Bifidobacterium animalis subsp. lactis BPL1 HT (BPL1 HT)

Bifidobacterium animalis subsp. lactis BPL1 HT is a heat-treated postbiotic derived from the probiotic strain B. animalis subsp. lactis CECT 8145 [1, 8]. It is not a traditional therapeutic target but rather a therapeutic agent used to manage metabolic health and obesity [4, 11]. The 'HT' designation refers to the heat-inactivation process, which renders the bacteria non-viable while preserving bioactive components such as lipoteichoic acid (LTA) [2, 5]. LTA acts as a key effector molecule, interacting with host receptors like Toll-like receptor 2 (TLR2) and modulating the insulin/IGF-1 signaling pathway [2, 9]. This modulation leads to the activation of FOXO transcription factors (e.g., DAF-16), which regulate lipid metabolism, antioxidant responses, and longevity [5, 7]. Clinical studies have demonstrated that BPL1 HT can significantly reduce abdominal visceral fat, waist circumference, and insulin resistance in adults with obesity [8, 11]. It has also shown promise in improving metabolic and behavioral outcomes in children with Prader-Willi syndrome [1, 12]. As a postbiotic, it offers advantages in terms of shelf-stability and safety compared to live probiotic formulations [6, 8]. While BPL1 HT is not a target for conventional pharmacological drugs, it is often incorporated into dietary supplements and functional foods as an active ingredient to support weight management and metabolic balance [4, 11]. Its role in modulating the gut-brain axis and cardiovascular health is also an area of active research [14, 15].

Other names

BPL1CECT 8145Heat-treated BPL1Heat-inactivated Bifidobacterium animalis subsp. lactis BPL1Bifidobacterium animalis subsp. lactis CECT 8145BPL1-HT

BPL1 HT functions as a postbiotic agent that modulates host metabolic pathways, primarily the insulin/IGF-1 signaling pathway, through its cell wall component lipoteichoic acid (LTA) [2, 5]. LTA interacts with host receptors such as Toll-like receptor 2 (TLR2), triggering downstream signaling that activates FOXO transcription factors like DAF-16 [2, 9]. This activation promotes the expression of genes involved in lipid oxidation and antioxidant defense, leading to reduced fat accumulation and improved insulin sensitivity [5, 11]. Additionally, BPL1 HT has been suggested to influence the GLP-1 pathway, contributing to satiety and glucose regulation [6].