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Aspirin has lower antiplatelet activity in diabetic patients. Our aim is to study the roles of acute hyperglycemia and hyperlipidemia on aspirin function in diabetic subjects with and without cardiovascular disease. Using urine thromboxane (pg/mg creatinine) and VerifyNow (Aspirin Resistance Measures-ARU), we investigated diabetic subjects during a 2-hour glucose challenge (n=49) or a 4-hour fat challenge (n=11). All subjects were currently taking aspirin (81 or 325 mg). After fat ingestion, urine thromboxane increased in all subjects (Mean ± SE before: after) (1209 ± 336: 1552 ±371, P=.01), while we noted a trend increase in VerifyNow measures (408±8: 431±18, P=.1). The response to glucose ingestion was variable. Diabetic subjects with cardiac disease and dyslipidemia increased thromboxane (1693±364: 2799 ± 513, P<.05) and VerifyNow (457.6 ± 22.3: 527.1 ± 25.8, P<.05) measures after glucose. We conclude that saturated fat ingestion increases in vivo thromboxane production despite aspirin therapy.