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1 Department of Medicine, University of Sydney, Sydney, NSW, Australia
2 Department of Clinical Biochemistry, Royal Prince Alfred Hospital, Sydney, NSW, Australia
3 The Diabetes Centre, Royal Prince Alfred Hospital, Sydney, NSW, Australia
4 The Diabetes Centre, Royal Prince Alfred Hospital, Sydney, NSW, Australia; Department of Medicine, University of Sydney, Sydney, NSW, Australia
* To whom correspondence should be addressed. E-mail: david.celermajer{at}email.cs.nsw.gov.au.
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 older age. Post-prandial vascular responses were assessed in three groups of subjects; fifteen type 2 diabetic subjects (age 58 ± 8yrs), 15 age, gender and BMI-matched older controls (age 57 ± 9 years), and 15 healthy young controls (age 33 ± 7yrs). Studies were carried out before, 3 and 6 hours after a standardized high-fat meal (1030 kcal, 61g fat). Forearm microvascular flows were measured using strain-gauge plethysmography and large artery function by ultrasound. Resting blood flow and hyperemic "area under curve" (AUC) flow were not significantly different in the diabetic subjects (resting 117 ± 42% & AUC 134 ± 46% of pre-meal values) compared with the age-matched controls (resting 131 ± 39% & AUC 134 ± 47%, p = NS), however the response in the diabetics was blunted when compared with young controls (resting 171 ± 67% & AUC 173 ± 99% of pre-meal 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 post-prandial 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 non-diabetic and diabetic adults, related to aging rather than insulin resistance.
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