Background and Aims A novel bioactive peptide, mitochondrial‐derived peptide (MOTS‐c), has recently attracted attention as a potential prevention or therapeutic option for obesity and type 2 diabetes mellitus (T2DM). MOTS‐c profiles have not yet been reported in human obesity and T2DM. We aimed to determine circulating MOTS‐c levels in obesity and explore the association between MOTS‐c levels and various metabolic parameters. Methods In this case‐control study, 40 obese children and adolescents (27 males) and 57 controls (40 males) were recruited in the Hubei Province of China in 2017. Circulating MOTS‐c levels were measured, clinical data (eg, glucose, insulin, and lipid profile) were recorded, and anthropometric measurements were performed. Finally, we investigated correlations between MOTS‐c levels and related variables. Results MOTS‐c levels were significantly decreased in the obese group compared with the control group (472.61 ±22.83 vs 561.64 ±19.19 ng/mL, P <.01). After classification by sex, MOTS‐c levels were significantly decreased in obese male children and adolescents compared to their counterparts (465.26 ±24.53 vs 584.07 ±21.18 ng/mL, P <.001), while they were comparable between the obese and healthy female subjects (487.89 ±49.77 vs 508.85 ±38.76 ng/mL, P >.05). Further, MOTS‐c levels were negatively correlated with body mass index (BMI), BMI SD score, waist circumference, waist‐to‐hip ratio, fasting insulin level, homeostasis model assessment of insulin resistance (HOMA‐IR), and glycated hemoglobin (HbA1c) in the male cohort. Conclusions Circulating MOTS‐c levels were decreased in obese male children and adolescents and correlated with markers of insulin resistance and obesity.

Post-weaning diarrhoea (PWD) in piglets is associated with colonization of the intestine with bacterial pathogens. In this study, we evaluated the use of recombinant porcine β-defensin 2 (rpBD2) as a medicated feed additive for weaned piglets. The crude extract from the culture supernatant of rpBD2-expressing Pichia pastoris was used as a medicated feed additive for weaned piglets. Dietary treatments included a positive control (basal diet + antibiotics, designated PC) and three different rpBD2 treatments without antibiotics (basal diet supplemented with 1, 5, or 15 g of crude rpBD2/kg basal diet, designated 1PD, 5PD, and 15PD, respectively). Of all the treatments, 5PD had the greatest impact on the weaned piglets. It increased their body weight, average daily weight gain, average daily feed intake, and intestinal villus height in the duodenum and jejunum, and reduced the incidence of PWD. The diversity of the cecal digesta and mucosa microflora was compared between the weaned piglets in the PC and 5PD groups. Piglets treated with 5PD had lower diversity indices and fewer bacterial pathogens in their cecal digesta and mucosa than the PC group. Our results demonstrate that crude rpBD2 could provide an alternative to the traditional antibiotic feed additives given to weaned piglets.

Inflammation contributes greatly to the pathogenesis of bronchopulmonary dysplasia. In previous studies, we showed that blocking neutrophil influx by treatment with SB265610, a selective CXCR2 antagonist, could partly reduce superoxide accumulation and preserve alveolar development in 60% O 2 -exposed newborn rats. The purpose of this study was to further investigate the role of neutrophils in the formation of reactive oxygen and nitrogen species mediating hyperoxia-impaired lung development. We found that hydroxyl radical formation and lipid peroxidation in rat lungs were significantly increased during 60% O 2 exposure. These increases were attenuated by the administration of SB265610. In addition, SB265610 largely inhibited protein nitration induced by hyperoxia. SB265610 partly prevented the hyperoxia-enhanced bronchoalveolar lavage (BAL) protein content in 60% O 2 -exposed animals. Our results demonstrate that neutrophils have a pivotal role in hydroxyl radical formation, lipid peroxidation and protein nitration. Taken together with our previous studies, the present findings show that blocking neutrophil influx protects alveolar development and improves lung function in part by preventing reactive oxygen/nitrogen species accumulation. I nflammation is a common mechanism uniting factors linked to the development of bronchopulmonary dysplasia (BPD), such as oxidative stress, mechanical injury, and defective antioxidant defenses (1). Premature newborns born to mothers with chorioamnionitis are at high risk of developing BPD (2). Likewise, premature newborns with respiratory distress syndrome (RDS) with elevated neutrophil counts in tracheal aspirates at birth are at high risk of developing BPD (3). In the baboon model of BPD, neutrophil chemokine IL-8 is elevated in tracheal aspirates a few days after delivery (4).While there are no published studies that directly and specifically antagonize neutrophil influx in premature newborn babies, a number of experimental models show beneficial effects. Depletion of circulating neutrophils in preterm lambs lessened the severity of pulmonary leak of protein and fluid in experimental RDS (5). Blocking hyperoxia-induced pulmonary neutrophil influx in newborn rats by treatment with neutralizing antibodies to neutrophil chemokines (6) prevented impaired lung compliance (7), DNA oxidation (8), and protected alveolar development (7) in 95% O 2 -exposed newborn rats.To determine the mechanisms by which blocking neutrophil influx could protect lung development, we exposed newborn rat pups to air or FiO 2 ϭ 0.6 for two weeks and treated them with SB-265610, a small molecule selective antagonist of C-X-C chemokine receptor-2 (CXCR2), a dominant neutrophil chemokine receptor. In our previous studies, SB265610 prevented neutrophil accumulation, partly reduced tissue superoxide accumulation, and accelerated alveolar development (9). To determine whether blocking neutrophil influx through this approach could reduce pulmonary hydroxyl radical accumulation, lipid peroxidation, ...