Alpha cell function interacts with diet to modulate prediabetes and Type 2 diabetes |
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| Institution: | 1. Lipids and Atherosclerosis Unit, Department of Internal Medicine, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Spain;2. CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Córdoba, Spain;3. Department of Cell Biology, Physiology and Immunology, University of Cordoba, Córdoba, Spain;4. Nutrition and Genomics Laboratory, J.M.-US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA;5. IMDEA Alimentación, Madrid, Spain;6. CNIC, Madrid, Spain;1. Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE;2. Department of Cellular and Molecular Medicine, Cleveland Clinic, Cleveland, OH, USA;1. HOPE Cardiometabolic Research Team and Department of Physiology, College of Health Sciences, University of Ilorin, Nigeria;2. Cardiovascular Unit, Department of Physiology, College of Health sciences, Osun State University, Osogbo, Nigeria;3. Department of Public Health, Kwara State University, Malete, Nigeria;4. Cardiovascular Research Institute and Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-842, Republic of Korea;1. Food and Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada, R3T 2N2;2. Canadian Centre for Agri-Food Research in Health and Medicine, St. Boniface Hospital Research Centre, Winnipeg, MB, Canada, R2H 2A6;3. Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Winnipeg, MB, Canada, R2H 2A6.;1. Division of Endocrinology, Beth Israel Deaconess Medical Center (BIDMC), Harvard Medical School, 330 Brookline Ave, Slosberg-Landay SL-419, Boston, MA 02215, USA;2. Ansh Labs, Webster, TX 77598, USA |
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| Abstract: | Alpha- and beta-cells dysfunction is implicated in the development of Type 2 diabetes mellitus (T2DM). We aimed to evaluate whether alpha- and beta-cell dysfunction may precede prediabetes (PreDM) and T2DM development. Furthermore, we explored the role of two healthy diets (Mediterranean and low-fat diets) modulating these processes. We included 462 patients from the CORDIOPREV study without T2DM at baseline, of which 272 were PreDM. During follow-up, 107 patients developed T2DM (T2DM-incident group), 30 developed PreDM (PreDM-incident group), 86 regressed to normoglycemia (PreDM-regression group) and 29 patients remained without PreDM or T2DM criteria (control group), according to the American Diabetes Association diagnosis criteria. We measured glucose, insulin, glucagon and GLP-1 plasma levels in the OGTT performed at baseline and after 2 years of follow-up. Patients were randomized to consume two healthy diets, a Mediterranean (>35%) and a low-fat (<30%). At baseline we already observed higher levels of glucagon and glucagon/insulin (G/I) ratio in the T2DM-incident group compared with PreDM-incident and control groups. T2DM Risk Assessment by COX analysis using G/I ratio at 30 min after an OGTT was able to assess the T2DM risk with an HR of 2.514. The two dietary models differentially influenced the PreDM regression. Specifically, the consumption of Mediterranean diet was associated with a decrease in G/I ratio (P=.034), whereas the low-fat diet reduced insulin levels (P=.002). Our results suggest that alpha-cell dysfunction precedes the T2DM development. This process seems to be independent of diet consumed. However the PreDM regression might be differentially modulated by diets. |
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