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Alpha cell function interacts with diet to modulate prediabetes and Type 2 diabetes

Roncero-Ramos, Irene, Jimenez-Lucena, Rosa, Alcala-Diaz, Juan F., Vals-Delgado, Cristina, Arenas-Larriva, Antonio P., Rangel-Zuñiga, Oriol A., Leon-Acuña, Ana, Malagon, María M., Delgado-Lista, Javier, Perez-Martinez, Pablo, Ordovas, Jose M., Camargo, Antonio, Lopez-Miranda, Jose
The Journal of nutritional biochemistry 2018 v.62 pp. 247-256
Mediterranean diet, blood glucose, glucagon, glucagon-like peptide 1, glucose, healthy diet, insulin, islets of Langerhans, low fat diet, models, noninsulin-dependent diabetes mellitus, patients, risk, risk assessment
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.