Background: Time-restricted feeding is an emerging dietary intervention that is becoming increasingly popular. There are, however, no randomised clinical trials of time-restricted feeding in overweight patients with type 2 diabetes. Here, we explored the effects of time-restricted feeding on glycaemic regulation and weight changes in overweight patients with type 2 diabetes over 12 weeks. Methods: Overweight adults with type 2 diabetes (n = 120) were randomised 1:1 to two diet groups: time-restricted feeding (n = 60) or control (n = 60). Sixty patients participated in a 10-h restricted feeding treatment program (ad libitum feeding from 8:00 to 18:00 h; fasting between 18:00 and 8:00 h) for 12 weeks. Results: Haemoglobin A1c and body weight decreased in the time-restricted feeding group (− 1.54% ± 0.19 and − 2.98 ± 0.43 kg, respectively) relative to the control group over 12 weeks (p < 0.001). Homeostatic model assessment of β-cell function and insulin resistance changed in the time-restricted feeding group (0.73 ± 0.21, p = 0.005; − 0.51 ± 0.08, p = 0.02, respectively) compared with the control group. The medication effect score, SF-12 score, and the levels of triglycerides, total cholesterol and low-density lipoprotein cholesterol were improved in the time-restricted feeding group (− 0.66 ± 0.17, p = 0.006; 5.92 ± 1.38, p < 0.001; − 0.23 ± 0.08 mmol/L, p = 0.03; − 0.32 ± 0.07 mmol/L, p = 0.01; − 0.42 ± 0.13 mmol/L, p = 0.02, respectively) relative to the control group. High-density lipoprotein cholesterol was not significantly different between the two groups. Conclusion: These results suggest that 10-h restricted feeding improves blood glucose and insulin sensitivity, results in weight loss, reduces the necessary dosage of hypoglycaemic drugs and enhances quality of life. It can also offer cardiovascular benefits by reducing atherosclerotic lipid levels. Trial registration: This study was registered with the Chinese Clinical Trial Registry (ChiCTR-IPR-15006371).

Purpose: Sleep duration is thought to play a key role in the development of metabolic syndrome. However, the results have been inconsistent. Methods: We conducted a systematic review and meta-analysis of cohort studies and searched publications in PubMed, Embase, Cochrane Central Register of Controlled Trials, and Clinicaltrials.gov. The summary relative risks (RRs) were estimated using a random model. The sensitivity analysis was performed by sequentially excluding each study to test the robustness of the pooled estimates. Finding: We included 13 studies involving 300,202 patients in which short sleep and long sleep significantly increased the risk of metabolic syndrome 15% (RR = 1.15, 95%CI = 1.09-1.22, p < 0.001) and 19% (RR = 1.19, 95%CI = 1.05-1.35, p < 0.001). Moreover, the relationship between sleep duration and metabolic syndrome risk presented a U-shaped curve. Short and long sleep increased the risk of obesity by 14% (RR = 1.14, 95%CI = 1.07-1.22, p<0.001) and 15% (RR = 1.15, 95%CI = 1.00-1.30, p = 0.04), and high blood pressure 16% (RR = 1.16, 95%CI = 1.02-1.31, p = 0.03) and 13% (RR = 1.13, 95%CI = 1.04-1.24, p = 0.01), respectively. Short sleep can potentially increase the risk of high blood sugar by 12% (RR = 1.12, 95%CI = 1.00-1.15, P = 0.05). Implications: Based on our findings, sleep is a behavior that can be changed and is economical. Clinically doctors and health professionals should be encouraged to increase their efforts to promote healthy sleep for all people.

Diabetic nephropathy (DN) is characterized by tubulointerstitial fibrosis caused by epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. Although ferroptosis promotes DN development, the specific pathological process that is affected by ferroptosis in DN remains unclear. Herein, EMT-related changes, including increased α-smooth muscle actin (α-SMA) and Vimentin expression and decreased E-cadherin expression, were observed in the renal tissues of streptozotocin-induced DN mice and high glucose-cultured human renal proximal tubular (HK-2) cells. Treatment with ferrostatin-1 (Fer-1) ameliorated these changes and rescued renal pathological injury in diabetic mice. Interestingly, endoplasmic reticulum stress (ERS) was activated during EMT progression in DN. Inhibiting ERS improved the expression of EMT-associated indicators and further rescued the characteristic changes in ferroptosis caused by high glucose, including reactive oxygen species (ROS) accumulation, iron overload, increased lipid peroxidation product generation, and reduced mitochondrial cristae. Moreover, overexpression of XBP1 increased Hrd1 expression and inhibited NFE2-related factor 2 (Nrf2) expression, which could enhance cell susceptibility to ferroptosis. Co-immunoprecipitation (Co-IP) and ubiquitylation assays indicated that Hrd1 interacted with and ubiquitinated Nrf2 under high-glucose conditions. Collectively, our results demonstrated that ERS triggers ferroptosis-related EMT progression through the XBP1-Hrd1-Nrf2 pathway, which provides new insights into potential mechanisms for delaying EMT progression in DN.

Ferroptosis-related characteristic changes were found in diabetic wound models. Inhibition of ferroptosis improved inflammatory infiltration of diabetic wounds. PI3K/AKT signal pathway was rescued by restraining of ferroptosis. Mitigation of ferroptosis in diabetic wound promoted the wound healing.