Adipose tissue expression of tumor necrosis factor-alpha (TNF-α) has been implicated in the pathogenesis of obesity-linked insulin resistance and the dyslipoproteinemia of insulin resistance. This study has two aims: (1) to compare select inflammatory mediators in non-smoking, normoglycemic male subjects with and without the atherogenic dyslipoproteinemia (ADL), and (2) to determine the effects of statin therapy on select inflammatory mediators.ADL subjects had higher levels of insulin (16.7 +/- 7.5 versus 11.6 +/- 5.9μIU/mL, P = 0.008), soluble TNF receptor superfamily 1B (sTNFRSF1B) (3.3 +/- 0.7 versus 2.7 +/- 0.5ng/mL, P = 0.005), and interleukin-6 (IL-6) (2.6 +/- 2.2 versus 1.3 +/- 1.8pg/mL, P = 0.006) as compared to those of the non-ADL subjects. After adjustment for age, sTNFRSF1B (P = 0.003) was more predictive of ADL than high-sensitivity C-reactive protein (hs-CRP) (P = 0.047). Statin therapy did not change sTNFRSF1B, TNF-α, IL-6, hs-CRP, whereas soluble TNF receptor superfamily 1A (sTNFRSF1A) increased slightly (P = 0.048). A high level of sTNFRSF1B is a strong marker of the pro-inflammatory state in this sample of male ADL subjects.