Effect of a Diet Rich in Interesterified, Non-Interesterified and Trans Fats on Biochemical Parameters and Oxidative Status of Balb-c Mice

The aim of this study was to investigate the effects of different modified fats on the body weight, biochemical profile, and biomarkers of hepatic oxidative status in Balb-c mice. The animals were divided into four groups and fed for 75 days with a normolipidic (Control Group, CG) or hiperlipidic diets (40% kcal) containing a commercial interesterified fat (IFG) rich in palmitic acid (39%);a blend of non-interesterified fat (NIFG), with 2-fold less saturated fatty acids at the sn-2 position of triacylglycerols;or a partially hydrogenated vegetable oil (PHFG), source of trans fatty acid (20%) and of linolenic acid (6%). The mice of the IFG and NIFG presented similar results in all evaluated parameters. The serum biochemical profile and hepatic oxidative stress markers in mice of the PHFG were similar to CG, except for total cholesterol (TC) which was significantly higher (p < 0.05) for the mice of the PHFG. The mice feed with interesterified fat (IFG) showed serum TC (p < 0.01), non-HDL-C (p < 0.05), glucose (p < 0.05) and hepatic reduced glutathione values (2.7 fold, p < 0.05) and glutathione reductase activity (2.4 fold, p < 0.001) significantly higher when compared to the mice fed with partially hydrogenated vegetable oil (PHFG). The hydrogenated fat source of trans fatty acid (20%) had less important metabolic effects than fats containing amounts of palmitic acid (interesterified or non-interesterified). Our results suggest that the replacement of hydrogenated fats by interesterified fats may not be such a simple solution to reduce or eliminate trans fatty acids in foods.

Assessing the response of human primary macrophages to defined fibrous architectures fabricated by melt electrowriting

The dual role of macrophages in the healing process depends on macrophage ability to polarize into phenotypes that can propagate inflammation or exert anti-inflammatory and tissue-remodeling functions.Controlling scaf-fold geometry has been proposed as a strategy to influence macrophage behavior and favor the positive host response to implants.Here,we fabricated Polycaprolactone(PCL)scaffolds by Melt Electrowriting(MEW)to investigate the ability of scaffold architecture to modulate macrophage polarization.Primary human macrophages unpolarized(M0)or polarized into M1,M2a,and M2c phenotypes were cultured on PCL films and MEW scaffolds with pore geometries(square,triangle,and rhombus grid)characterized by different angles.M0,M2a,and M2c macrophages wrapped along the fibers,while M1 macrophages formed clusters with rounded cells.Cell bridges were formed only for angles up to 90◦.No relevant differences were found among PCL films and 3D scaffolds in terms of surface markers.CD206 and CD163 were highly expressed by M2a and M2c macrophages,with M2a macrophages presenting also high levels of CD86.M1 macrophages expressed moderate levels of all markers.The rhombus architecture promoted an increased release by M2a macrophages of IL10,IL13,and sCD163 compared to PCL films.The proangiogenic factor IL18 was also upregulated by the rhombus configuration in M0 and M2a macrophages compared to PCL films.The interesting findings obtained for the rhombus architecture represent a starting point for the design of scaffolds able to modulate macrophage phenotype,prompting investigations addressed to verify their ability to facilitate the healing process in vivo.

Exercise-Dependent Modulation of Bone Metabolism and Bone Endocrine Function:New Findings and Therapeutic Perspectives

Physical inactivity is the fourth leading cause of mortality worldwide;regardless of geographic location and income,it is a contributing risk factor to the other three causes.Physical activity is really a drug,a poly-pill;its“regular use”can reduce this risk throughout the activation of a plethora of responses in virtually all the body tissues.The beneficial effects of physi-cal activity on cardiovascular function and hemodynamics are mainly mediated by skeletal muscle,adipose tissue and the immune system via the usage,delivery and distribution of metabolic substrates and improvement in inflammatory status.There is emerging evidence for exercise-dependent changes in bone metabolism as well;with improved bone quality,reduced fracture risk and increased bone endocrine function,the last of which modulates energy metabolism through its effects on pancreatic islet cells,skeletal muscle and adipose tissue.Bone endocrine function relies on the integration of biomechani-cal stimuli and endocrine signals from other organs and tissues.Here I review current concepts about exercise-dependent modulation of bone endocrine function and its beneficial effects on whole-body metabolism.Several molecular mechanisms have been identified that support this exercise-stimulated bone-mediated metabolic effect and,among these,Wnt signaling,fibroblast growth factor-23,bone morphogenic protein-7,osteocalcin,RANK/RANKL/OPG axis,and lipocalin-2 gave the largest evidences.In conclusion,beside the controversies surrounding technical aspects of the exercise,the efficacy of physi-cal activity in preventing/treating metabolic and inflammatory dysfunctions also passes throughout the bone.