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The literature suggests a bidirectional relationship between testosterone (T) and iron, but mechanisms underlying this relationship remain unclear. We investigated effects of iron on advanced glycation end products (AGEs) in obesity-related androgen deficiency. In total, 111 men were recruited, and iron biomarkers and N(<i>ɛ</i>)-(carboxymethyl)lysine (CML) were measured. In an animal study, rats were fed a 50% high-fat diet (HFD) with (0.25, 1, and 2 g ferric iron/kg diet) or without ferric citrate for 12 weeks. Obese rats supplemented with &gt;1 g iron/kg diet had decreased testicular total T compared to HFD alone. Immunohistochemical staining showed that &gt;1 g of ferric iron increased iron and AGE retention in testicular interstitial tissues, which is associated with increased expression of the receptor for AGEs (RAGE), tumor necrosis factor-α, and nitric oxide. Compared with normal weight, overweight/obese men had lower T levels and higher rates of hypogonadism (19% vs. 11.3%) and iron overload (29.8% vs.15.9%). A correlation analysis showed serum total T was positively correlated with transferrin saturation (<i>r</i> = 0.242, <i>p</i> = 0.007) and cathepsin D (<i>r</i> = 0.330, <i>p</i> = 0.001), but negatively correlated with red blood cell aggregation (<i>r</i> = −0.419, <i>p</i>&lt;0.0001) and CML (<i>r</i> = −0.209, <i>p</i> &lt; 0.05). In conclusion, AGEs may partially explain the underlying relationship between dysregulated iron and T deficiency.