Collagen peptides have been widely studied for their beneficial effects on skin health; however, their potential role in hair growth remains insufficiently explored. This study aimed to investigate the effects of orally administered low-molecular-weight fish collagen peptide (SH-GT) on hair regrowth and its underlying mechanisms in a hair-removed C57BL/6J mouse model. Mice were administered SH-GT (100, 300, or 600 mg/kg body weight) or a positive control (Pansidil, 400 mg/kg) daily for 28 days. SH-GT significantly enhanced hair regrowth, as evidenced by the increased hair growth area. Histological analysis revealed increased dermal thickness and visible hair follicle structures in SH-GT-treated groups. At the molecular level, SH-GT upregulated proliferation-related proteins, including PCNA and Cyclin D1, and activated Wnt/β-catenin signaling. In addition, SH-GT enhanced PI3K/Akt/mTOR signaling, suggesting improved cellular growth and survival. Conversely, SH-GT suppressed hair growth inhibitory pathways by reducing BMP4 expression and decreasing Smad phosphorylation. Furthermore, SH-GT increased the mRNA expression of growth factors such as IGF-1, HGF, VEGF, EGF, and FGF7. In conclusion, SH-GT promotes hair regrowth by simultaneously activating proliferation-related signaling pathways and suppressing inhibitory mechanisms, thereby improving the dorsal skin microenvironment associated with hair regrowth. These findings suggest that SH-GT may serve as a promising functional ingredient for improving hair growth.

This study investigated the effects and mechanisms of broccoli extract containing more than 99.0% β-NMN (BRC) on UVB-induced skin damage, including moisture loss, oxidative stress, inflammation, wrinkle formation, and melanin production, using in vitro and in vivo models. BRC treatment significantly alleviated UVB-induced skin dehydration, oxidative stress, and inflammatory responses, as well as inhibited wrinkle formation and melanin synthesis. Mechanistically, BRC enhanced skin hydration and barrier function by upregulating hyaluronic acid synthases and genes related to sphingolipid metabolism, while simultaneously suppressing NF-κB signaling and COX-2 expression, thereby re-ducing inflammation. Moreover, BRC promoted collagen synthesis by activating the TGF-βR1/Smad3/Collagen pathway and prevented extracellular matrix degradation by inhibiting JNK/c-Fos/c-Jun/MMPs signaling. In addition, BRC modulated the cAMP/PKA/CREB/MITF/TRPs pathway, leading to reduced melanin production. These findings suggest that BRC supplementation may effectively protect against UVB-induced skin damage, supporting its potential application as a functional ingredient for skin health.

Background/Objectives: Kaempferia parviflora (KP), also known as black ginger, has been reported to exert metabolic regulatory effects, yet its influence on skeletal muscle glucose handling remains unclear. Because impaired glucose uptake in skeletal muscle is a major contributor to insulin resistance and type 2 diabetes mellitus (T2DM), this study investigated the effects of KP on glucose uptake and the GLUT4 signaling pathway both in vitro and in vivo. Methods: The effects of KP extract on glucose uptake and GLUT4-related signaling proteins were evaluated in differentiated C2C12 myotubes. In parallel, C57BL/6J and db/db mice were orally administered KP extract at varying doses for six weeks to evaluate its metabolic effects in vivo. Results: KP significantly increased glucose uptake in C2C12 myotubes, accompanied by increased GLUT4 expression and upregulation of GLUT4-related signaling proteins. In diabetic mice, KP administration improved fasting glucose, glucose tolerance and GLP-1 level while lowering insulin and HbA1c levels. Skeletal muscle tissues exhibited increased GLUT4 expression and modulation of downstream regulators involved in glucose homeostasis. Conclusions: These findings indicate that KP improves skeletal muscle glucose metabolism primarily through activation of the GLUT4 pathway. Taken together, KP may serve as a potential functional ingredient for regulating muscle glucose utilization and mitigating metabolic disturbances associated with T2DM.

Terminalia bellirica extract (TBE) has long been utilized in Ayurvedic medicine across Indian and surrounding regions for diverse therapeutic applications. Despite its traditional prominence, systematic investigations addressing the anti-obesity efficacy and underlying mechanisms remain limited. In this study, we evaluated the anti-obesity potential of TBE using both 3T3-L1 adipocyte and high-fat diet (HFD)-induced mice model. In vitro studies using 3T3-L1 adipocytes demonstrated that TBE significantly inhibited lipid accumulation and downregulated key genes involved in adipogenesis and lipogenesis, while upregulating genes promoted lipolysis and energy metabolism. To validate these cellular effects in a physiological context, mice were randomly assigned to six groups: normal control (NC), HFD-induced obese (C), HFD with metformin (100 mg/kg b.w., PC), and HFD with TBE at 50, 100, and 200 mg/kg b.w. Consistent with the in vitro findings, TBE supplementation significantly reduced body weight gain, adipose tissue mass, and adipocyte size in HFD-induced obese mice. Taken together, these results indicate that TBE exerts anti-obesity effects through modulation of adipose tissue metabolic pathways, highlighting its therapeutic potential for obesity management.