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1Department of Medicine, University of Sydney, and 2Department of Clinical Biochemistry and 3Diabetes Centre, Royal Prince Alfred Hospital, Camperdown, Australia
Submitted 21 July 2004 ; accepted in final form 27 October 2004
A fatty meal induces vasodilatation (of both resting and stimulated forearm flow) in healthy young adults, an effect most likely mediated by the vasodilator actions of insulin. We therefore hypothesized that an impaired meal-related vascular response might be an in vivo marker of vascular insulin resistance, related to the presence of diabetes and/or higher age. Postprandial vascular responses were assessed in three groups of subjects: 15 Type 2 diabetic subjects (age 58 ± 8 yr), 15 age-, gender-, and body mass index (BMI)-matched older control subjects (age 57 ± 9 yr), and 15 healthy young control subjects (age 33 ± 7 yr). Studies were carried out before and 3 and 6 h after a standardized high-fat meal (1,030 kcal, 61 g fat). Forearm microvascular flows were measured by strain gauge plethysmography and large-artery function by ultrasound. Resting blood flow and hyperemic area under curve (AUC) flow were not significantly different in diabetic subjects (resting 117 ± 42% and AUC 134 ± 46% of premeal values) compared with age-matched controls (resting 131 ± 39% and AUC 134 ± 47%); however, the response in diabetic subjects was blunted compared with young controls (resting 171 ± 67% and AUC 173 ± 99% of premeal values; P = 0.02 and P = 0.18, respectively). On multiple regression analysis, we found that increasing age (but not BMI or diabetes) was significantly associated with impaired postprandial vascular responses (resting: r = 0.4, P = 0.002; AUC: r = 0.4, P = 0.006). Therefore, meal ingestion results in impaired vasodilator responses in older nondiabetic and diabetic adults, related to aging rather than insulin resistance.
Type 2 diabetes; insulin resistance
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