[Effect of Autophagy to Drug Resistance of B-cell Lymphoma Cells].

OBJECTIVE: To investigate the effect of autophagy on the drug resistance of different human lymphoma cells. METHODS: 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. RESULTS: 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. CONCLUSION: The higher autophagy activity in lymphoma cells, the lower chemotherapy resistance of the lymphoma cells after autophagy was inhibited.

[Biological Characteristics of Immunophenotype, Stem Cell Gene and Colony Forming Ability in Side-Population Cells of Jeko-1 Cell Line].

AbstractObjective: To investigate the in vitro biological characteristics of side-population(SP) cells in mantle cell lymphoma(MCL). METHODS: 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. RESULTS: SP cells in JeKo-1 cells could be enriched by continuous sorting and in vitro cultureing, and it was found that CD19-/IgM- accounted for (2.79±0.82)%,CD19-/IgM+accounted for (70.99±13.61)%,CD19+/IgM-accounted for (0.55±0.25)%, and CD19+/IgM+accounted for (25.67±14)%. Bmi-1,CD133, C-MYC and Nanog genes were highly expressed in SP cells, but were low expressed in non-SP cells (P<0.05). Compared with non-SP cells, SP cells had stronger colony forming ability (P<0.05). CONCLUSION: JeKo-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： CD19-/IgM-、CD19-/IgM+、CD19+/IgM-、CD19+/IgM+, and show stronger gene expression of stem cells and self-renewal ability in vitro.

[Expression and Significance of LncRNA RP11-513G11.1 in Peripheral Blood of Patients with Diffuse Large B-Cell Lymphoma].

OBJECTIVE: 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. METHODS: 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. RESULTS: Compared with normal control group, the expression of RP11-513G11.1 significantly increased in DLBCL patients (P<0.001). 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) (P<0.05). 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（P<0.001）. The median progression-free survival time and overall survival time of chemotherapy-sensitive patients were significantly longer than those of chemotherapy-resistant patients (P<0.001). 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（P<0.05）. CONCLUSION: RP11-513G11.1 is highly expressed in patients with DLBCL, which is related with the prognosis of DLBCL patients.

[Associations of glycated albumin level with coronary artery disease].

OBJECTIVE: To explore the associations of the level of glycated albumin (GA) with coronary artery disease (CAD). METHODS: 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 Prevention & Treatment of Blood Lipid Abnormality in Chinese Adults. RESULTS: (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 P < 0.05). (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)%, P < 0.01). And the level of GA was higher in the patients with 1-vessel ((14.8 ± 2.1)% vs (13.3 ± 1.7)%, P < 0.05) and multi-vessel lesions ((15.1 ± 2.1)% vs (13.3 ± 1.7)%, P < 0.05) than that in the non-CAD counterparts (all P < 0.05). 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. CONCLUSIONS: 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.

[Relationship between glycated albumin level and pancreatic ß cell function in newly diagnosed type 2 diabetics].

OBJECTIVE: To explore the relationship between glycated albumin (GA) level and pancreatic ß cell function in newly diagnosed type 2 diabetics. METHODS: 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 ß cell function (HOMA-ß). ΔI30/ΔG30 was used to evaluate early-phase insulin secretion after a glucose load. RESULTS: (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, P < 0.01). 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, P < 0.01). (3) GA was negatively correlated with body mass index (BMI) (r = -0.112, P < 0.01), HOMA-ß (r = -0.350, P < 0.01) and ΔI30/ΔG30 (r = -0.263, P < 0.01). (4) Multivariant stepwise regression analysis showed that HbA1c, FPG, 3 hPG and ΔI30/ΔG30 were independent factors of GA level. CONCLUSION: Glycated albumin level is closely correlated with the function of early-phase insulin secretion in newly diagnosed type 2 diabetics.

Liver enzymes concentrations are closely related to prediabetes: findings of the Shanghai Diabetes Study II (SHDS II).

OBJECTIVE: 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. METHODS: 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. RESULTS: 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]. CONCLUSION: Serum ALT and GGT concentrations were closely related to pre-diabetes and diabetes in the Shanghai population and positively associated with insulin resistance.

[Combined utility of hemoglobin A1c and glycated albumin in diabetic screening].

OBJECTIVE: To assess the validity of combined detection of hemoglobin A1c (HbA1c) and glycated albumin (GA) in diabetic screening. METHODS: 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. RESULTS: (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 (P < 0.01). (2) Pearson correlation analysis demonstrated that HbA1c had a positive association with GA (r = 0.75, P < 0.01). (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 (P > 0.05). (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%, P < 0.01). CONCLUSION: 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.

Relationship between serum osteocalcin and glycaemic variability in Type 2 diabetes.

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 (P < 0.001) 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 ß-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 (P < 0.001). Multiple stepwise regression analysis indicated that baseline osteocalcin was the single parameter that best predicted the change in MAGE (ß = -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.

Combined assessment of glycated albumin and fasting plasma glucose improves the detection of diabetes in Chinese subjects.

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.

SLC22A2 gene 808 G/T variant is related to plasma lactate concentration in Chinese type 2 diabetics treated with metformin.

AIM: To investigate the potential relationship between the SLC22A2 gene polymorphism and blood lactate concentration in Shanghai Hans suffering from type 2 diabetes mellitus (T2DM). METHODS: The SLC22A2 single nucleotide polymorphism (SNP) 808G/T was genotyped in 400 T2DM patients, including a metformin-treated group (n=200) and a non-metformin-treated group (n=200). Fasting plasma lactic acid levels were measured with an enzyme-electrode assay. Biochemical indexes, including plasma alanine aminotransferase (ALT), creatinine (Cr), and glycolated hemoglobin (HbA1c), were also measured. RESULTS: The fasting plasma lactate concentration in the metformin-treated group was significantly higher than that in the non-metformin-treated group (1.29+/-0.45 mmol/L vs 1.18+/-0.44 mmol/L, P=0.015). Additionally, the ratio of patients with hyperlactacidemia was 8% (16/200) for the metformin-treated group and 5.5% (11/200) for the non-metformin-treated group, with no lactic acidosis found in either group. The frequency of the SLC22A2 808G/T T allele was 12.9%. Patients with the mutant genotype (TT) had a higher blood lactate concentration in the metformin-treated group than those in the non-metformin-treated group (t=2.492, P=0.013). This trend was not observed in the GG and GT genotypes when compared with metformin-treated and non-metformin-treated groups. Patients with the mutant genotype (TT) in the metformin-treated group also had a higher incidence of hyperlactacidemia compared with the GG genotype (40.0% vs 6.9%, P=0.050) in the metformin-treated group and the GG (6.0%, P=0.042) or GT (4.3%, P=0.043) genotypes in the non-metformin-treated group. In the metformin-treated group, there were significant gender differences in lactate concentrations in the TT (2.18+/-0.15 vs 1.04+/-0.27 mmol/L, P=0.008) and GG genotypes (1.40+/-0.51 vs 1.19+/-0.35 mmol/L, P=0.004). The lactate levels of women with the TT genotype were the highest in the metformin-treated group, but differences in lactate levels among the genotypes were not observed in the non-metformin-treated group. CONCLUSION: There is an 808G/T polymorphism in the SLC22A2 gene in Chinese Hans with T2DM. The 808G>T variance in the SLC22A2 gene can affect the plasma lactate level and the incidence of hyperlactacidemia in T2DM patients undergoing metformin therapy. Additionally, the female patients carrying the TT genotype are prone to lactatemia.

Glipizide controlled-release tablets, with or without acarbose, improve glycaemic variability in newly diagnosed Type 2 diabetes.

1. The aim of the present study was to compare the effects of glipizide controlled-release (CR) tablets monotherapy with that of glipizide CR tablets plus acarbose on glycaemic variability in newly diagnosed Type 2 diabetes (T2DM) patients using a continuous glucose-monitoring system (CGMS). 2. Forty newly diagnosed T2DM patients whose glycated haemoglobin A1c (HbA1c) levels ranged from 7.0% to 9.8% were randomized to either monotherapy or combination therapy. Overall glycaemic control and blood glucose variability were evaluated by CGMS parameters. 3. After 8 weeks treatment, fasting and postprandial blood glucose, HbA1c, glycated albumin (GA), mean blood glucose (MBG), mean amplitude of glycaemic excursions (MAGE), postprandial incremental area under the curve (AUC(pp)) and homeostasis model assessment of insulin resistance decreased significantly in both groups (P < 0.01). There was also a significant decrease in the mean of daily differences (MODD) in the combination therapy group. Mean changes in MBG, MAGE, MODD and AUC(pp) were significantly greater in the combination therapy group than in the monotherapy group (all P < 0.01), whereas no significant differences were found in the mean changes of HbA1c and GA. Multivariate regression analysis showed that the decrement in AUC(pp) was significantly associated with decreases in MAGE. 4. In conclusion, glipizide CR tablets alone or in combination with acarbose can improve overall blood glucose levels and glycaemic variability. Combination therapy using glipizide CR tablets and acarbose was more effective in reducing intraday and day-to-day glycaemic variability than glipizide CR tablet monotherapy.

Relationship of plasma creatinine and lactic acid in type 2 diabetic patients without renal dysfunction.

BACKGROUND: 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. METHODS: 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. RESULTS: The mean lactic acid level and the proportion of hyperlactatemia of metformin group were significantly higher than that of non-metformin group (P < 0.01), 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. CONCLUSIONS: 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.

The protective effect of the RAS inhibitor on diabetic patients with nephropathy in the context of VEGF suppression.

AIM: The aim of the present study was to explore whether renin angiotensin system (RAS) inhibitor can reduce the production of vascular endothelium growth factor (VEGF). Further, we sought to elucidate the correlation between VEGF level and certain clinical parameters, such as albumin excretion rate (AER), before and after treatment with angiotensin type 1 receptor blocker. METHODS: We recruited 166 type 2 diabetic patients at various stages of diabetic nephropathy (DN) and 46 healthy control subjects for a cross-sectional study. We recruited another 42 hypertensive type 2 diabetic patients with microalbuminuria for a longitudinal study involving a 6-month irbesartan treatment protocol. Urinary VEGF (uVEGF) levels were determined using ELISA. RESULTS: In the cross-sectional study, hypertensive type 2 diabetic patients who received RAS inhibitor presented lower uVEGF levels than those who did not receive the RAS inhibitor. Statistical analysis indicated that uVEGF level was independently correlated with the AER. In the longitudinal study involving the 6-month irbesartan treatment, we demonstrated that uVEGF levels decreased significantly in patients who achieved a 50% AER reduction (remission group, n=32). In contrast, uVEGF levels remained unchanged in patients who did not exhibit a 50% AER reduction (nonremission group, n=10). Furthermore, the change in uVEGF was significantly correlated with the change in AER (r=0.65, P<0.01) before and after 6 months of irbesartan treatment. This result held true even after we had adjusted for the decrease in average blood pressure. CONCLUSION: The protective effect of the RAS inhibitor in DN patients is associated with the suppression of VEGF. Accordingly, it may be possible to use uVEGF as a marker of DN progression. We suggest that uVEGF may be an important target for therapeutic intervention in the context of DN.

[Association of muscle segment homeobox gene 1 polymorphisms with nonsyndromic cleft lip with or without cleft palate].

OBJECTIVE: 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. METHODS: 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. RESULTS: MSX1 genes of exon 1 mutation was not been found in the NSCL/P and unrelated normal subjects by SSCP. CONCLUSION: 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.

[Glycated albumin level and its influential factors in type 2 diabetes mellitus].

OBJECTIVE: 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. METHOD: 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. RESULTS: (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 (P < 0.001). GA was positively correlated with FPG, 2hPG, and mean blood glucose (MBG) (all P < 0.01). (3) GA value was negatively correlated with BMI (P < 0.01). (4) Multiple stepwise regression analysis showed that HbA1c, BMI, and FPG were the main influential factors of GA. CONCLUSION: (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.

[Obesity in type 2 diabetes, its features and specificity].

OBJECTIVE: To study the features and specificity of body fat depot abnormalities in type 2 diabetic patients. METHODS: 366 Chinese aged >or= 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). RESULTS: 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) (P < 0.0001), 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) (P < 0.0001, < 0.00001, = 0.0014 respectively); (4) central distribution of body fat (WHR, WFR and VA + SA/FA) (P < 0.0001, = 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. CONCLUSION: 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.