<p>Advanced glycation end products (AGEs) are formed through non-enzymatic glycation reactions and accumulate in tissues, particularly under pathological conditions such as diabetes mellitus. These compounds are linked to the progression of diabetic complications, including nephropathy, retinopathy, and cardiovascular disease, through mechanisms such as oxidative stress and chronic inflammation. Emerging evidence suggests significant sex-specific differences in AGE formation, accumulation, and their biological effects, influenced by hormonal variations, dietary patterns, and metabolic differences. While the underlying biochemistry of AGE formation, such as the Maillard reaction and dicarbonyl compound activity, is well-characterized, the implications of these processes for clinical outcomes remain underexplored. This mini-review highlights the interplay between molecular mechanisms and sex-specific factors in AGE-related pathophysiology. It further discusses potential therapeutic approaches targeting AGE formation and receptor-mediated pathways, emphasizing the importance of integrating sex-specific considerations into diabetes management. Bridging molecular insights with clinical practice could advance personalized treatment strategies for diabetic complications.</p>