess the validity of glycated albumin (GA) and fasting plasma glucose (FPG) as a screening tool for the early detection of diabetes in Chinese subjects. 2. A total of 1971 outpatient subjects underwent a 75 g oral glucose tolerance test (OGTT) and GA measurement. The receiver operating characteristic curve (ROC) was plotted to examine the sensitivity, specificity, and positive and negative predictive values of GA and FPG in detecting undiagnosed diabetes at the different cut-off levels. 3. The prevalence of impaired glucose regulation and diabetes was 27.40% and 38.30%. For these diabetic individuals, 4.64% had isolated fasting hyperglycemia, 50.86% had isolated postprandial hyperglycemia and 44.50% had both. Using ROC analysis, a GA of 17.1% gave an optimal sensitivity of 76.82% (95% confidence interval: 73.64-79.79%) and specificity of 76.89% (74.42-79.23%) for the diagnosis of diabetes. Likewise, a FPG of 6.1 mmol/L gave an optimal sensitivity of 80.93% (77.94-83.67%) and specificity of 85.94% (83.86-87.84%). If subjects met both criteria, they were regarded as having diabetes; the positive predictive value of the combined criteria, FPG ≥ 6.1 mmol/L and GA ≥ 17.1%, was relatively high (84.79% (81.62-87.60%)), and this would have avoided 76% of the OGTT in our survey. 4. In conclusion, a GA value of 17.1%, an optimal cut-off in Chinese subjects, identified a high proportion of potential diabetic individuals. Simultaneous measurement of FPG and GA would enhance the sensitivity of diabetes screening in our population and avoid 76% of OGTT.

As one of most widely-used biguanides, metformin can induce the lactic acidosis in patients with renal failure though its incidence is very low. However, lactic acidemia induced by metformin was reported in patients without renal dysfunction. It is unclear that whether lactatemia exists in diabetic patients with normal renal function in Chinese or not and its influencing factors. This study aimed to clarify the influencing factors of lactic acid, and identify a practiced clinical marker to predict the hyperlactacidemia in diabetics with normal renal function.The clinical data and venous blood samples of 1024 type 2 diabetic patients treated with (n = 426) or without metformin (n = 599) were collected. The lactic acid was assayed by enzyme-electrode method. The biochemical indexes included creatinine (Cr) and hepatase were measured with enzymatic procedures. The lactic acid concentrations of different Cr subgroups were compared, and the correlation and receiver operating characteristic curve analysis were used.The mean lactic acid level and the proportion of hyperlactatemia of metformin group were significantly higher than that of non-metformin group (P0.01), but no lactic acidosis was found in all patients. The correlation and multiple stepwise regression analysis indicated that the correlative factors of lactic acid in turn were Cr, metformin, alanine transferase (ALT), body mass index (BMI), Urine albumin (Ualb), and blood urea nitrogen (BUN) in total patients; and Cr, ALT, BMI and BUN in non-metformin treated patients; Cr and ALT in metformin-group. The lactate concentration increased with the increment of Cr levels, and reached its peak at Cr 111-130 micromol/L, and the optimal cutoff of Cr in predicting hyperlactacidemia was 96.5 micromol/L.Metformin can increase the incidence of lactatemia in type 2 diabetic patients without renal dysfunction. Cr, ALT, and BMI are independent associated factors of blood lactic acid levels. There is low proportion of lactatemia in type 2 diabetics without metformin therapy, the optimal cutoff of Cr to predict lactatemia in these patients is 96.5 micromol/L.

Muscle segment homeobox gene (MSX)1 has been proposed as a gene in which mutations may contribute to nonsyndromic cleft lip with or without cleft palate (NSCL/P). To study MSX1 polymorphisms in NSCL/ P by means of polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP), and investigate the association of MSX1 exons 1 polymorphisms with NSCL/P.DNA were extracted from blood samples from NSCL/P and unrelated normal subjects. Genome DNA from peripheral leukocyte with these blood samples were extracted, which was used as template to amplify desired gene fragment of MSX1 exons 1 by means of polymerase chain reaction (PCR). The PCR products were examined by single-strand conformation polymorphism (SSCP). The MSX1 exons 1 polymorphisms were examined by sequencing if mutations were found.MSX1 genes of exon 1 mutation was not been found in the NSCL/P and unrelated normal subjects by SSCP.No correlation between MSX1 exon 1 and NSCL/P was found. MSX1 exon 1 may not be a key gene (susceptibility gene) in NSCL/P.

To provide evidence for assessing glycated albumin (GA) appropriately cliniccally through determining the GA level of type 2 diabetes mellitus (DM) patients and analyzing its influential factors.Continuous glucose monitor system was used to monitor the levels of fasting plasmic glucose (FPG), 2-hour post-prandial plasmic glucose (2hPG), GA, and glycated hemoglobin (HbA1c) in 445 type 2 DM in-patients.(1) The mean GA value was 24.9% +/- 7.0% and the mean HbA1c was 8.9% +/- 2.2%. (2) GA value was associated with HbA1c (P0.001). GA was positively correlated with FPG, 2hPG, and mean blood glucose (MBG) (all P0.01). (3) GA value was negatively correlated with BMI (P0.01). (4) Multiple stepwise regression analysis showed that HbA1c, BMI, and FPG were the main influential factors of GA.(1) GA value has good relationship with HbA1c, a golden standard to reflect the glycemic control in a long period. (2) BMI should be concerned when assessing GA value of DM patients, especially of the obese and thin subjects.

To study the features and specificity of body fat depot abnormalities in type 2 diabetic patients.366 Chinese agedor= 40, 287 with type 2 diabetics and 79 without type 2 diabetics, hypertension and dyslipidemia, underwent the following examinations: (1) total body fat depots, defined by body mass index (BMI); (2) regional body fat depots, including waist circumference (W), hip circumference (H), femoral circumference (F), intra-abdominal fat area (VA), abdominal subcutaneous fat area (SA) and femoral subcutaneous fat area (FA); (3) ratio between regional and body fat depots (W/BMI, H/BMI, F/BMI, VA/BMI, SA/BMI and FA/BMI); (4) body fat distribution, including W and H ratio (WHR), W and F ratio (WFR), VA + SA/FA, and VA/SA; and (5) tissue insulin sensitivity, expressed by homeostasis model assessment index for insulin resistance (HOMA-IR).The body fat depot abnormalities observed in type 2 diabetes were as follows: (1) increase in total body fat depots (BMI) (P = 0.0013); (2) increase in abdominal fat depots (W) (P0.0001), mainly accounted for absolute and relative increases in intra-abdominal fat depots (VA, VA/SA and VA/BMI) P = 0.0011, 0.0025, 0.0008 respectively; (3) relative decrease in hip and femoral subcutaneous fat depots (H/BMI, F/BMI and FA/BMI) (P0.0001,0.00001, = 0.0014 respectively); (4) central distribution of body fat (WHR, WFR and VA + SA/FA) (P0.0001, = 0.0002, = 0.0002 respectively) by increase in intra-abdominal fat depots as well as decrease in hip or femoral body fat depots. The degree of abnormalities in body fat depots and the degree of tissue insulin resistance were in parallel with the number of other metabolic diseases (hypertension and dyslipidemia) associated in type 2 diabetic patients. Stepwise regression analysis indicated that increase in total body fat depots was the major independent contibuting factor for tissue insulin resistance. Moreover, increase in intra-abdominal fat depots and decrease in femoral fat depots were also independent contributing factors for insulin resistance.Increase in intra-abdominal fat depots as well as decrease in femoral subcutaneous fat depots is not only the features of body fat distribution observed in diabetic patients, but also in subjects with metabolic syndrome.