30 min), the lysate supernatants were used to determine gliotoxin reductase activity (A 340 nm ) in the presence of gliotoxin (9 M) and NADPH (200 M) at pH 7.2 (a modified version of Hill et al
By slowing gastric emptying, it reduces the time stomach acid has to work on B12-protein bonds
10.1016/j.jsbmb.2016.07.016 147 WeingrtnerO.LtjohannD.JiS.WeisshoffN.ListF.SudhopT.et al (2008)
Key Benefits: Accelerates fat metabolism by transporting fatty acids into mitochondria for energy production Boosts natural energy levels and combats physical fatigue Supports brain function and cognitive clarity Promotes cardiovascular health by improving fat utilization in the heart Enhances exercise performance and endurance Improves recovery time and reduces muscle soreness Optimizes weight management as part of a fat-loss protocol Superior absorption via subcutaneous injectionunmatched by oral or capsule forms Why Injectable L-Carnitine
Molecular mechanisms of cutaneous ageing To interpret the effects of dermatological peptides, the molecular alterations of cutaneous ageing must be understood: Intrinsic ageing (chronological) Decreased collagen synthesis by fibroblasts (1% per year after 30) AGE accumulation (Advanced Glycation End-products) by non-enzymatic glycation Fibroblastic senescence with SASP (Senescence-Associated Secretory Phenotype), chronic pro-inflammatory secretion Dermal atrophy , reduced vascularisation, loss of subcutaneous adipocytes Extrinsic ageing (photoageing) UV-B damage : cyclobutane pyrimidine dimers, keratinocyte DNA alteration UV-A and oxidative stress : ROS, lipid peroxidation, protein carbonylation MMP overexpression (MMP-1, MMP-3, MMP-9) via AP-1 activation, degrading collagen and elastin Solar elastosis : accumulation of degraded and dystrophic elastin in the dermis Dermatological peptides act at different levels of these cascades: anabolic stimulation (GHK-Cu, Matrixyl), catabolic inhibition (MMP modulation), anti-oxidant protection (GHK-Cu), inflammatory signalling modulation
