Sean M Lanting1, Kimberley L Way2, Angelo Sabag2, Rachelle N Sultana2, Nathan A Johnson2, Michael K Baker3, James A Gerofi4, Ian D Caterson4, Stephen M Twigg5, Vivienne H Chuter6. 1. Faculty of Health and Medicine, School of Health Sciences, University of Newcastle, Australia. Electronic address: sean.lanting@newcastle.edu.au. 2. Faculty of Medicine and Health, Discipline of Exercise and Sports Science, University of Sydney, Camperdown, Australia; The Boden Collaboration for Obesity, Nutrition, Exercise and Eating Disorders, Charles Perkins Centre, University of Sydney, Camperdown, Australia; The Charles Perkins Centre, University of Sydney, Camperdown, Australia. 3. School of Exercise Science, Australian Catholic University, Strathfield, Australia. 4. The Boden Collaboration for Obesity, Nutrition, Exercise and Eating Disorders, Charles Perkins Centre, University of Sydney, Camperdown, Australia; The Charles Perkins Centre, University of Sydney, Camperdown, Australia. 5. The Charles Perkins Centre, University of Sydney, Camperdown, Australia; School of Medicine, University of Sydney, Camperdown, Australia. 6. Faculty of Health and Medicine, School of Health Sciences, University of Newcastle, Australia; Priority Research Centre for Physical Activity and Nutrition, University of Newcastle, Australia.
Abstract
BACKGROUNDS AND AIMS: Obesity and diabetes independently contribute to cutaneous microvascular dysfunction via pathological processes that are not fully understood. We sought to determine if obesity severity is associated with cutaneous microvascular dysfunction and measures of peripheral arterial disease in adults with type 2 diabetes in cross-sectional observational study design. METHODS AND RESULTS: Primary outcomes were post-occlusive reactive hyperaemia as determined by laser-Doppler fluxmetry (peak flux post-occlusion, time to peak flux post-occlusion, peak as a percentage of baseline, and area under the curve [AuC] index post-occlusion to pre-occlusion). Secondary outcomes were ankle- and toe-brachial indices (ABI and TBI) and systolic toe pressure. Thirty-six participants (20 men, 16 women) with mean age 55 ± 8 years, BMI of 36 ± 5 kg/m2 and duration of diabetes 8 ± 6 years underwent measurements. After adjusting for age and duration of diabetes, SAT and total percentage body fat were able to explain 29% (p = 0.001) and 20% (p = 0.01) of variance of AuC index models, as well as 29% (p = 0.02) and 18% (p = 0.02) of peak as a percentage of baseline models, respectively. Though TBI demonstrated moderate, significant correlations with SAT (r:0.37, p = 0.04) and total percentage body fat (r:0.39, p = 0.03), these were not upheld by regression analyses. Neither ABI nor systolic toe pressure significantly correlated with any measure of adiposity or obesity. CONCLUSION: These findings demonstrate impairment in cutaneous microvascular function related to adiposity and obesity severity in adults with type 2 diabetes, suggesting that obesity may pathologically effect cutaneous microvascular function in the absence of overt macrovascular disease, warranting further investigation.
BACKGROUNDS AND AIMS: Obesity and diabetes independently contribute to cutaneous microvascular dysfunction via pathological processes that are not fully understood. We sought to determine if obesity severity is associated with cutaneous microvascular dysfunction and measures of peripheral arterial disease in adults with type 2 diabetes in cross-sectional observational study design. METHODS AND RESULTS: Primary outcomes were post-occlusive reactive hyperaemia as determined by laser-Doppler fluxmetry (peak flux post-occlusion, time to peak flux post-occlusion, peak as a percentage of baseline, and area under the curve [AuC] index post-occlusion to pre-occlusion). Secondary outcomes were ankle- and toe-brachial indices (ABI and TBI) and systolic toe pressure. Thirty-six participants (20 men, 16 women) with mean age 55 ± 8 years, BMI of 36 ± 5 kg/m2 and duration of diabetes 8 ± 6 years underwent measurements. After adjusting for age and duration of diabetes, SAT and total percentage body fat were able to explain 29% (p = 0.001) and 20% (p = 0.01) of variance of AuC index models, as well as 29% (p = 0.02) and 18% (p = 0.02) of peak as a percentage of baseline models, respectively. Though TBI demonstrated moderate, significant correlations with SAT (r:0.37, p = 0.04) and total percentage body fat (r:0.39, p = 0.03), these were not upheld by regression analyses. Neither ABI nor systolic toe pressure significantly correlated with any measure of adiposity or obesity. CONCLUSION: These findings demonstrate impairment in cutaneous microvascular function related to adiposity and obesity severity in adults with type 2 diabetes, suggesting that obesity may pathologically effect cutaneous microvascular function in the absence of overt macrovascular disease, warranting further investigation.