Aim:The effects of exercise intervention and to assess its long-term efficacy in preventing subsequent cardiovascular events in patients with type 2 diabetes were little known on randomized controlled trial. Methods: Thirty-eight type 2 diabetic patients (21 men and 17 women) were assigned to either the exercise group (n 21) or the control group without exercise training (n 17) by simple randomization. The exercise training group was scheduled for aerobic and resistance exercise programs for 3 months. After the 3-month, we investigated endothelial function, insulin resistance, adipocytokines and inflammatory markers. The endothelial function was evaluated by examining a flow-mediated endothelium-dependent vasodilatation (FMD). Furthermore, we followed the incidence of cardiovascular events for 24 months. Results: After 3-month, HbA1C was decreased significantly in both groups. FMD was increased from 7.3 4.7% to 10.9 6.2% only in the exercise group ( p 0.05). Long-term follow-up data showed that the control group developed cardiovascular events more frequently than did the exercise group ( p 0.05). Conclusions: Exercise improves endothelial dysfunction independently of glycemic control and insulin sensitivity in patients with type 2 diabetes. The beneficial effects of 3-month exercise to reduce cardiovascular events persist for 24 months. J Atheroscler Thromb, 2010; 17:828-833.

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Growth factor signaling via insulin receptor (IR) and IGF-1 receptor (IGF1R) plays several important roles in the pathogenesis of metabolic syndrome and diabetes. OSI-906 (linsitinib), an anti-tumor drug, is an orally bioavailable dual inhibitor of IR and IGF1R. To investigate the recovery from metabolic changes induced by the acute inhibition of IR and IGF1R in adult mice, mice were treated with OSI-906 or a vehicle for 7 days and the results were analyzed on the last day of injection (Day 7) or after 7 or 21 days of withdrawal (Day 14 or Day 28). On day 7, the visceral white fat mass was significantly reduced in mice treated with OSI-906 accompanied by a reduced expression of leptin and an increased expression of the lipolysis-related genes Lpl and Atgl. Interestingly, the lipoatrophy and the observed changes in gene expression were completely reversed on day 14. Similarly, liver steatosis and β cell proliferation were transiently observed on day 7 but had disappeared by day 14. Taken together, these results suggest that this model for the acute inhibition of systemic IR/IGF1R signaling may be useful for investigating the recovery from metabolic disorders induced by impaired growth factor signaling.

Background: Ovarian cancer (OC) is a leading cause of cancer-related death in women, and thus an accurate diagnosis of the predisposition and its early detection is necessary. The aims of this study were to determine whether serum exosomal microRNA-34a (miR-34a) in ovarian cancer could be used as a potential biomarker. Methods: Exosomes from OC patients' serum were collected, and exosomal miRNAs were extracted. The relative expression of miR-34a was calculated from 58 OC samples by quantitative real-time polymerase chain reaction. Results: Serum exosomal miR-34a levels were significantly increased in early-stage OC patients compared with advanced-stage patients. Its levels were significantly lower in patients with lymph node metastasis than in those with no lymph node metastasis. Furthermore, its levels in the recurrence group were significantly lower than those in the recurrence-free group. Conclusions: Serum exosomal miR-34a could be a potential biomarker for improving the diagnostic efficiency of OC.

Aims/Introduction Liraglutide and empagliflozin suppress cardiovascular events. However, reports on their long‐term combined use with insulin therapy or direct comparisons of these drugs are limited. Materials and Methods This open‐label, parallel‐group, randomized controlled trial compared the effects of liraglutide and empagliflozin combined with insulin therapy in type 2 diabetes patients . Adult type 2 diabetes outpatients undergoing stable insulin therapy with glycated hemoglobin levels of 7.0–9.5% were enrolled. Participants received 0.9 mg/day liraglutide or 10 mg/day empagliflozin for 24 weeks. The primary end‐point was the change in glycated hemoglobin levels from week 0 to 24. Body composition was assessed by dual‐energy X‐ray absorptiometry. Results A total of 64 insulin‐treated patients were randomized to receive liraglutide or empagliflozin. We analyzed 61 patients (30 liraglutide and 31 empagliflozin) who could be followed up. Liraglutide induced greater changes in glycated hemoglobin and glycated albumin than empagliflozin (glycated hemoglobin −1.24 ± 0.15% vs −0.35 ± 0.11%, P < 0.0001; glycated albumin −4.4 ± 0.6% vs −2.4 ± 0.5%, P < 0.01). Bodyweight (−1.3 ± 0.4 kg vs −1.5 ± 0.3 kg, P = 0.69) or body fat mass/lean tissue mass; urinary albumin excretion (median −5.3 mg/g‐creatinine [interquartile range −60.6, 9.9 mg/g‐creatinine] vs −12.9 mg/g‐creatinine [interquartile range −70.8, −2.0 mg/g‐creatinine], P = 0.23); and frequency of hypoglycemia did not differ significantly between the groups over a period of 24 weeks. There were no cases of study discontinuation owing to adverse effects. Conclusions Liraglutide addition to ongoing insulin therapy more effectively reduced glycated hemoglobin and glycated albumin levels than empagliflozin in patients with inadequately controlled type 2 diabetes.