Tobacco use among persons displaying type II diabetes exponentially increases negative health consequences and mortality rates. Especially troubling, diabetic persons who smoke display reduced rates of tobacco cessation as compared to non-diabetic smokers. Diabetes is a metabolic syndrome that consists of insulin resistance due to disruptions in insulin signaling. Insulin has been shown to modulate mesolimbic reward circuitry in response to drugs of abuse, such as nicotine. This study utilized the conditioned place preference paradigm (CPP) to examine nicotine reward in a rat model of insulin resistance induced by the consumption of a high-fat diet (HFD). Rats were placed on a HFD for 5 weeks, after which they were assessed for insulin resistance via blood glucose measurements after an insulin challenge. The results revealed that the HFD produced significant increases in body weight compared to control-diet rats. The HFD produced two subsets of animals that displayed insulin resistance or insulin sensitivity. Interestingly, insulin resistant rats exhibited higher nicotine CPP than control-diet rats. Also, rats that displayed insulin sensitivity exhibited suppressed nicotine CPP as compared to control-diet rats. This suggests that neither the increased body weight nor the HFD per se in the HFD insulin resistant rats contributed to the enhanced nicotine reward. These findings suggest that following a HFD, animals that display insulin resistance undergo neural changes related to insulin signaling that alter brain reward systems in a manner that promotes the rewarding effects of nicotine.