Daedong Kim

Cancer cachexia (CC) is a multifactorial metabolic syndrome characterized by systemic inflammation, muscle wasting, and adipose tissue depletion. Amaranth ( Amaranthus caudatus L.), a pseudocereal rich in proteins, squalene, and tocotrienols, exhibits strong antioxidant and anti‐inflammatory activities. Enzymatic hydrolysis of amaranth proteins enhances bioavailability and physiological potency. Korean mint ( Agastache rugosa ) extract, abundant in flavonoids such as tilianin and acacetin, has been reported to suppress inflammatory and oxidative pathways. However, the combined effect of amaranth hydrolysate and Korean mint extract (AKE) on cancer cachexia has not been elucidated. CT26 tumor‐bearing mice (six‐week‐old male BALB/c) were orally administered AKE (125 or 250 mg/kg/day) for 14 days. AKE attenuated cachexia‐induced weight loss (3.6%–10.3%, p < 0.01) and preserved muscle (13.6%–15.8%, p < 0.01) and fat mass (36.0%–40.8%, p < 0.01). Grip strength was significantly improved. AKE suppressed serum pro‐inflammatory cytokines and inhibited muscle protein degradation by downregulating muscle RING‐finger protein‐1 and muscle atrophy F‐box expression. It also enhanced protein synthesis by activating the protein kinase B/mammalian target of rapamycin pathway. In adipose tissue, AKE reduced AMP‐activated protein kinase browning while promoting adipogenesis via proliferator–activated receptor gamma, CCAAT/enhancer‐binding protein alpha, and Sterol regulatory element‐binding protein 1 upregulation. These findings demonstrate that AKE mitigates cancer‐induced muscle and fat loss by modulating inflammation, proteolysis, and metabolic remodeling, highlighting its potential as a multi‐targeted nutritional strategy for managing cancer cachexia.

Background/Objectives: Cancer cachexia involves progressive skeletal muscle and adipose tissue loss, which is further aggravated by cisplatin chemotherapy via increased systemic inflammation, tissue catabolism, and renal toxicity. The present study aimed to evaluate whether a combination of amaranth protein hydrolysate and Agastache rugosa extract (AKE) could attenuate cisplatin-associated cachexia and nephrotoxicity in CT26 tumor-bearing mice. Methods: Cancer cachexia was induced by subcutaneous CT26 cell inoculation in 6-week-old male BALB/c mice, followed by a 7-day tumor establishment period. Cisplatin was then administered intraperitoneally, and AKE (125 or 250 mg/kg/day) was given daily by oral gavage for 14 days. Results: AKE administration significantly alleviated cisplatin-induced body weight loss and systemic inflammation, accompanied by preservation of skeletal muscle and adipose tissue mass, as well as increased myofiber cross-sectional area and adipocyte size. AKE markedly reduced serum inflammatory cytokines, blood urea nitrogen, and creatinine levels, indicating protection against cisplatin-induced renal injury. Mechanistically, AKE suppressed renal apoptosis through inhibition of mitogen-activated protein kinase signaling. In skeletal muscle, AKE attenuated muscle atrophy by modulating protein turnover pathways, including downregulation of muscle-specific ubiquitin ligases and restoration of Akt/mTOR and FoxO3a signaling. Furthermore, AKE mitigated adipose tissue wasting by suppressing AMP-activated protein kinase-dependent browning and restoring adipogenic signaling involved in lipid storage and differentiation. Conclusions: These findings demonstrate that AKE confers comprehensive protection against cisplatin-induced cachexia and nephrotoxicity by coordinately preserving muscle and adipose tissue and attenuating renal injury, suggesting its potential as a functional nutritional strategy to alleviate chemotherapy-associated tissue wasting.

2′‐Fucosyllactose (2′‐FL) is a component of human milk oligosaccharides and has undergone extensive investigation for potential health benefits. However, its potential to prevent androgenic alopecia (AGA) has not been reported. In this study, we investigated the protective effect of 2′‐FL on hair damage in a testosterone‐induced AGA mouse model. The administration of 2′‐FL significantly reduced hair loss and increased both hair length and thickness in an AGA mouse model. Mechanistically, administration of 2′‐FL increased hair follicle size and growth factor expression associated with hair growth. 2′‐FL enhanced β‐catenin signaling by activating AKT and ERK. In addition, 2′‐FL suppressed apoptosis signaling and inflammatory cytokines in the dorsal skin of AGA mice. These results underscore the potential of 2′‐FL as a therapeutic agent for AGA.

The beneficial effects of Akkermansia muciniphila (Akk) on gut health and inflammation reduction have been demonstrated; however, scientific evidence of hair growth enhancement by Akk has not been reported. Therefore, this study was undertaken to investigate the effect of Akk on improving testosterone-mediated hair growth inhibition. Hair growth inhibition was induced through subcutaneous injection of testosterone into the shaved dorsal skin of C57BL/6 male mice. Live and pasteurized Akk were orally administered at a concentration of 1 x 10(8 )colony-forming unit. After 5 weeks, hair length and skin tissues were analyzed. The live and pasteurized Akk significantly stimulated hair growth, countering the inhibitory effect of testosterone compared to the testosterone-alone group. Hematoxylin and eosin staining revealed a significant increase in hair follicle size in the Akk-treated group. An increase in beta-catenin levels, which are associated with hair growth and cell cycle progression, was also observed. Moreover, the Akk-treated group exhibited increased levels of fibroblast growth factors, including Fgf7, Igf1, Fgf7, Fgf10, and Fgf21. However, no significant difference was observed between the live and pasteurized Akk groups. These results underscore the potential of live and pasteurized Akk in improving testosterone-mediated hair growth inhibition.