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Objective Offspring of patients with type 2 diabetes (OPDs) exhibits endothelial dysfunction (ED) associated with a chronic inflammatory state. N-3 polyunsaturated fatty acids (n-3 PUFA) may have antioxidant and anti-inflammatory properties that are beneficial for cardiovascular and metabolic health. Therefore, in the present study, we tested the hypothesis that dietary supplementation with fish oil rich in n-3 PUFA may improve ED in otherwise healthy OPDs. Methods and design A double-blind, placebo-controlled trial was conducted with 50 OPDs. Participants were randomized to treatment with either placebo or n-3 PUFA (2 g/day) for 12 weeks. Before and after treatment we evaluated endothelial function (using flow-mediated dilation (FMD) of the brachial artery), circulating inflammatory markers (adiponectin, TNF-α, and high sensitivity-CRP), and insulin resistance (QUICKI). Results No significant changes were observed in study outcomes in subjects treated with placebo. By contrast, when compared with baseline values, subjects treated with n-3 PUFA had significant improvement in FMD (9.1 ± 5.8% vs. 11.7 ± 4.4%, p = 0.02) that was accompanied by decreased plasma triglycerides (117 ± 73 mg/dl vs. 86 ± 44 mg/dl, p = 0.001) and TNF-α levels (8.9 ± 2.3 pg/ml vs. 6.8 ± 2.7 pg/ml, p = 0.001), and a trend towards increased plasma adiponectin levels (7.8 ± 4.5 μg/ml vs. 9.5 ± 5.1 μg/ml, p = 0.09). When data were analyzed by multiple regression analysis, decreased TNF-α after treatment with n-3 PUFA predicted increased FMD. Conclusion Dietary supplementation with n-3 PUFA significantly improved endothelial function and reduced pro-inflammatory markers in OPDs. Thus, fish oil consumption may have beneficial cardiovascular and metabolic health effects in otherwise healthy subjects predisposed to diabetes and its vascular complications.

Introduction: Preclinical research suggests a role of Glucagon Like Peptide-1 Receptors (GLP-1R) on the regulation of human bronchial tone. We investigated the effect of GLP-1R agonists on lung function of Type 2 Diabetes Mellitus (T2DM) population without co-existing chronic obstructive respiratory disorders. Methods: This was a prospective cohort study that examined change in lung function measurements over two years of T2DM patients (n = 32) treated with metformin monotherapy (control cohort), metformin plus GLP-1R agonists (GLP-1R agonists cohort), or metformin plus insulin (insulin cohort). Results: After 24 months of treatment, the forced expiratory volume in 1 s (FEV 1 ) significantly (p < 0.05) increased from baseline in the GLP-1R agonists cohort (218 ml [95%CI 88-246]), but not in the control and insulin cohorts (94 ml [95%CI -28 -216] and 26 ml [95%CI -174 -226], respectively; p > 0.05 vs. baseline). The average increase in FEV 1 in the GLP-1R agonists cohort was significantly greater than that in the control and insulin cohorts (delta: 110 ml [95%CI 18-202] and 177 ml [95%CI 85-270], respectively, p < 0.05). The forced vital capacity (FVC) also increased significantly more in the GLP-1R agonists cohort than in the control and insulin cohorts (overall delta FVC: 183 ml [95%CI 72-295], p < 0.05). The maximal expiratory flow at 50-75% significantly (p < 0.05) improved from baseline in the GLP-1R agonists cohort, but not in the control and insulin cohorts (p > 0.05). Conclusion:Our preliminary results suggest a potential new therapeutic perspective to treat airway disorders with GLP-1R agonists.

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