This study aimed to evaluate different parameters in the green process of organic Spirulina biomass (SB) C-phycocyanin (C-PC) extraction to understand the impact on weight and oral glucose tolerance of C-PC extract in Swiss mice fed with a high-fat diet (HFD). The proximate composition and antioxidant activity were analyzed in Spirulina by-products: SB, C-PC, and Remaining biomass (RB). The protein content on a dry basis was 52.05% in SB and 61.16% in RB and 118.97 μg/g in C-PC. The antioxidant activity was equal for SB and C-PC but higher than RB. However, RB can be considered a promising ingredient, promoting the sustainable use of the whole SB. Swiss mice were distributed in five groups: control diet (CD), HFD, HFD plus Spirulina biomass (HFDS), HFD plus C-PC (HFDC), and HFD plus remaining biomass (HFDR). HFDS increased the delta weight of the animals and showed glucose intolerance compared to the CD and HFDC groups. The results demonstrated that the supplementation of 500 mg/kg of body weight of SB in the HFDS group did not show antiobesogenic potential with an HFD, but it is essential to conduct further studies to bring other interesting responses regarding C-PC biological in vivo effects.

Lifestyle changes regarding diet composition and exercise training have been widely used as a non-pharmacological clinical strategy in the treatment of obesity, a complex and difficult-to-control disease. Taking the potential of exercise in the browning process and in increasing thermogenesis into account, the aim of this paper was to evaluate the effect of resistance, aerobic, and combination training on markers of browning of white adipose tissue from rats with obesity who were switched to a balanced diet with normal calorie intake. Different types of training groups promote a reduction in the adipose tissue and delta mass compared to the sedentary high-fat diet group (HS). Interestingly, irisin in adipose tissues was higher in the resistance exercise (RE) and aerobic exercise (AE) groups compared to control groups. Moreover, in adipose tissue, the fibroblast growth factor 21 (FGF21), coactivator 1 α (PGC1α), and peroxisome proliferator-activated receptor gamma (PPARγ) were higher in response to resistance training RE compared with the control groups, respectively. Additionally, uncoupling protein 1 (UCP1) showed higher levels in response to group AE compared to the HS group. In conclusion, the browning process in white adipose tissue responds differently toward different training exercise protocols, with resistance and aerobic training efficient in activating different biomarkers of the browning process, upregulating irisin, FGF21, PGC1α, PPARγ, and UCP1 in WAT, which together may suggest an improvement in the thermogenic process in the adipose tissue. Considering the experimental conditions of the present investigation, we suggest future research to pave new avenues to be applied in clinical practices to combat obesity.

C-phycocyanin (CPC), a bioactive compound derived from Spirulina, has been described as a molecule with antioxidant and anti-inflammatory properties. It has also been demonstrated that sustainably obtained CPC effectively inhibited body mass gain, regulated serum leptin and resistin levels, and prevented the onset of a pro-inflammatory state in Swiss mice fed a hyperlipidic diet. These results highlighted the anti-obesogenic potential of CPC. Brown adipose tissue (BAT) has been identified as a promising target in the treatment of obesity, playing a role in energy expenditure. In this study, Swiss mice fed a high-fat diet were supplemented with 500 mg/kg body weight of CPC daily for 12 and 16 weeks. BAT was collected, and Western blot and ELISA were performed. A reduction in pro-inflammatory cytokines, as well as a decrease in leptin levels was observed in the tissue, which was also associated with a reduction in BAT relative weight to body mass. Furthermore, CPC administration was able to modulate uncoupling protein 1 (UCP1) levels, which is crucial in the thermogenesis process. Therefore, this study demonstrated that supplementation with CPC reduces inflammatory cytokines associated with detrimental effects in the BAT, emerging as a tool in combating obesity and improving BAT function.

Modified citrus pectin (MCP), a polysaccharide from citrus fruits, modulates galectin-3 (Gal-3) and immune responses. Although MCP exhibits notable immunomodulatory effects, its role in drug-induced splenic and systemic toxicity remains unexplored. This study investigated the effects of MCP modulation on splenic immune remodeling and galectin expression in a rat model of cisplatin-induced toxicity. Wistar rats were divided into four groups ( n = 5 animals/group): control (SHAM), MCP (100 mg/kg/day for 7 days), cisplatin (CIS, 10 mg/kg/day for 3 days), and MCP + CIS. Spleens were collected 6 h after the final cisplatin dose. Cisplatin induced splenic structural disorganization and selectively reduced nitric oxide levels without broadly affecting antioxidant enzymes. Cisplatin treatment was associated with increased CD3⁺ T cell labeling and enhanced tissue expression of Gal-1, -3, and − 9. MCP administration did not restore splenic architecture but promoted increased hemosiderin deposition in the red pulp, suggestive of enhanced erythrophagocytosis and altered iron handling, and markedly reduced CD3⁺ T cell immunoreactivity. MCP associated with cisplatin also reduced Gal-1 and Gal-3 levels and altered the relationship between galectins and splenic immune cell populations. Correlation analyses revealed positive associations between Gal-1, -3, and − 9 and CD68⁺ macrophages, as well as a selective association between Gal-3 and CD3⁺ T cells, exclusively in MCP + CIS animals. MCP does not mitigate cisplatin-induced splenic damage but alters immune cell distribution and galectin-related responses during cisplatin exposure.

Xanthan gum is commonly used in the food industry to adjust food consistency and to improve the safety of swallowing liquids and food in people with dysphagia. The pro-inflammatory effect of xanthan gum is acknowledged in the literature. This study aimed to examine the effect of chronic xanthan gum supplementation in the diet on intestinal inflammatory processes in adult Wistar rats at three different doses. After the tenth week of treatment, white adipose tissue (epididymal, retroperitoneal, and mesenteric) was collected, and the distal colon was dissected and processed for cytokine and immunohistochemical analysis. Fecal matter from the colon was used for microbiota analysis. In general, the addition of xanthan gum at all doses promoted an inflammatory state as demonstrated by the high presence of lymphocytes. Also, it modified the content of the pro-inflammatory cytokines IL-1β and TNF-α compared to the control group. Regarding the colon barrier markers, xanthan gum increased the Claudin 2 and ZO-1 levels. The α diversity and relative abundance of Bacterioidetes (B), Firmicutes (F), F/B ratio were similar among the groups. Elusimicrobiota was increased. Our research, using an experimental model, confirmed the clinical assumption that xanthan gum is associated with the development of necrotizing enterocolitis in neonates. We validated the biological mechanism and metabolic pathway in the intestine of the deleterious effect of continuous use of xanthan gum. In conclusion, dietary xanthan gum induced moderate-grade inflammation and modified the colon gut barrier. Recent advances in the study of xanthan gum underscore the need for translational research bridging experimental findings and clinical practice.

Environmental exposure to heavy metals, particularly cadmium (Cd), has been increasingly associated with obesity, metabolic dysfunction, chronic inflammation, and related disorders such as type 2 diabetes and cardiovascular diseases. Adipose tissue (AT), a paracrine and endocrine organ central to systemic energy and inflammatory homeostasis, is a major site of heavy metal accumulation and a key target of Cd toxicity. However, the mechanisms by which Cd disrupts adipocyte function, especially through epigenetic pathways, remain poorly understood. In this study, we investigated the effects of Cd on epigenetic regulators, antioxidant enzyme activity, inflammatory mediators, and adipogenic programming in human adipose-derived stromal/stem cells (hASCs) and differentiated adipocytes. Cd exposure altered histone modifiers associated with lysine 27 of histone 3 (H3K27), disrupted redox balance in a concentration-dependent manner, impaired adipogenic differentiation and lipid accumulation, and modulated inflammatory and adipokine responses according to differentiation stage and Cd concentration. Our findings suggest that Cd compromises adipose cell homeostasis through mechanisms involving epigenetic dysregulation, oxidative stress imbalance, and altered adipogenic and inflammatory signalling. These observations point to possible long-term metabolic consequences of environmental Cd exposure due to its accumulation in adipose tissue.