Antti Viljanen1,2,3, Minna Soinio4, Carol Yim-Lui Cheung5,6, Jarna C Hannukainen7, Henry K Karlsson3, Tien Yin Wong6,8, Alun D Hughes9, Paulina Salminen10, Pirjo Nuutila3,4, Eija Vesti2, Robyn J Tapp11,12. 1. Medilaser Turku, Cor Group, Turku, Finland. 2. Department of Ophthalmology, University of Turku and Turku University Hospital, Turku, Finland. 3. Turku PET Centre, University of Turku and Turku University Hospital, Turku, Finland. 4. Department of Endocrinology, Turku University Hospital, Turku, Finland. 5. Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Ma Liu Shui, Hong Kong. 6. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore, Singapore. 7. Turku PET Centre, University of Turku, Turku, Finland. 8. Office of Academic and Clinical Development, Duke-NUS Medical School, National University of, Singapore, Singapore. 9. Institute of Cardiovascular Science, University College London, London, UK. 10. Department of Surgery, University of Turku, and Turku University Hospital, Turku, Finland. 11. Population Health Research Institute, St Georges, University of London, London, UK. rtapp@sgul.ac.uk. 12. Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Australia. rtapp@sgul.ac.uk.
Abstract
STUDY AIM: Retinal microvasculature changes reflect systemic small vessel damage from obesity. The impact of bariatric surgery induced weight loss on the microvasculature is relatively unknown. We hypothesized that weight loss following bariatric surgery would be associated with improved structural changes in the retinal microvasculature, reflecting an overall improvement in microvascular health. METHODS: The study included 22 obese subjects scheduled for bariatric surgery (laparoscopic Roux-en-Y gastric bypass or a sleeve gastrectomy) and 15 lean, age-matched controls. Ophthalmic examination, including fundus photography, was performed at baseline and 6-months. Retinal microvasculature caliber was analysed quantitatively using a semi-automated computer program and summarized as central retinal artery equivalent (CRAE) and venular equivalent (CRVE). RESULTS: Mean weight loss at 6 months was 26.1 kg ± 8 kg in the bariatric surgery group. Retinal artery caliber increased (136.0 ± 1.4 to 141.4 ± 1.4 µm, p = 0.013) and venular caliber decreased (202.9 ± 1.9 to 197.3 ± 1.9 µm, p = 0.046) in the bariatric surgery group by 6 months, with no change in arteriolar (136.6 ± 1.1 to 134.5 ± 1.2, p = 0.222) or venular (195.1 ± 2.1 to 193.3 ± 2.2, p = 0.550) caliber in the control group. The arteriolar to venular ratio increased in the bariatric surgery group, with no change in the control group at 6 months. CONCLUSIONS: The findings suggest obesity-related microvascular changes are reversible after bariatric surgery-induced weight loss. The capacity for the retinal microvasculature to improve following bariatric surgery suggests plasticity of the human microvasculature early in the disease course.
STUDY AIM: Retinal microvasculature changes reflect systemic small vessel damage from obesity. The impact of bariatric surgery induced weight loss on the microvasculature is relatively unknown. We hypothesized that weight loss following bariatric surgery would be associated with improved structural changes in the retinal microvasculature, reflecting an overall improvement in microvascular health. METHODS: The study included 22 obese subjects scheduled for bariatric surgery (laparoscopic Roux-en-Y gastric bypass or a sleeve gastrectomy) and 15 lean, age-matched controls. Ophthalmic examination, including fundus photography, was performed at baseline and 6-months. Retinal microvasculature caliber was analysed quantitatively using a semi-automated computer program and summarized as central retinal artery equivalent (CRAE) and venular equivalent (CRVE). RESULTS: Mean weight loss at 6 months was 26.1 kg ± 8 kg in the bariatric surgery group. Retinal artery caliber increased (136.0 ± 1.4 to 141.4 ± 1.4 µm, p = 0.013) and venular caliber decreased (202.9 ± 1.9 to 197.3 ± 1.9 µm, p = 0.046) in the bariatric surgery group by 6 months, with no change in arteriolar (136.6 ± 1.1 to 134.5 ± 1.2, p = 0.222) or venular (195.1 ± 2.1 to 193.3 ± 2.2, p = 0.550) caliber in the control group. The arteriolar to venular ratio increased in the bariatric surgery group, with no change in the control group at 6 months. CONCLUSIONS: The findings suggest obesity-related microvascular changes are reversible after bariatric surgery-induced weight loss. The capacity for the retinal microvasculature to improve following bariatric surgery suggests plasticity of the human microvasculature early in the disease course.
Authors: Robyn J Tapp; Christopher G Owen; Sarah A Barman; Roshan A Welikala; Paul J Foster; Peter H Whincup; David P Strachan; Alicja R Rudnicka Journal: Obesity (Silver Spring) Date: 2020-07-29 Impact factor: 5.002
Authors: Robyn J Tapp; Christopher G Owen; Sarah A Barman; David P Strachan; Roshan A Welikala; Paul J Foster; Peter H Whincup; Alicja R Rudnicka Journal: Diabetologia Date: 2022-07-19 Impact factor: 10.460