OBJECTIVE:Bariatric surgery has become the most effective treatment for morbid obesity. Increasing evidence showed that bariatric surgery can alleviate insulin resistance and influence thyroid function. This study aimed to investigate the relationship between changes in thyroid function and adipose tissue insulin resistance (adipo-IR) after bariatric surgery. METHODS:A total of 287 non-diabetic participants with regular thyroid function were recruited and divided into the lean, overweight and obese groups. Among them, 50 morbidly obese patients submitted to bariatric surgery. RESULTS:The obese group had a higher level of adipo-IR, thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), FT3/free thyroxine (FT4) and metabolism disorders than the lean and overweight groups. BMI was correlated with TSH, FT3, FT3/FT4 and adipo-IR (r = 0.309, 0.315, 0.322 and 0.651, respectively, all P < 0.001). Adipo-IR was significantly correlated with TSH (r = 0.402, P < 0.001), FT3 (r = 0.309, P < 0.001), and FT3/FT4 (r = 0.228, P < 0.05). Bariatric surgery resulted in a sharp decline in BMI, adipo-IR, TSH, FT3 and FT3/FT4 levels, meanwhile, metabolic disorders improved. The decrease in BMI after bariatric surgery was significantly correlated with reductions in adipo-IR (r = 0.577, P < 0.001) and TSH (r = 0.401, P = 0.005). Interestingly, the fasting blood glucose, fasting insulin, adipo-IR and TSH in the higher TSH group decreased more remarkably than in the lower TSH group. CONCLUSION:Obese individuals with higher TSH levels had an obvious metabolic improvement after bariatric surgery.

Background: This study was to research the efficacy of fenofibrate in the treatment of microalbuminuria in the patients with type 2 diabetes mellitus (T2DM) and hypertriglyceridemia.Methods: Type 2 diabetic patients (56) with microalbuminuria and hypertriglyceridemia aged 30 to 75 were randomly divided into the fenofibrate treatment group(n=28) and the control group (n=28) for 180 days. Urinary microalbumin /creatinine ratio (UACR) and other metabolic parameters were compared at baseline, during treatment and after treatment.Results: After 180 days, the reduction of levels of fasting blood glucose (FBG) and glycosylated hemoglobin (HbA1c) in two groups were no differences. In treatment group, uric acid (UA) (296.42 ± 56.41 vs 372.46 ± 72.78), triglyceride (TG) [1.51(1.17, 2.06) vs 3.04(2.21, 3.29)], and UACR [36.45 (15.78,102.41) vs 129.00 (53.00, 226.25)] were significantly decreased compared with the baseline. The high-density lipoprotein cholesterol (HDL-C) levels were significantly increased (1.22 ± 0.26 vs 1.09 ± 0.24) compared with the baseline. The decrease in UACR [-44.05(-179.47, -12.16) vs -8.15(-59.69, 41.94)]in treatment group was significantly higher compared with the control group. The decrease in UACR was positively associated with the decreases in TG ( r = 0.447, P = 0.042) and UA ( r = 0.478, P = 0.024) after fenofibrate treatment.Conclusion: In the patients with hypertriglyceridemia and type 2 diabetes mellitus, fenofibrate can improve microalbuminuria and do not increase the deterioration of glomerular filtration rate

Aims/Introduction. This study is aimed at (1) investigating the change of β-cell dysfunction as baseline fasting glucose progresses in newly diagnosed patients with T2DM and (2) finding whether body mass index (BMI) has different degrees of impact on insulin secretion as baseline fasting glucose progresses. Materials and Methods. 661 patients with newly diagnosed T2DM were enrolled in the present study. A 75 g oral glucose tolerance test was used to calculate HOMA-β, HOMA-IR, early-phase insulin secretion index (EISI, calculated as ΔI30/ΔG30), and area under the insulin releasing curve (AUCI0-180). Patients were divided into low, medium, and high FBG groups. Each group was further divided into lean, overweight, and obese subgroups according to BMI. Results. A decrease of EISI and HOMA-β and an increase of HOMA-IR were shown among different FBG groups significantly. In the medium FBG group, AUCI0-180, EISI, HOMA-β, and HOMA-IR in obese patients were higher than those in lean and overweight patients. In the low and high FBG groups, AUCI0-180, HOMA-β, and HOMA-IR in obese patients were higher than those in other subgroups. BMI was positively associated with high EISI in the medium FBG group but failed to yield a significant association with EISI in the low and high FBG groups. Conclusions. During the progression of baseline FBG, β-cell dysfunction and insulin resistance worsened. As FBG increased, increased BMI had a positive influence on β-cell dysfunction in all FBG groups. The independent factors that correlated to EISI differed with the increasing of baseline FBG.

Aims: Our aim was to search for clinical predictors of good glycemic control in patients starting or intensifying oral hypoglycemic pharmacological therapy. Methods: A multicenter, prospective cohort of 499 diabetic subjects was enrolled in this study: patients with newly diagnosed diabetes (NDM group) or poor glycemic control with oral antidiabetic drugs (OADs) (PDM group). All subjects then started or intensified OADs therapy and followed up for 91 days. Glycemic control was determined according to HbA1c at day 91 with HbA1c <7% considered good. Results: The proportions of patients with good glycemic control after follow up for 91 days were 66.9% and 34.8% in NDM group and PDM group respectively. Logistic regression analysis showed that the change in GA at 28 days was the only predictor of good glycemic control in NDM patients (OR = 1.630, 95% CI 1300-2.044, P < 0.001). In PDM patients, changes in GA at 28 days, CPI, baseline HbA1c, diabetic duration, and BMI were all independent predictors of good glycemic control (All P < 0.05). Conclusions: GA decline is a good predictor of future success in newly diagnosed patients. In patients intensifying therapy, beside GA decline, other individualized clinical characteristics should also be considered. (C) 2018 Elsevier Inc. All rights reserved.

Objective This study was performed to investigate the serum vascular endothelial growth factor (VEGF) levels in Chinese patients with impaired glucose tolerance (IGT) and newly diagnosed type 2 diabetes mellitus (T2DM). Methods A total of 189 subjects (41 controls, 40 patients with IGT, and 108 patients with newly diagnosed T2DM) were recruited. Serum VEGF levels were determined by ELISA; other metabolic parameters were assessed by standard laboratory methods. Results There were significant differences in serum VEGF levels among the T2DM, IGT, and control groups (T2DM vs. controls: 72.00 [45.40, 98.35] pg/mL vs. 53.10 [36.30, 116.25] pg/mL; IGT vs. controls: 78.17 [55.52, 137.25] pg/mL vs. 53.10 [36.30, 116.25] pg/mL). Moreover, serum VEGF levels were positively associated with the homeostasis model assessment for insulin resistance (HOMA-IR) value. Multiple linear regression analysis indicated that the HOMA-IR value was an independent risk factor for elevated serum VEGF level. Conclusions Both IGT and T2DM patients exhibited increased serum VEGF levels, compared with controls; increased serum VEGF level was positively associated with the HOMA-IR value. Therefore, the increased serum VEGF level might partially result from increased insulin resistance in these patients.

BACKGROUND:Fibroblast growth factor (FGF)-21 is an important regulator of glucose metabolism. In the present study, we investigated whether plasma levels of FGF-21 changed in patients with newly diagnosed type 2 diabetes mellitus (T2DM) and assessed the effects of metformin treatment on plasma FGF-21 levels.MATERIALS AND METHODS:The plasma FGF-21 levels and the metabolic parameters of 226 patients with newly diagnosed T2DM and 100 sex- and age-matched normal glycemic tolerant (NGT) controls were measured. Seventy-four patients among of the 226 patients with T2DM were treated with metformin throughout the 12-week study period. The fasting plasma FGF-21 and high-sensitivity C-reactive protein (hs-CRP) levels were measured using enzyme-linked immunosorbent assay kits.RESULTS:The patients with T2DM had significantly higher fasting plasma FGF-21 levels (302.2 pg/mL [range, 201.3-454.4 pg/mL] vs. 104.5 pg/mL [range, 71.6-185.6 pg/mL]; P < 0.00) and hs-CRP levels (2.63 ± 2.81 mg/L vs. 1.58 ± 2.16 mg/L; P < 0.00) than the NGT subjects. The fasting plasma hs-CRP and FGF-21 levels were significantly decreased in the T2DM group after metformin treatment compared with pretreatment (respectively, 2.56 ± 1.75 mg/L vs. 3.28 ± 1.89 mg/L [P < 0.05] and 232.6 pg/mL [range, 154.3-307.8 pg/mL] vs. 313.9 pg/mL [range, 227.7-474.2 pg/mL] [P < 0.01]).CONCLUSIONS:In patients with T2DM, the plasma FGF-21 levels are increased but are significantly decreased after metformin treatment. Metformin may play a role in reducing the FGF-21 levels in patients with T2DM, likely through the amelioration of glucose-lipid metabolism and inflammation.