Lactococcus chungangensis CAU 28 alleviates diet-induced obesity and adipose tissue metabolism in vitro and in mice fed a high-fat diet

Obesity, which has become a major public health problem, can arise from complex dyslipidemia, insulin resistance, and immune responses, among other mechanisms. Some Lactobacillus strains effectively ameliorate obesity; however, the beneficial effects of Lactococcus spp., which are often used as dairy starters, remain unclear. In the present study, we evaluated the efficacy of Lactococcus chungangensis CAU 28 using the 3T3-L1 cell line and obese mice fed a high-fat diet. Overall, administration of Lc. chungangensis CAU 28 effectively resolved obesity associated with weight gain and lipid accumulation. In differentiated 3T3-L1 cells, Lc. chungangensis CAU 28 treatment significantly diminished the total lipid quantity, inhibited triglyceride formation, and prevented the proliferation of adipogenic transcription factors (fatty acid synthase, adiponectin, peroxisome proliferator-activated receptor-gamma, and CCAAT-enhancer-binding protein-α) associated with lipid accumulation. In the obesity mouse model, wherein the intake of Lc. chungangensis CAU 28 effectively reduced body weight gain, along with fat differentiation and accumulation (white fat; abdominal and subcutaneous). Furthermore, Lc. chungangensis CAU 28 increased serum adiponectin levels, decreased serum leptin levels, and effectively regulated adipokine secretion. It also increased the high-density lipoprotein:cholesterol ratio, reduced total cholesterol and triglyceride levels, reduced the low-density lipoprotein:cholesterol ratio, and affected obesity-regulated inflammatory cytokines IL-6, tumor necrosis factor-α, IFN-γ, and IL-1β. Additionally, Lc. chungangensis CAU 28 was associated with an increase in the CD3+CD4+CD8- phenotype among obese mice. Thus, the administration of Lc. chungangensis CAU 28 induced antiobesity effects, suggesting potential applications of this species as a supplement for obesity mitigation.