Collagen supplementation (CS) has emerged as a promising therapeutic approach with potential benefits for managing metabolic syndrome (MetS)-related risk factors. This narrative review integrates human evidence with preclinical mechanistic insights into the metabolic actions of collagen. Anti-obesity effects are attributed to increased satiety, gastric distension, GLP-1 secretion, and enhanced fatty acid oxidation mediated by PPAR-α activation and AMPK signalling. In type 2 diabetes, collagen improves glucose homeostasis by enhancing insulin sensitivity, upregulating GLUT-4, and inhibiting DPP-IV, thereby prolonging incretin activity (GLP-1, GIP) and supporting β-cell function. The antihypertensive effect of collagen peptides (CP) is primarily linked to angiotensin-converting enzyme (ACE) inhibition, which reduces angiotensin II levels while promoting bradykinin-mediated vasodilation and nitric oxide release. Additionally, CP has shown potential in improving lipid profiles by modulating PPAR-γ and AMPK, increasing HDL-C and reducing LDL-C and triglycerides. Emerging evidence also supports a role for collagen in restoring gut microbiota balance, increasing short-chain fatty acid production, and reducing pro-inflammatory and oxidative pathways, contributing to systemic metabolic regulation. Overall, these findings suggest CS exerts multi-targeted benefits on MetS components through modulation of endocrine, inflammatory, and metabolic pathways. Nevertheless, larger, long-term clinical trials are warranted to determine optimal dosing regimens, evaluate long-term efficacy, and further elucidate microbiota-mediated effects.