ECE2023 Rapid Communications Rapid Communications 1: Diabetes, Obesity, Metabolism and Nutrition 1 (6 abstracts)
Angiotensin-converting enzyme in type II diabetes: effects of combined training on cardiovascular components and blood components
Andreia Matos 1,2,3 , Ângela Gil 1,2 , Isanete Alonso 1,4 , João P. Magalhães 5 , Ana Carolina Santos 1,2 , Rogério Ribeiro 6 , João F. Raposo 6 , Luís B. Sardinha 5 & Manuel Bicho 1,2
1Genetics Laboratory, Ecogenetics and Human Health, Instituto de Saúde Ambiental-ISAMB, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal; 2Instituto de Investigação Científica Bento da Rocha Cabral, Lisbon, Portugal, 3i3S-Instituto de Investigação e Inovação em Saúde, Tumour and Microenvironment Interactions Group, University of Porto, Porto, Portugal; 4Hospital St. Louis, Lisbon, Portugal; 5Exercise and Health Laboratory, Interdisciplinary Centre for the Study of Human Performance, Faculty of Human Kinetics, University of Lisbon, Lisbon, Portugal; 6Education and Research Center, APDP, Lisbon, Portugal
Objectives: The angiotensin-converting enzyme (ACE1) gene is one of the most studied genes in the pathogenesis of type II diabetes (T2DM) and cardiovascular disease. However, in the context of exerciSemodels in T2DM, they are not yet fully understood. We intended to characterize the genetic profile of individuals with T2DM from an inter-individual point of view using prognostic markers and cardiovascular risk. On the other hand, relate it with the profile obtained with the type of training: high-intensity intervals (HIIT) with resistance (RT); and moderate continuous (MCT) with RT.
Methods: Subjects with T2DM (n=80, 59 years old) underwent a 1-year randomized clinical trial (clinicaltrials.gov ID:NCT03144505) and were randomized into three groups (control, n=27; HIIT with RT, n=25; MCT with RT, n= 29). Biochemical parameters were determined by ELISA or standard methods at baseline and after 1 year of follow-up. ACE1 I/D genetic polymorphism was determined by PCR-RFLP.
Results: After 1 year, training had implications for c-peptide, insulin levels and basophil percentage in T2DM. Interestingly, although no differences were observed in the distribution of ACE1 genotypes, we observed that ACE1 DD (versus ID+II) individuals showed changes in VO2 max percentages, both in the initial phase of the study and after 12 months of training and follow-up. This finding may be related to a state of pseudo-hypoxia, due to aldosterone dysregulation and concomitant increase in sodium reabsorption in T2DM. When we used the Mendelian randomization model, that is, selecting the DD genotype of ACE1, we verified that individuals submitted to HIIT (versus control) presented alterations both in the percentage of monocytes, as in the mean of mean globular hemoglobin and mean corpuscular volume (P<0.05). On the other hand, in the same model, but for the MCT, we only verified that the DD individuals from ACE1 presented alterations in the number of platelets at the end of the training period.
Conclusions: Some blood count components have been associated with cardiovascular risk in patients with T2DM. With this study, we observed a differential profile between patients with DMII in the cardiovascular component possible related with ACE1 polymorphism.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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