Chlorella vulgaris (C. vulgaris) is unicellular green algae consumed worldwide as a functional food. The immune stimulatory function of C. vulgaris is known; however, no study has elucidated its immune regulatory potential and associated microbiome modulation. In the current study, we aimed to validate the immune regulatory role of C. vulgaris mediated through two mechanisms. Initially, we assessed its ability to promote the expansion of the regulatory T cell (Treg) population. Subsequently, we investigated its impact on gut microbiota composition and associated metabolites. The supplementation of C. vulgaris altered the gut microbiota composition, accompanied by increased short-chain fatty acid (SCFAs) production in mice at homeostasis. We later used C. vulgaris in the treatment of a DSS-induced colitis model. C. vulgaris intervention alleviated the pathological symptom of colitis in mice, with a corresponding increase in Treg levels. As C. vulgaris is a safe and widely used food supplement, it can be a feasible strategy to instigate cross-talk between the host immune system and the intestinal flora for the effective management of inflammatory bowel disease (IBD).

Background: The high incidence of metabolic syndrome in the elderly poses a significant challenge to the healthcare system, emphasizing the need for interventions tailored to geriatric patients. Given the limited focus on females in previous studies, this research aimed to evaluate the effects of dietary curcumin on obesity and NAFLD outcomes in naturally aged (18-month-old) female mice. Methods: Female C57BL/6 mice aged 18 months were fed a normal chow diet (NCD) and a HFHSD, with or without curcumin (0.4% w/w), for an 8-week period. Parameters included food intake, body weight, insulin tolerance test (ITT), glucose tolerance test (GTT), percentage fat mass, hepatic triglyceride, and cholesterol levels, and a histological examination for NAFLD detection, qPCR, and immunoblotting analyses were performed. Results: The cumulative body weight gain after 8 weeks in the aged female mice supplemented with curcumin and fed an HFHSD was significantly lower (10.84 ± 1.09 g) compared to those fed a HFHSD alone (15.28 ± 1.26 g). Curcumin supplementation also resulted in reduced total body fat (HFHSD group 50.83 ± 1.71% vs. HFHSD+CUR 41.46 ± 3.21%), decreased epidydimal fat mass (HFHSD: 3.79 ± 0.29 g vs. HFHSD+CUR: 2.66 ± 0.30 g), and repaired adipogenic signaling in the white adipose tissue. Furthermore, curcumin lowered triglyceride and cholesterol deposition in the liver, preventing hepatic steatosis and improving hepatic insulin sensitivity. Conclusions: Curcumin demonstrates the ability to ameliorate the deleterious effects of HFHSD in aged female mice by reducing body fat composition, modulating adipogenic signaling in the white adipose tissue, and improving insulin homeostasis and non-alcoholic fatty deposition in the liver.

Objectives: Obesity is associated with cardiac remodeling characterized by cardiomyocyte hypertrophy and fibrosis, eventually leading to heart failure. This study aimed to evaluate whether dietary matcha supplementation could be effective in reducing high-fat, high-sugar diet (HFD)-induced cardiac remodeling in mice, and whether this effect is linked to changes in the gut microbiota along the gut–heart axis. Methods: Six-week-old C57BL/6J mice were randomly divided into normal chow diet (NCD) or HFD (without matcha, 0.2% matcha, or 1% matcha) groups. Dietary intervention continued for 10 weeks with continuous monitoring of body weight. After completion of the intervention, hearts were collected, weighed, and processed for histological examination of cardiomyocyte size with wheat germ agglutinin (WGA) staining and collagen deposition with Picrosirius Red staining. The gut microbiome was evaluated using 16S rRNA sequencing of gDNA from feces, and correlation analysis was performed between microbial taxa and cardiometabolic parameters. Results: After 10 weeks of dietary intervention, heart weight was significantly lower in mice treated with 1% matcha than in HFD controls. WGA staining showed a significant increase in cardiomyocyte size in the HFD group compared with the NCD group, whereas both the 0.2% and 1% matcha-supplemented groups revealed significantly smaller cardiomyocytes than the HFD controls. In addition, both matcha doses significantly reduced cardiac collagen deposition relative to HFD controls. In the gut, matcha supplementation displayed a marked increase in the abundance of beneficial gut microbiota, including Ligilactobacillus, Lactobacillus, and Oscillospiraceae, while reducing pathogenic Enterobacteriaceae and Klebsiella, particularly at the high dose. Conclusions: Dietary matcha supplementation attenuated HFD-induced cardiac hypertrophy and fibrosis in mice, independently of body weight, in association with modulation of the gut microbiota along the gut–heart axis. Future studies should determine whether the observed reductions in cardiac hypertrophy and fibrosis translate into measurable improvements in cardiac function and whether the associated gut microbiota alterations exert causal effects on cardiac remodeling.