The present study investigated the potential health-promoting effects of heat-inactivatedLactobacillus gasseriTMC0356 (TMC0356) on the metabolic syndrome (MS) and the probable mechanisms underlying these effects using an MS rat model. For the purpose of the study, sixty Sprague–Dawley rats were randomly divided into five groups: a control group fed a conventional diet, an MS model group fed a high-fat and high-salt (HFS) diet and three TMC0356 test groups (low-, medium- and high-dose groups) fed an HFS diet supplemented with TMC0356 at 41·8, 83·5 and 167·0 mg/kg body weight (BW) per d, respectively. Food intake and BW were measured weekly. Fasting blood glucose (FBG), lipid profiles and blood pressure (BP) were measured at 0, 5, 10 and 15 weeks. Organ coefficients, immune cell counts and serum insulin, adiponectin, C-reactive protein (CRP), IL-6, TNF-α, IgG and secretory IgA levels were measured at the 15th week after diet intervention. The HFS diet increased the BW, liver or fat:BW ratio, FBG, homeostatic model assessment of insulin resistance, adiponectin, serum LDL-cholesterol and total cholesterol levels and BP (P< 0·01). Average food and energy intakes in the three TMC0356 groups were significantly lower than those of the MS model group. All the metabolic indices, except BP, were markedly improved (P< 0·05) by oral administration of low and medium doses of TMC0356. The thymus index in the medium-dose group and lymphocyte, CRP, IL-6, TNF-α and IgG levels in all the three TMC0356 groups were significantly increased (P< 0·05 orP< 0·01) compared with those in the MS model group. These results suggest that TMC0356 can improve the metabolic characteristics of MS rats by suppressing appetite. Additionally, the enhancement of inflammatory immune response may be, at least in part, the mechanism underlying the health-promoting effects of TMC0356 on the MS.

Aim This study was conducted to investigate the chronic injury of peritoneal glucose injection on the peritoneum and intestine and the protective effects of omega‐3 polyunsaturated fatty acid (ω‐3PUFA) during peritoneal dialysis (PD). Methods Peritoneal dialysis animal models were established by intraperitoneal injection of 4.25% glucose for 28 days. Protein expression in ileum and peritoneum was measured by immunofloresence and immunohistochemistry. Protein expression in macrophages was measured by Western blot. Fibrosis was analyzed by Masson staining. Results Peritoneal dialysis significantly increased the structural injury and decreased junction‐related protein ZO‐1 and occludin expression in ileum, the expression of proteins relating to the activation of M2 (Erg2, IRF4), but not M1 (CD38, IRF5) macrophages. PD significantly increased the expression of TGF‐β1, VEGF and ALK5 protein in peritoneal tissues. PD significantly increased fibrosis (Masson staining) and the expression of fibroblast marker α‐SMA in peritoneal tissues. Injection of macrophage clean reagent and ω‐3PUFA significantly inhibited M2 activation, and decreased Masson staining, α‐SMA, TGF‐β1, VEGF and ALK5 protein expression in peritoneal tissues in PD treated rats. ω‐3PUFA injection significantly decreased PD‐induced injury in ileum and normalized the expression of ZO‐1 and occludin in the ileum of PD rats. Conclusion Omega‐3 fatty acids can provide a protective role on PD‐induced peritoneal fibrosis and injury of the intestine.

The chemokine (C-X3-C motif) ligand 1 (CX3CL1), also named fractalkine (FKN), has been implicated in psychiatric disorders and functions as a novel adipocytokine. However, no attention has been paid to the role of FKN in anorexia nervosa (AN). The current study was performed to explore FKN levels in AN to determine its role in the involvement of AN. A total of 96 girls aged 11-18 years with AN (n=34), healthy controls (HC; n=32) and simple obesity (OB, n=30) were enrolled in the cross-sectional study. Blood samples were collected during the fasting state. Serum FKN concentrations were determined using ELISA. The skinfold thickness (TSF) of the biceps and triceps as well as mid-arm muscle circumference (MAMC) were used to determine the nutritional status. Our results showed that serum FKN levels were significantly lower in the AN group than in the control and OB groups. After adjusting for body mass index (BMI), FKN concentrations in the AN group were statistically higher than in the HC and OB groups. Significant correlations between serum FKN and body weight, BMI, Cole index and serum insulin were observed. In addition, serum FKN levels were positively related to TSF and MAMC in all subjects. Serum FKN concentrations are attenuated in girls with AN compared with healthy adolescents and are positively related to nutritional status. The lower FKN levels may be regulated by nutrition status and response to starvation. After adjusting for BMI, higher FKN levels may reflect that persistent inflammation is present in patients with AN.