Latino youth are disproportionately impacted by obesity, prediabetes and type 2 diabetes (T2D). Pediatric obesity is characterized by abnormal increases in proinflammatory markers, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNFα), and monocyte chemoattractant protein-1 (MCP-1) and reductions in antiinflammatory markers, high molecular weight adiponectin (HMW Adpn) and interleukin10 (IL-10). Interleukin-1 receptor antagonist (IL-1ra) is an anti-inflammatory that is positively associated with obesity. IL-6, TNF-α, MCP-1 and IL-1ra have been associated with reduced insulin sensitivity and β-cell dysfunction, two central pathophysiologic mediators of glucose intolerance, while HMW Adpn and IL-10 have been associated with increased insulin sensitivity and β-cell function. The United States Diabetes Prevention Program (DPP) supported lifestyle intervention as the cornerstone approach for preventing T2D among adults with prediabetes, yet no studies to date have assessed the efficacy of an adapted DPP among Latino youth with prediabetes. In this dissertation, three studies were conducted. The first cross-sectional study among Latino youth with prediabetes and obesity (n=65) demonstrated that MCP-1 (β=-0.001, p=0.027; β=0.03, p=0.033), HMW Adpn (β=0.2, p<0.001; β=-2.2, p=0.018), and IL-1ra (β=-0.03, p=0.006; β=0.09, p=0.009) significantly predicted insulin sensitivity (measured by whole body insulin sensitivity index, WBISI) and glucose tolerance (measured by 2-hr glucose concentrations from an oral glucose tolerance test), respectively. Only HMW Adpn significantly predicted β-cell function, measured by oral disposition index, or oDI (β=0.6, p<0.001). The second study was a randomized control trial that demonstrated the efficacy of lifestyle intervention (INT, n=79) for improving oDI among Latino youth with prediabetes and obesity, compared to a usual care control (UCC, n=38) group. No differences were found for changes in WBISI (Δ0.1, p=0.899) or 2-hr glucose (Δ-7.2, p=0.260) between groups. The third study was a secondary analysis (INT n=46, UCC n=29) that demonstrated no significant effects on IL-6, TNF-α, MCP-1, HMW Adpn, IL10, or IL-1ra (all interactions, p>0.05).