Obesity caused by a high-fat diet (HFD) affects gut microbiota linked to the risk of type-2 diabetes (T2D). This study evaluates live cells and ethanolic extract (SEL) of Lactobacillus sakei Probio65 and Lactobacillus plantarum Probio-093 as natural anti-diabetic compounds. In-vitro anti-diabetic effects were determined based on the inhibition of α-glucosidase and α-amylase enzymes. The SEL of Probio65 and Probio-093 significantly retarded α-glucosidase and α-amylase enzymes (p < 0.05). Live Probio65 and Probio-093 inhibited α-glucosidase and α-amylase, respectively (p < 0.05). In mice fed with a 45% kcal high-fat diet (HFD), the SEL and live cells of both strains reduced body weight significantly compared to HFD control (p < 0.05). Probio-093 also improved blood glucose level compared to control (p < 0.05). The gut microbiota modulatory effects of lactobacilli on HFD-induced diabetic mice were analyzed with qPCR method. The SEL and live cells of both strains reduced phyla Deferribacteres compared to HFD control (p < 0.05). The SEL and live cells of Probio-093 promoted more Actinobacteria (phyla), Bifidobacterium, and Prevotella (genus) compared to control (p < 0.05). Both strains exerted metabolic-modulatory effects, with strain Probio-093 showing more prominent alteration in gut microbiota, substantiating the role of probiotics in gut microbiome modulations and anti-diabetic effect. Both lactobacilli are potential candidates to lessen obesity-linked T2D.

Cellular aging has drawn the attention of researchers, scientists, and biotech businesses for the treatment of a number of medical conditions. Cellular aging is primarily defined by consistent cessation of proliferative development in response to internal and external stressors, including DNA damage, telomere shortening, mitochondrial dysfunction, and regulation of the senescence-associated secretory phenotype (SASP). Disturbances involving these factors may contribute to age-related disease development. Therefore, the current review aims to explore anti-aging factors targeting DNA damage response and SASP regulation and their detailed signaling networks. In addition, it provides an opportunity for researchers to identify not only anti-aging targets, but also anti-aging therapeutic strategies based on identified and non-identified targets.